Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241612EnglishN2014June23General SciencesINHIBITION OF CORROSION OF MILD STEEL IN 1M SULPHURIC ACID BY A NEW SCHIFF BASE
English0111P.M. DasamiEnglish K. ParameswariEnglish S. ChitraEnglishAim: Corrosion is a serious problem faced by all the industries. The use of inhibitors is a simple and cost effective method to control corrosion. This paper reports the synthesis of a novel Schiff base and its application as corrosion inhibitor for mild steel. Methodology: Inhibition behaviour of synthesized Schiff base for the corrosion of mild steel in 1M H2SO4was studied by weight loss measurements, potentiodynamic polarization, and andelectrochemical impedance spectra. Results: The results revealed that the efficiency depends on concentration of the inhibitor and temperature. The inhibitor obeys Langmuir isotherm indicating monolayer adsorption on the mild steel surface. Thermodynamic parameters show that the adsorption of the inhibitor on mild steel surface occurs through electrostatic attraction. Polarization studies show that the inhibitor behaves as mixed type in 1M H2SO4 affecting both anodic metal dissolution and cathodic hydrogen evolution. The formation of surface adsorptive film of the Schiff base on the mild steel surface was confirmed by SEM and EDX studies. Conclusion: The prepared Schiff base is found to be a very good inhibitor for the mild steel corrosion in sulphuric acid media even at low concentration offers more than 90% inhibition efficiency.
EnglishInhibitors, Schiff base, Thiadiazoles, Potentiodynamic polarization, Langmuir isotherm, Impedance.INTRODUCTION
Corrosion is an electrochemical process by which metallic surfaces react with their environment causing the metal to lose its material properties due to surface deterioration. The use of inhibitors is one of the most practical methods for protection of metal against corrosion, especially in acidic media.Organic compounds contain mainly oxygen, sulfur, nitrogen atoms, and multiple bonds in the molecules that facilitate the adsorption of the molecules on the metal surface1,2. The polar unit is regarded as the reaction center for the adsorption process. Thus, polar organic compounds are adsorbed on the metal surface, forming a charge transfer complex bond between their polar atoms and the metal. The size, orientation, shape and charge on the molecule determine the degree of adsorption and hence the effectiveness of the inhibitor. Various Schiff bases have been reported as effective corrosion inhibitors for steel. In the present work, the efficiency of a new synthesized Schiff base (TDIQ) as inhibitor for the corrosion of mild steel in 1M sulphuric acid was evaluated on the basis of weight loss,lectrochemical impedance spectroscopy (EIS), Tafel polarization data and SEM- EDX studies.
MATERIALS AND METHODS
Chemical composition of the mild steel The experiments were performed with cold rolled mild steel specimen of chemical composition (C=0.20%, Mn=1%,Si-0.05%,S=0.025%,P=0.25% and Fe=98%) Structure of the inhibitor (TDIQ
Corrosion monitoring methods Weight loss measurements were carried out with rectangular mild steel plates of dimension 3cm× 1cm× 0.1cm. The polished, preweighed plates were immersed in 1M H2SO4 containing various concentrations of the inhibitor for 3 hrs, then reweighed. From the loss in mass, inhibition efficiency was calculated. The effect of temperature on the inhibition efficiency was determined by carrying out the weight loss measurements at higher temperatures (303K-333K) The electrochemical studies were carried out with IVIUM Compactstat(potentiostat/galvanostat), using mild steel rod embedded in Teflon with exposed area 0.785 cm2 . The potential range is - 200 to +200 mV with respect to the open circuit potential at a scan rate of 1mV/sec. For impedance measurements, the sweep frequency is from 10Hz to 0.01KHz with a signal amplitude of 10mV SEM micrographs for the mild steel were recorded after 3 hrs of immersion in 1MH2SO4 solution with and without inhibitor. The synergistic effect was studied with 1mM KCl, KBr and KI in 1MH2SO4 with various concentration of the inhibitor, where inthepreweighed steel specimenwere immersed for 3 hours. From the weight loss, inhibition efficiency was calculated.
RESULTS \
Weight loss measurements Table-1 gives the Inhibition efficiencies obtained from the weight loss measurements of mild steel for different concentrations of the inhibitor. It is clear that the inhibition efficiency increased as the concentration of the inhibitor increased from 0.1mM to 0.5mM. Effect of temperature and thermodynamic parameters In order to study the effect of temperature on the inhibition efficiency and to determine the activation energy for the corrosion process, the weight loss studies were carried out at higher temperature(303K-333K).The results are given in the Table -2. It may be noted that the inhibition efficiency decreased with temperature. The corrosion rate (CR) of the mild steel in acidic media is related to the temperature by the ArrheniusequationLog CR = log A – Ea/ 2.303 RT Where CR is the corrosion rate, Ea is the apparent activation energy, R is the molar gas constant, T is theabsolute temperature and A is the frequency factor. The plot of log CR and 1/T gives linear plots(Fig.1) and the value of Ea is obtained from the slope of the straight line (Table -3) were calculated from the slope of the straight lines. An alternative form of Arrhenius equation is Corrosion rate= RT/Nhexp(?S 0 ads/R) exp(- ?H0 ads/RT) Where h is Planck’s constant, N is Avagrado number, ?S0 is the entropy of activation and ?H0 is the enthalpy of activation. Fig.2 shows a plot of log corrosion rate against 1/T. A straight line is obtained with slope of ?H0 ads/R and interceptlnR/Nh + ?S0 ads/R from which the values of ?H0 ads, ?G0 adsand ?S0 ads are calculated and are listed inTable -3. Langmuir Adsorption Isotherm Langmuir isotherm is an ideal isotherm for physical or chemical adsorption where there is no interaction between the adsorbate and adsorbent3 . A graph plotted between concentrationvs C/? gives a linear behaviour. Assumption of Langmuir relates the concentration of the adsorbate in the bulkof the electrolyte (C) to the degree of surface coverage (?) according to the equation, C/?= 1/K + C Where ‘K’ is the equilibrium constant of adsorption. Potentiodynamic polarisation study Potentiodynamicpolarisation studies on the mild steel have been made for the inhibitor in 1M H2SO4. The electrochemical parameters such as Icorr(corrosion current) and Ecorr(corrosion potential) obtained from Tafel plot for the inhibitor (Fig. 4) is given in Table 4. The Icorrvalue decreases as compared to the blank value and at 0.5mM of inhibitor, the Ecorr value is slightly shifted towards negative direction. Tafel constants ba and bcare affected with increase in concentration of the inhibitor. Electrochemical impedance spectroscopy Nyquist plot of mild steel in uninhibited and inhibited acidic solutions containing various concentrations of TDIQ are given in Fig-5.The impedance parameters derived from Nyquist plots are given in Table -5. It was observed that there is a gradual decrease in Cdl(double layer capacitance) value with increase in concentration from 0.05 to 0.5 mM, whereas the Rct(charge transfer resistance) increases with the concentration of the inhibitor. Effect of halide ions The synergistic effect provided by the addition of halide ions such as I-, Br-, and Cl- to the solutioncontaining 1M H2SO4 and the inhibitor was studied by weight loss method and the data is presented in Table-6. Analysis of the data reveals that the addition of halides to the inhibitorincreases the inhibition at each concentration of the inhibitor used. It has been reported that the surface of iron is found to be positively charged in an inhibitor free sulphuric acid media4 . When the inhibitor is added, the nitrogen atoms present get protonated to form a cation. Hence they would be less strongly adsorbed. However, when halide ions are added,they are strongly chemisorbed on the positively charged steel surface. This makes the organic cations to be adsorbed on the layer of the anions. This is called co-operative adsorption and is responsible for the increased IE of the inhibitor in presence of halide ions. Scanning Electron Microscopy Studies The surface morphology of carbon steel surface was evaluated by Scanning Electron Microscopy (SEM). Fig. 6,7and 8show the SEM image of the polished mild steel surface, steel surface immersed in 1M H2SO4and with TDIQ.It is clear that in the absence of the inhibitor, the surface is highly corroded. However in the presence of inhibitor the rate of corrosion is suppressed. EDX Studies Energy-dispersive X-ray (EDX) spectroscopy was used to determine the elements present on the metal surface before and afterexposure to the inhibitor solution. Fig. 9 and 10 show the EDX graph for the mild steel immersed in 1M H2SO4and with TDIQ. The EDX graph shows that the presence of nitrogen, sulphur, oxygen atoms present in the inhibitor, which is adsorbed on the mild steel surface.
DISCUSSION
The inhibition efficiency increased as the concentration of the inhibitor increased.The behavior may be attributed to an increase in surface coverage,? by the adsorption of inhibitor on the mild steel surface, in the aggressive solution, which restricts the dissolution of the metal. The inhibition efficiency decreased with temperature. This may be attributed to desorption of the inhibitor molecule from metal surface at higher temperature5 .This is also supported byEa (Activation energy) value, which is higher in the presence of inhibitor as compared with that in the absence which is characteristics of physisorption of the inhibitor andformation of an absorptive film of electrostatic nature6 . Negative ?G0 ads(change in Gibb’s Free energy of adsorption) values indicate spontaneity of the adsorption process and the values are less than 40kJ/mol showing that the inhibitor is adsorbed on mild steel by physisorption. The negative sign of enthalpy ?H0 ads(change in enthalpy of adsorption) reflects the exothermic nature ofsteel dissolution. Negative entropy imply that the formation of activated complex is the rate determining step and represents an association rather than dissociation and that a decrease in disorder occurs7 . Applicability of Langmuir isotherm to the adsorption of inhibitor on mild steel confirms the formation of monolayer adsorption where there is interaction between the adsorbate and the adsorbent8 . In the electrochemical studies, Icorr is reduced in presence of Schiff base showing the efficiency of the inhibitor.Tafel constants ba and bcare affected with increase in concentration of the inhibitor suggests that the inhibitor is mixed type9 . In the EIS study, the Nyquist plots are semicircular in appearance indicating that charge transfer process controls the corrosion of mild steel10. The decrease in Cdl value results from increase in surface coverage by the inhibitor, which lead to an increase in Inhibition Efficiency (IE). The synergistic influence of halide ions is more for I- ion which may be attributed to the large size and ease of polarisibility of I- ion which facilitates stronger chemisorption with iron surface. The SEM image observations suggest that the inhibitor forms a protective layer on the surface that prevents the attack of acid on the metal11. The EDX studies inferred that the molecule interactedstrongly with the metal through sulphur atom12 . Corrosion inhibition mechanism From the obtained results of various experimental techniques used, it was concluded that the synthesized Schiff base inhibit the corrosion of mild steel in 1M H2SO4 by adsorption at the metal–electrolyte interface. Two modes of adsorption can be considered. The physical adsorption requires the presence of charged metal surface and charged inhibitor species in the solution, while chemisorption involves charge sharing or charge transfer from the inhibitor to the metal surface. TDIQ,whichposseses N and S atoms with lone pair of electrons and also π electrons of the aromatic rings. The thermodynamic parameters suggest a physisorption mechanism prevails with the studied Schiff base. The effective performance of the inhibitor may be due to the electrostatic interaction between the positively charged Fe surface and the π electron of aromatic rings and azomethine group and also the lone pair of the electron on N and S atoms.
CONCLUSION
The synthesized Schiff base is a very good inhibitor for the corrosion of mild steel in 1M H2SO4. The inhibition efficiency increases with increase in concentration of the inhibitor and decrease with temperature. The inhibitor acts by adsorption on the mild steel surface and the adsorption obeys Langmuir isotherm. Electrochemical studies show that the inhibitor is mixed type but slightly cathodic. SEM and EDX studies revealed the formation of a protective film of the inhibitor on the steel surface.
ACKNOWLEDGEMENT
Authors acknowledge theimmense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=830http://ijcrr.com/article_html.php?did=830REFERENCES
1. Bentiss F, Traisnel M, Hildebrand HF, Lagrenee M, 2,5 –bis (4- dimethylaminophenyl)-1,3,4- oxadiazoleand 2,5-bis (4-dimethylaminophenyl)1,3,4- thiadiazole as corrosion inhibitors for mild steel in acidic media.Corro. Sci. 2004; 46: 2781-2792
2. Ozcan M, Dehri I, Erbil M, Organic sulphur containing compounds as corrosion inhibitors for mild steel in acidic media: correlation between inhibition efficiency and chemical structure. Appl. Surf. Sci., 2004; 236: 155- 164.
3. Elawady GY, El-Said IA, Fouda AS, Anion surfactants as corrosion inhibitors for aluminium dissolution in HClsolutions.Int.J.Electrochem. Sci, 2008; 3: 177-190.
4. Martinex. S, Stern. I, Thermodynamic characterization of metal dissolution and inhibitor adsorption processes in the low carbon steel/mimosa tannin/suphuric acid system. Appl. Surf. Sci. 2002; 199: 83-89
5. Ananthkumar Ra S, Sankar A, Ramesh kumarS,Corrosion Inhibition Of Mild Steel In 0.5M H2SO4 By 1-(2-Methyl-4-(2- Methylphenyldiazenyl) Phenyl) Azonapthalen-2-ol. Am. J. of Engg Res. (AJER), 2013; Volume-02, Issue-09: 17-22.
6. PopovaS,SokolovaA, Raicheva S, ChristovM., AC and DC study of the temperature effect on mild steel corrosion in acid media in the presence of benzimidazolederivatives.Corro. Sci.2003; 45: 33-58 Bockris JOM., ReddyAKN., Mod.Electrochem.,vol 2, Plenum Press, Newyork (1977) 126
7.
8. Chitra. S, ParameswariK., Vidhya. M,Kalishwari M, and SelvarajA., Sulpha Schiff bases are corrosion inhibitors for mild steel in 1M H2SO4, Int. J. Electrochem. Sci., 2011; 6: 4593
9. Bentiss. F, Lebrini M, LagreneM. , Thermodynamic characterisation of metal dissolution and inhibitor adsorption processes in mild steel /2,5-bis(n-thionyl)- 1,3,4- thiadiazoles / hydrochloric acid system,Corros. Sci2005;47: 2915-2931.
10. Jayaprabha C, Sathiyanarayanan S, VenkatachariG., Influence of metal cations in the inhibitive effect of polyaniline for iron in 0.5M H2SO4, Mater.chem.and phy 2005; 107: 350.
11. Shaju KS,Joby Thomas K, Vinod P. Raphael, and Aby Paul, Electrochemical and Surface Morphological Studiesof Carbon Steel Corrosion by a Novel Polynuclear SchiffBase in HCl Solution. ISRN Electrochem, 2013; http://dx.doi.org/10.1155/2013/820548
12. Rajappa SK, Venkatesha TV, Praveen BM, Chemical treatment of zinc surface and its corrosion inhibition studies. Bull. Mater. Sci., 2008;31: pp. 37–41.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241612EnglishN2014June23General SciencesINTER CORRELATION STUDIES AMONG YIELD AND ITS CONTRIBUTING TRAITS IN BREAD WHEAT GENOTYPES GROWN IN HARYANA, INDIA (TRITICUM AESTIVUM L.)
English1218Sumit ChhibberEnglish Divya JainEnglishThe attainment of maximum crop yield is an important objective in most breeding programmes. Grain yield is a complex trait influenced by a number of yield contributing traits. Information on the association of morpho-agronomic traits with grain yield forms a basis for any successful breeding programme. The present study was conducted to estimate the inter-relationships and interdependence between grain yield and its contributing as well as influencing traits by computing coefficients of simple, partial and multiple correlations analysis for the currently cultivated three bread wheat genotypes in Haryana, namely, HD 2932, HD 2967 and HD 2851.The varieties were evaluated for the traits-shoot height, tiller numbers, grain yield, 1000-grain weight, vegetative dry matter content, reproductive dry matter content, biological yield and harvest index. The results revealed that the grain yield depicts significant positive correlation with shoot height, tiller number, vegetative dry matter content, and reproductive dry matter content and biological yield. Based on the results, it is reasonable to assume that high yield of wheat plants in these genotypes could be obtained by selecting breeding materials with high tiller number, reproductive dry matter content and biological yield.
EnglishTriticumaestivum L., correlations, grain yield, biological yield.INTRODUCTION
Wheat, (Triticumaestivum L.), an allohexaploid belongs to the family Poaceae. It is accorded a premier place among cereals because of the vast acreage devoted to its cultivation, high nutritive value and its association with some of the earliest and most important civilizations of the world. Wheat is the second most important staple food after rice in India grown on about 29.8 million hectares and generally provides about 50% of the calories and protein requirement to a vast majority of the Indian population.The production of wheat in the country has increased significantly from 75.81 million MT in 2006-07 to an all time record high of 94.88 million MT in 2011-12 [1]. Currently, India is second largest producer of wheat in the world. To meet the demand of rising population, the major efforts of wheat breeders have been directed towards improving its grain yield. Grain yield is a quantitatively inherited character highly influenced by environmental factors and exhibits a profound genotype-environment interaction [2],[3]. Therefore, direct improvement of yield has not been possible through traditional breeding techniques. Instead traits affecting and influencing yield have been identified and selection has been exerted on those characters which show a close association with grain yield. Yield contributing traits can be identified through morphological and molecular markers [4],[5]. Morphological characters whichcontribute towards grain yield of wheat crop include characters like plant height, leaf area, spike length, number of spikelets/spike, iller number and 1000-grain weight [2], [6], [7]. An estimate of this inter-relationship and interdependence between yield and its contributing as well as its influencing traits is important for effective utilization of the genetic stock [2], [8], [9] and [10]. The correlation coefficient analysis is useful in the identification of the characters that are positively correlated with yield [11], [12], [13],[14].The quantification and interpretation of these correlations can result in mistakes on selection strategies, since a high correlation can be the result of a third trait or a group of traits affecting these traits. In this scenario, partial and multiple correlations are the tools available to the plant breeder for better understanding the causes involved in associations between traits [15],[16]. Therefore, an attempt was undertaken to estimate correlations existing between grain yield, its components and other metric traits in three bread wheat genotypes grown in Haryana, India namely,HD 2932, HD 2967 and HD 2851. The information could be used to define the suitable criteria for further yield improvement in these varieties.
MATERIALS AND METHODS
The experimental plot was designed at a private farm in village Galoli, district Yamuna Nagar, Haryana in 2012-2013 main cropping season. Certified seeds of three varieties commonly grown in Haryana, namely, HD 2932, HD 2967 and HD 2851 were sown in a randomized block design having three replications in the first week of November. Each replication had one row of 5 metre length of each one of genotype. Row to row distance was maintained roughly 18-20 cm and plant to plant distance was kept approximately 6cm. Recommended agronomic practices were applied to the experimental material throughout the growing period. Data of randomly selected 10 plants per replication of the three varieties currently cultivated in India, namely, HD 2851, HD 2932 and HD 2967was recorded for the traits shoot height, effective tiller numbers, grain yield, 1000-grain weight, vegetative dry matter content weight, reproductive dry matter content weight and biological yield.The data obtained was subjected to coefficients of simple, partial and multiple correlations analysis according to the method proposed by Falconer [8],[17].
RESULTS AND DISCUSSION
The three wheat varieties HD 2851, HD 2932 and HD 2967 present an interesting aspect of the existence of positive and significant correlation among various metric traits in these varieties [Table 1]. Grain yield is positively correlated with shoot height, tiller number, vegetative dry matter content, and reproductive dry matter content and biological yield. Positive correlation of grain yield with shoot height has been reported by other workers [18],[19],[20],[21],[22],[23]. Similarly, positive correlation with tiller number has also been reported in different wheat genotype [6],[10],[15],[24]. Vegetative dry matter content and reproductive dry matter content are positively correlated with tiller number, grain yield and biological yield. Both these traits have insignificant negative correlation with plant height. Biological yield is positively correlated with tiller number, grain yield, and vegetative dry matter content and reproductive dry matter content. Positive correlation between biological yield and grain yield suggest that grain yield can be increased by increasing biological yield as it would help to accumulate more photosynthates to developing grain. This result concurs with the findings of many investigators [25], [26], [27], [28],[29],[30]. Correlation between 1000 grain weight and grain yield is insignificant.Insignificant correlation between grain weight and grain yield has been reported in other bread wheat varieties [31],[32], [33]. Partial correlation also indicates that significant and positive correlation retains between grain yield and shoot height and insignificant correlation persists between grain yield and grain weight even when the influence of various metric traits studied are partialled out one by one [Table 2]. Likewise the correlation between grain yield and vegetative dry matter content; and grain yield and biological yield stays significant and positive when the influence of shoot height, tiller number and grain weight are partialled out one by one [Table 3]. Significant correlation exists between grain yield and tiller number when the influence of shoot height, grain weight and vegetative dry matter content is partialled out. Keeping grain yield as the dependent variable and other traits shoot height, tiller number, grain weight, vegetative dry matter content, reproductive dry matter content and biological yield as the independent variable, the coefficient of multiple correlation values are high, positive and significant[Table 3]. This indicates a high dependence of the variance in grain yield over the variances in the above mentioned traits. However, the correlation between grain yield and tiller number is insignificant in association with trait grain weight [Table III]. Thus, these traits appear to have low contribution to the variance in grain yield. The positive correlation between grain yield and shoot height clearly indicate that increase in grain yield will be accompanied by increase in shoot height.The increase in shoot height is not useful as the partitioning of the resources may lose balance and tilt towards shoot height increments [25],[33]. The positive correlation of grain yield with vegetative dry matter content and biological yield supports this contention. This contention is further supported by the existence of positive correlation among vegetative dry matter content, reproductive dry matter content and biological yield in the three wheat varieties. Partial correlations and multiple correlations also indicate strong dependence of grain yield over shoot height, tiller number, vegetative dry matter content and biological yield. Vegetative dry matter content and biological yield being exponential components of shoot height and negatively correlated with shoot height, therefore, the correlation studies in HD 2851, HD 2932 and HD 2967 for various metric traits indicate that the increase in grain yield is possible in these varieties through breeding for an increase in effective tiller numbers of wheat genotypes, high reproductive dry matter content, vegetative dry matter content and biological yield.
CONCLUSION
Based on the correlation studies, it is recommended that the increase in grain yield in HD 2851, HD 2932 and HD 2967 is possible through breeding for an increase in effective tiller numbers, high reproductive dry matter content, vegetative dry matter content and biological yield.
ACKNOWLEDGEMENT
The authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / Publishers of all those articles, journals and books from where the literature for this paper has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=831http://ijcrr.com/article_html.php?did=831REFERENCES
1. Annual Report (2012 – 13): Directorate of Wheat Research, Karnal - 132001 (India)
2. Drikvand, R., Bihamta, M.R., Najafian,Goodarz., Ebrahami,Asa.(2013). Kernel Quality Association and Path Analysis in Bread Wheat. International Journal of Biology,5 (3): 73-79.
3. Mohammadi, M., Peyman, S., Karimizadeh, R. (2014). Sequential Path Analysis for Determination of Relationship between Yield and Yield Components in Bread Wheat (Triticumaestivum L.) Not Sci Biol. 6(1):119- 124.
4. Naghavi,M.R., Monfared, S.R., Ahkami, A.H. and Ombidbaksh, M.A.(2009). Genetic variation of durum wheat landraces and cultivars using morphological and protein markers. Int. J. Biol. Life Sci.,1(2): 68-70.
5. Collard, .B.C.Y., Jahufer, M.Z.Z., Brouwer, J.B. and Pang, E.C.K.(2005). An introduction to markers, quantitative trait loci (QTL) mapping and marker-assisted selection for crop improvement: The basic concepts. Euphytica142: 169-196.
6. Degewione,A., Dejen, T. and Sharif, M. (2013).Genetic variability and traits association in bread wheat (Triticumaestivum L.) genotypes. International Journal of Agricultural Sciences 1(2): 19-29.
7. Fellahi,Z.,Hannachi,A.,Bouzerzour,H. And Boutekrabt,A.(2013). Correlation between traits and path analysis coefficient for grain yield and other quantitative traits in bread wheat under semi arid conditions. Journal of Agriculture and Sustainability 3(1):16-26 .
8. Falconer D.S. and Mackay T.F.C., 1996, Introduction to quantitative genetics. 4th ed. Benjamin Cummings, England.
9. Kumar,S., Dwivedi,N.K. ,Tyagi,N.K., Kumar,S. (2003). Genetic variability in some metric traits and its contribution to yield in wheat (Triticumaestivum L.). Progressive Agric., 3(1-2):152-153.
10. S.J. Khan, Kalimullah.,Irfaq, M., Rahman, H.U. (2012). Genetic variability, correlation and diversity studies in Bread wheat (Triticumaestivum L.) germplasm. The Journal of Animal and Plant Sciences, 22(2): 330-333.
11. D. M., Langade.,Shahi, J. P., Srivastava, K., Singh, A., Agarwal, V. K ., Sharma, A. (2013). Appraisal of Genetic Variability and Seasonal Interaction for Yield and Quality Traits in Maize (Zea mays L.), Plant Gene and Trait 4(18) : 95-103.
12. Ahmad S.Q., Khan S., Ghaffar M., and Ahmad F.( 2011). Genetic diversity analysis for yield and other parameters in maize (Zea mays L.) genotypes, Asian J. Agric. Sci., 3(5):385-388.
13. Mohammadia S.A., Prasanna B.M., and Singh, N.N. (2003). Sequential path model for determining interrelationship among grain yield and related characters in maize, Crop Sci., 43:1690-1697.
14. Maqbool,R., Sajjad,M., Khaliq,I., Aziz-urRehman, Khan,A.S. and Khan, S.H.(2010). Morphological Diversity and Trait Association in bread wheat (Triticumaestivum L.) American-Eurasian J.Agric. & Environ. Sci. 8(2):216-224.
15. Muhammad Zeeshan, WaheedArshad, Muhammad Imran Khan, Shiraz Ali, Muhammad Tariq (2014). Character association and casual effects of polygenic traits in spring wheat (Triticumaestivum L.) genotypesInternational Journal of Agriculture, Forestry and Fisheries. 2(1): 16-21.
16. Savii G., Nedelea, G.(2012). Estimation of interrelationships among different yield traits in winter wheat: Journal of Horticulture, Forestry and Biotechnology, Volume 16(1), 115-118.
17. Falconer,D.S. (1981). Introduction to quantitative genetics. Longman(London and New York).
18. Law,C. N. , Snape, J. W. and Worland, A. J.(1978). The genetical relationship between height and yield in wheat. Heredity 40, 133– 151.
19. Mohtasham,M., Peyman, S., Rahmatollah, K. and Mohammad Kazem, S. (2012). Relationships between Grain Yield and Yield Components in Bread Wheat under different water availability (Dryland and Supplemental Irrigation Conditions).Not.Bot.Horti. Agrobo. 40(1):195-200.
20. Ali, MA., Abbas, A., Awan, SI., Jabran, K., Gardezi, SDA. (2011). Correlated response of various morpho-physiological characters with grain yield in sorghum landraces at different growth phases. J. Animal Plant Sci. 21(4):671- 679.
21. Leilah, AA. And Al-Khateeb, SA. (2005). Statistical analysis of wheat yield under drought conditions.J. Arid. Env. 61:483-496.
22. SaifUllahAjmal, NahidZakir, Muhammad YaqoobMujahid(2009). Estimation of Genetic Parameters and Character Association in WheatJ.Agric.Biol.Sci.1(1):15-18.
23. Jamali,R and Jamali, KD (2008): Correlation and regression studies in semi dwarf wheat(Triticumaestivum L.) Proceedings of the 11th International Wheat Genetics Symposium, Brisbane Australia 675-677.
24. Beheshtizadeh, H., Rezaie, A., Rezaie, A. and Ghandi, A. (2013).Principal component analysis and determination of the selection criteria in bread wheat (TriticumaestivumL.) genotypes.Intl. J. Agri. Crop Sci. Vol., 5 (18), 2024-2027.
25. Bahari,N., Bighdilu, B.B., Karpisheh,L (2014): Studying the correlation and analyzing the path coefficient between grain weight and the traits related to remobilization of assimilates in bread wheat genotypes. J. Bio. &Env. Sci. Vol. 4, No. 3, p. 303-308.
26. Khan, A., Barma, N. C. D., Hasan, M. M., Alam, M. A. and M. K. Alam (2014). J. Agric. Res., 52(1) p.11-23.
27. Chaturvedi, B. K. and R. R. Gupta(1995). Selection parameters for some grain and quality attributes in spring wheat (T. aestivum L.). Agric. Sci. Digest. 15(4): 186-190, Karnal, India.
28. Subhani, G. M., S. Ahmed and M. A. Chowdhury(2000). Correlation and path coefficient analysis in bread wheat under drought stress and normal conditions. Pakistan J. Biolog. Sci. 3 (1): 72-77.
29. Singh, I., A. S. Radhu and Y. Tindal (1997). Harvest index a better selection criterion for yield improvement in bread wheat. Haryana Agril. Univ. J. Res. 7(1): 27-30.
30. Fellahi, Z., Hannachi, A., Bouzerzour, H. and Boutekrabt, A. (2013). Journal of Agriculture and SustainabilityVolume 3, Number 1 , 16- 26.
31. MoneimBabuFatih, A.(1986).Genotypic and phenotypic associations of grain yield, grain protein and yield related characteristics in wheat-Agropyron derivatives Hereditus 105: 14I-l53 .
32. Yousaf,A., Atta, B.M., Akhter,J., Monneveux,P. and Lateef, Z.(2008). Genetic Variability, Association and Diversity Studies in Wheat (Triticumaestivum L.) Germplasm.Pak. J. Bot., 40(5): 2087-2097.
33. Iftikhar, R., Khaliq I., Ijaz, M. and Rashid, M.A.R.(2012). Association Analysis of Grain Yield and its Components in Spring Wheat (Triticumaestivum L.) American-Eurasian J. Agric. & Environ. Sci., 12 (3): 389-392
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241612EnglishN2014June23HealthcareLIQUID BASED CYTOLOGY- IS IT A GOOD ALTERNATIVE?
English1927Sonti SulochanaEnglish Divya GopalanEnglish Chitra SrinivasanEnglishThe objectives of the study were to evaluate Liquid Based Cytology (LBC) over conventional Pap smear with respect to adequacy of smear, preservation of morphological features, clarity of background, detection of infective organisms and dysplastic cells. Methodology: the samples were collected at the OBG clinic using the cytobrush, and Pap staining and analysis was done in the Department of Pathology. The sample size was 114. Under speculum examination, the cytobrush was introduced into the cervical os and scraped. The material was smeared onto a slide to prepare a conventional Pap smear. The brush was then dropped into a vial containing the preservative. This sample was then subjected to processing which dispersed the sample to separate the representative cells and unwanted cell debris. A smear was then prepared using the required cells. Both smears were stained by the routine Pap stain and examined under a microscope. Their findings were recorded and the differences were analyzed. Results: There was not much difference in the sensitivity between the conventional Pap smear and LBC in detecting infective organisms. However dysplastic changes were detected in two smears using LBC whereas this was not possible using the conventional smear. Conclusion: Using LBC it was possible to detect infective organisms even when their load was low. Since the cells are in a monolayer, and the smear is uniformly prepared, the quality of the smear is improved thereby decreasing the screening time and easier to read. Therefore LBC can be considered superior to conventional smear with respect to adequacy of smear, preservation of morphological features, clarity of background, detection of infective organisms like bacterial vaginosis, trichomonas vaginalis, Candida etc and dysplastic cells.
EnglishLBC, Pap smear, bacterial vaginosis, trichomonas vaginalis, Candida
Englishhttp://ijcrr.com/abstract.php?article_id=832http://ijcrr.com/article_html.php?did=832REFERENCES
1. Murthy NS, Chaudhry K, Saxena S. Trends in cervical cancer incidence--Indian scenario. Eur J Cancer Prev. 2005 Dec;14(6):513-8.
2. Automation assisted and liquid based cytology for cervical cancer Screening, MSAC application 1122, Assessment report, sept 2009;page2
3. Dr. Amal AbdElHafez, Lecturer of pathology, Faculty of medicine – Mansoura University, Egypt. Liquid based cytology, ppt- accessed on 7- 10-2013.
4. Pierre Martin-Hirsch, MD, PhD, Albertus G. Siebers, MSc, and Johan Bulten, MD, PhD, Arbyn et al. Liquid Compared With Conventional Cervical Cytology: Jan 2008;3:1
5. "http://en.wikipedia.org/wiki/Pap_test#Effecti veness-accessed on 7-10-2013.
6. Dr Hilary Fielder, Liquid based cytology-pilot project, 2003.
7. Robert Lotocki, MD, FRCSC, Medical Director, Cervix Check, Cancer Care Manitoba, New Cervical Screening Technologies: Liquid-Based Cytology and HPV Testing presentation, sept 2011.pdf, accessed on 7- 10-2013.
8. Payne et al. Health Technol Assess 2000;4(18):1-73)
9. National Institute for Clinical Excellence (2000) Guidance on the use of liquid-based cytology for cervical screening, October 2003; Page 6
10. "http://en.wikipedia.org/wiki/cervical screening-accessed on 7- 10-2013.
11. Edmund S. Cibas , Cervical and vaginal Cytology, Nov 2002;11:42 Page 4
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241612EnglishN2014June23HealthcareCANTHARIDIN POISONING IN TWO MONTH OLD INFANT: CASE REPORT
English2832Ibrahim Al HelaliEnglish Ali HakamiEnglish Saleh Al-QahtaniEnglishCantharidin is a lipid soluble irritant extracted from the blister beetle. Manifestations of cantharidin poisoning range from local vesiculobullous formation to systemic manifestations involving central nervous system, renal system and gastrointestinal system. We report a case of systemic cantharidin toxicity in 2 month old infant secondary to cutaneous cantharidin toxicity which was managed conservatively and discharged in good health after 6 days.
EnglishCantharidin, poison, blister beetle, infant, Saudi ArabiaINTRODUCTION
Cantharidin (haemolymph exudation through leg joints or/and antennal pores) is among the most widely known insect natural products and primarily found in the true blister beetles, Meloidae, and secondarily in false blister beetles, Oedemeridae. It was discovered in haemolymph and gonads of the blister beetle, commonly known as Spanish fly Lytta vesicatoria (Linnaeus), in quantity larger than any other member of blister beetles. It is one of the oldest-known toxins from insects and has been known to humans for more than 2000 years due to its physiological activities such as blistering. Also, it is highly toxic to a wide variety of animals, including birds, amphibians and mammals.1 Historically, the best known true blister beetle is the Spanish fly Lytta vesicatoria Linnaeus which fills its breathing tube with air and closes its breathing spiracles (pores) to elevate body pressure in order to force out some droplets of haemolymph containing the toxic cantharidin through its leg joints. Taken internally or absorbed through the skin, cantharidin (or cantharides) is highly toxic to mammals. For man, the most common beetle injury is not from a bite or sting but from the formation of blisters (dermatosis) when roughly contacted with the soft skin and from the cantharidiasis (cantharidin poisoning) when ingested orally.1 Few cases of cantharidin toxicity were reported in pediatrics through ingestion of the beetle itself but as far as we know there is only one reported case of cantharidin toxicity due to skin blistering secondary to skin contact with the beetle. In this case, we report cantharidin toxicity in 2 months old infant after skin contact with beetle blister.
CASE REPORT
A 2 -month - old Saudi girl previously healthy presented with one attack of generalized tonic clonic convulsion for 5 minutes. Convulsion was associated with high grader fever and irritability which started 2 days before. The girl had 3 attacks of coffee ground vomitous and 3 to 5 attacks of watery diarrhea with mucus but no blood. Her oral intake was poor. Her urine was concentrated and the color was dark yellow. There was no history of skin rash or contact with sick patient. She has no history of previous seizures or other medical problems. She is developmentally normal. Family history is noncontributory. Her family has no medical problems and living in Khamis Mushayt city (Aseer region) in the Southwest of Saudi Arabia. Family history is noncontributory. The family lives in Khamis Mushayt city (Aseer region) in the Southwest of Saudi Arabia. On arrival to pediatric emergency, she was in hypovolomic shock with Glasgow coma scale of 11/15. Capillary refill time was more 3 seconds. She was hypotensive with blood pressure of 70/32 mm Hg. Pulse rate was 160/minutes. Respiratory rate was 54/minutes and temperature was 39ºC. She was maintaining normal oxygen saturation at room air. The examination of the heart, respiratory system, gastrointestinal system was normal. She had hypertonia and hyper-reflexia for both upper and lower limbs with no apparent skin rash initially. Immediately, resuscitation was started with normal saline boluses and she showed response after the second bolus of normal saline informs of improving her blood pressure but she continued to be irritable. Her initial complete blood count showed leukocytosis (29000/cc), normal hemoglobin level (12.3 mg/dl) and normal platelets count (238000/cc). Blood urea nitrogen was 161 mg/dl and creatinine was 2.3 mg/dl. Her serum sodium was 156 mmol/l, potassium 4.8 mmol/l, calcium was 6.7mg/dl and serum ammonia was 157 mmol/l. Alkaline phosphatase was 351 u/l, serum alanine aminotransferase (ALT) was 275 u/l, Serum aspartate aminotransferase (AST) was 279 u/l and lactate dehydrogenase was 1215. Total bilirubin was 1.8 mg/dl. Her blood gases showed severe metabolic acidosis, PH:7.0, PCO2:27 and HCO3:10. Blood gases were normalized after 24 hours.
After stabilization she was shifted to pediatric ICU for close monitoring and management. Full sepsis screening was done including cerebrospinal fluid analysis and culture and was started on broad spectrum antibiotics. In the second day, her hemoglobin dropped to 7.2 mg/dl and here urine analysis showed numerous RBCs with 2 plus proteins and he was transfused with packed RBCs. During physical examination on day 2, a oval shape raised redness was observed on the lower part of the neck on the right side (Figure 1). It was about 1.5 by 1.0 cm in size in the middle of the redness there were 2 small ulcers with dirty sloughing base and ragged edges. The family did not notice this redness before but they mentioned that a beetle was seen in the clothes of the girl near to the site of redness earlier before the girl got sick. The family was asked if they can bring the beetle, which was brought in an empty water bottle (Figure 2). From here the beetle was identified to be Hycleus maculiventris (the family Meloidae) and the girl sickness was explained. The girl was continued on supportive care and she was improving with time and discharged on day 6 with completely normal clinical status and laboratory results. The sepsis screening which was done and came to be normal.
DISCUSSION
The case above described cantharidin toxicity resulting from the contact of blister beetles with the infant body. The beetle in this case was positively identified as Hycleus maculiventris (the family Meloidae). These beetles emit cantharidin laden body secretions which cause painful blisters and lesions on human skin when touched. Beetles of this species are usually black and yellow in colour with some being black and red, and others being all black.3 The bright colours that may warn would be predators, can unfortunately be attractive to children. Percutaneous absorption of cantharidin leading to systemict oxicity must not be under-rated since its high lipoid/ water partition coefficient permits rapid diffusion across the stratum corneum.10 As far as we know, this is the youngest patient who presented with cantharidin toxicity. There are few cases of cantharidin toxicity in children secondary to ingestion of the blister beetle.2,4,6 The clinical presentation was almost the same. Usually it starts by vomiting and abdominal pain shortly after the ingestion of the insect with drowsiness,2,4,6 Associated with fever in 3 patients. Some of those patients presented with gastrointestinal bleeding with different degrees and some with increasing liver enzymes.4 One patient presented with seizure.4 Renal involvement was there in most of patients with microscopic or gross heamaturea with renal impairment and electrolytes disturbance.2,4,6 Usually, the diagnosis was made by identifying the insect in the vomitus. The treatment were supportive in all cases and all patients were discharged in good health without any complications except one who died may be secondary to ingestion of large amount of insects.3 There is only one report of cantharidin toxicity in children secondary to skin contact with blister beetle.2 He presented with multiple blebs on his face and hand after touching the blister beetle and shortly after that he started to have heamaturea then he became quite deeply stuporous. The child's urine contained much protein and numerous erythrocytes and leucocytes, in proportions similar to those of whole blood. No ova were seen (vesical schistosomiasis does not occur in this district), and no organisms were found on examination of the fresh specimen or after staining. No casts were een.2 The blood showed a leucocytosis of 12,300 cells per cc. Leukocytosis was present in most cases of cantharidin toxicity including our patient. According to Craven and Polak (1954), cantharidin has a specific effect of inducing a leukoerythroblastic response.6 The faeces, though macroscopically normal, contained numerous erythrocytes. The bullae on skin and mucosa increased in size, coalesced, and then burst, leaving ulcers with a dirty sloughing base and ragged edges. He improved in 3 days time and went home in good health.2 In our report, the age of the child makes things difficult. She presented with high grade fever with seizure. This raised the possibility of central nervous system infection. The abnormal renal profile and electrolytes disturbance, can be explained initially by pre-renal hypovolomic shock and sepsis. The diagnosis of cantharidin toxicity was suspected after observing the skin lesion (most likely during the stage of ulcer) and by obtaining more history from the family about any presence of such insects at home and then by identification of the insect the diagnosis was made. In adults, there are a lot of reports about cantharidin toxicity9,11 and some reports about toxicity in animals.8 Spanish flies and other meloids have historically been used medicinally as aphrodisiacs, skin irritants, vesicants and abortifacients,1,4,10 such uses cause many cases of toxicity in adults. All patients with cantharidin were treated by general supportive measures based on the clinical presentation and they did well. There is no anti dote for cantharidin1,4,6 For topical exposure, the affected area should be cleaned with acetone, ether, fatty soap or alcohol, which helps to dissolve and dilute the cantharidin. Topical steroids may be applied to intact skin if it is symptomatic.7 CONCLUSION Cantharidin toxicity is difficult to diagnose and cases can be missed especially in young infants in the absence of history about contact with the insect. Awareness about such kind of presentation and high index of suspicion is highly needed.
ACKNOWLEDGMENT
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors/editors/ publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=833http://ijcrr.com/article_html.php?did=833REFERENCES
1. Karem S. Ghoneim. Enhancement of research interests in physiology and biochemistry of blister beetles (Coleoptera: Meloidae): A review. International Research Journal of Biochemistry and Bioinformatics. 2013, Vol. 3(4): 75-92.
2. Browne SG. Cantharidin Poisoning Due to a " Blister Beetle ". British Medical Journal. 1960, 1290-1291.
3. Tagwireyi D, Ball DE, Loga PJ, Moyo S. Cantharidin poisoning due to ``Blister beetle'' Ingestion. Toxicon. 2000, 38:1865-69.
4. Al-Binali A, Shabana M, Al-Fifi S, Dawood S, Shehri A, AlBarki A. Cantharidin Poisoning due to Blister Beetle Ingestion in Children. Two case reports and a review of clinical presentations. SQU Med J, 2010, 10( 2): 103-10.
5. Wertelecki W, Vietti TJ, Kulapongs P. Cantharidin Poisoning from Ingestion of a “Blister Beetle” Pediatrics, 1967, 39(2): 287.
6. Mallari RQ, Saif M, Elbualy MS, Sapru A. Ingestion of a Blister Beetle (Mecoidae Family). Pediatrics, 1996; 98; 458.
7. Moed L, Shwayder TA, Chang MW. Cantharidin Revisited a blistering defense of an ancient medicine. Arch Dermatol, 2001, 137: 1357-60.
8. Sánchez-Barbudo IS, Camarero PR, GarcíaMontijano M, Mateo R. Possible cantharidin poisoning of a great bustard (Otis tarda). Toxicon, 2012, 59: 100-3.
9. Jonathan S. Till and Bhagirath Majmudar, M.D . Cantharidin poisoning: review article. Southern Medical Journal, vol 74, No. 4
10. Nyazema N. Cantharidin Poisoning: A Review. S. Afr. Fam. Pract. 1989, 10: 70-3.
11. AlRumikan AS, Al-Hamdan NA. Indirect Cantharidin Food Poisoning Caused By Eating Wild Birds, AI-Majmaa, 1999. Saudi Epidemiology Bulletin, 1999, 6(4): 26.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241612EnglishN2014June23Healthcare"CYCLOOXYGENASE-2" - A VIBRANT CHEMICAL MEDIATOR IN A PLETHORA OFORAL LESIONS
English3342Aditi Amit ByatnalEnglish Subhalakshmi SenEnglish Amit ByatnalEnglish Monica Charlotte SolomonEnglishCyclooxygenase (COX) is an enzyme that is responsible for formation of important biological mediators called prostanoids, including prostaglandins, prostacyclin and thromboxane. Constituting a key regulatory enzyme of the ecosanoid biosynthetic pathway, COX catalyzes the conversion of arachidonic acid to protaglandinG2 (PGG2) and PGH2 and subsequently to a variety of eicosanoids. COX-2 is one of the isoforms of COX, which was upheld mainly as an inflammatory, inducible enzyme, having role different than that of COX-1. However, more recent studies are beginning to reveal additional functions of COX-2, especially in oral lesions.Most commonly studied area of interest being oral squamous cell carcinoma, along with salivary gland tumors, reactive inflammatory lesions and so on. The objective of this review is to discuss the role of COX-2 in various oral lesions.
EnglishCyclooxygenase, prostanoidsINTRODUCTION
The fascinating ability to treat fever and inflammation dates back about 3500 (400 B.C.) years ago to a time when the Greek physician Hippocrates prescribed an extract from willow bark and leaves. Later in the 17th century, the active ingredient of willow bark salicin was identified in Europe. The Kolbe company in Germany started mass producing salicylic acid in 1860. Acetylsalicyclic acid 1 (aspirin) the more palatable form of salicyclic acid was introduced into the market by Bayer in 18991 . However, the mechanism of action of anti-inflammatory and analgesic agents such as aspirin and indomethacin 2 remained elusive until the early 1960?s. This all changed in the seventies, when John Vane discovered the mechanism of action of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) thereby increasing our ability to develop novel anti-inflammatory therapies1 . The success of NSAIDs in treating various inflammatory conditions such as rheumatoid arthritis (RA) and osteoarthritis (OA) validated inhibition of the enzyme prostaglandin H synthase (PGHS) or cyclooxygenase (COX) as a highly suitable target in anti-inflammatory therapies1,2 . However, the gastrointestinal (GI) toxicities associated with widespread NSAID use proved to be a major drawback during long term therapy3 . COX, a central enzyme in the biosynthetic pathway to prostaglandins from arachidonic acid, is a protein that was purified more than 20 years ago and cloned in 1988. In the early 90?s, Needleman, Simmons and Herschman?s group reported the presence of an inducible isoform of the enzyme COX later identified as Cyclooxygenase-2 (COX-2)4,5. This discovery led to the hypothesis that anti-inflammatory prostaglandins (PGs) were produced through constitutive expression of Cyclooxygenase -1 (COX-)1, whereas the proinflammatory PGs were produced via induction of the COX-2 isoform6 .
DISCUSSION
COX-2 and inflammation
During the inflammatory process, the COX-1 micro RNA (mRNA) and protein activity do not change whereas a dramatic increase in COX-2 levels occurs leading to increased production of proinflammatoryPGs.The expression of COX-2 has been studied extensively in animal models of inflammation which provided strong evidence that induction of COX-2 enzyme is associated with inflammation. The COX-1 enzyme does not appear to be affected by the inflammatory process since similar levels of mRNA and protein are detected in both normal and inflamed tissue in animal models. PGs such as PGE2 and PGI2 produced via the COX-2 pathway magnify the degree of inflammation initiated by other mediators of inflammation such as histamine and bradykinin leading to increased vascular permeability and edema7 . COX-2 is not detectable in normal tissue but is detectable after induction by inflammatory stimuli. Selective COX-2 inhibitors exhibit good anti-inflammatory and analgesic activities in various animal models. In humans, COX-1 is found to be constitutively expressed in a wide range of tissues including the kidney, lung, stomach, small intestine and colon. Hence, COX-1 is considered a housekeeping enzyme responsible for maintaining basal prostaglandin levels, which is important for tissue homeostasis. In contrast, most tissues do not routinely express COX-2 constitutively. It is only in the central nervous system8 and seminal vesicles9where COX-2 has been demonstrated to be expressed normally. However, the stimulation of COX-2 in Src-transformed fibroblasts10 , endothelial cells and monocytes treated with the tumor promoter tetradecanoyl-phorbol-acetate or lipopolysaccharide create a notion that COX-2 is an inducible enzyme that produces prostaglandins during inflammatory and tumorigenic settings. Cyclooxygenase-2 and its function One of the first studies conducted after the discovery of two isoforms of COX was a screening of existing NSAIDs for those that had differential effects on inhibition of COX-1 vs. COX-2, and some were found to have a 20- to 70- fold selective preference11 . As a result, studies were done using differential inhibition of COX-1 or COX-2 activities to sort out the relative contributions of these isoforms under a variety of experimental conditions. COX-2 in Cancer Several population-based studies have detected a 40–50% decrease in relative risk for colorectal cancer in persons who regularly use aspirin and other NSAIDs12. Initial attempts to determine the molecular basis for these observations found that both human and animal colorectal tumors express high levels of COX-2, whereas the normal intestinal mucosa has low to undetectable COX-2 expression13. These findings led to the hypothesis that COX-2 may be playing a role in colon cancer growth and progression. Studies on cell culture models have shown that COX-2 expression contributes significantly to the tumorigenic potential of epithelial cells by increasing adhesion to extracellular matrix and making them resistant to apoptosis14. These phenotypic changes were shown to be reversible by treatment with a highly selective COX-2 inhibitor. Very recent work indicates that cyclooxygenase may play a vital role in the regulation of angiogenesis associated with neoplastic tumor cells15 . Hence, COX inhibitors may block the growth of blood vessels into developing tumors. COX-independent pathways also play an important role in the cancer chemopreventive properties of NSAIDs. Thus, it is understood that both COX-dependent and COXindependent pathways are involved in cancer chemoprevention
COX-2 in oral epithelial dysplasia and cancer
Expression of COX-2 has been evaluated in oral epithelial dysplasia and oral cancer. Results obtained are observed to be varying as depicted in ble 116-28 . It is well known that cancer cell development and survival is a multifactorial process, involving genetic mutation of normal cells as well as physiological changes within both cancer cells and also the body?s defense mechanisms29. Immune response to cancer cell development and progression is of particular importance as it might play a potential role in tumor formation. Unresolved immune responses, such as chronic inflammation, can promote the growth and progression of cancer. Within the immune system, cytotoxic CD8+ and CD4+ T cells, along with their characteristically produced cytokine interferon- γ (IFN-γ) function as the major anti-tumor immune effector cells, whereas tumor associated macrophages (TAM) or myeloidderived suppressive cells (MDSC) and their derived cytokines Interlukin-6, Tumor Necrosis Factor, Interlukin-1β and Interlukin-23 are generally recognized as dominant tumorpromoting forces. However, the roles played by CD4+, CD25+, Forkhead box (Fox) p3+ regulatory T lymphocytes and immunoregulatory cytokines such as Transforming Growth Factor -β in tumor development and survival remain elusive. These immune cells and the cellular factors produced from them, including both immunosuppressive and inflammatory cytokines, play dual roles in promoting or discouraging cancer development, and their ultimate role in cancer progression may rely heavily on the tumor microenvironment and the events leading to initial propagation of carcinogenesis30 . COX-2/PGE2 pathway has been demonstrated to influence every hallmark of cancer, including oral cancer. COX-2/PGE2 pathway has been suggested to play a role in suppression of apoptosis, via activation of the Ras-mitogen activated protein kinase (MAPK/ERK) pathway31. PGE2 has been reported to activate pro-survival pathways including PI3K/AKT pathway, protein kinase A signaling32 and activation of Epidermal Growth Factor (EGFR) signaling33. In addition to the apoptosis-suppressive effects of COX-2-derived PGE2, deregulated expression of COX-2 protein itself might also alter the susceptibility of cells to undergo apoptosis by reducing the cellular pool of its substrate arachidonic acid, which can stimulate apoptosis34. Aberrant activation of COX-2/PGE2 pathway might phenocopy activating mutations in the PI3K/ AKT and/or Ras-MAPK pathways, which could play an important role in promoting tumor progression. Indeed, deregulation of the COX-2/PGE2 pathway has been shown to behave in a similar manner to constitutively active Ras in murine intestinal adenomas, resulting in a positive feedback loop that boosts COX-2 expression and further stimulation of tumor growth35. COX2/PGE2 pathway prevents the receipt of antigrowth signals since over-expression of COX-2 has been reported to cause down-regulation of the TGFb type II receptor 14. The COX-2/PGE2 pathway, by enhancing cell survival and growth, serves to assist the cells for acquisition of further cellular alterations that contribute to immortalization and the progression towards the full malignant phenotype. Over-expression of COX-2 induces the production of angiogenic factors such as VEGF and basic fibroblast growth factor, which are instrumental in stimulating the formation of new blood vessels – a requirement for tumors should they wish to develop beyond a few millimeters in size36. The mechanism through which COX-2 might promote tumour vascularization is via the production of PGE2 and prostaglandin I2. These factors have been shown to participate in inducing endothelial cell dispersion and migration by integrin αVb3- mediated activation of the small guanosine 5?- triphosphatases Cdc42 and Rac37 . In vitro experiments have revealed that cells overexpressing COX-2 undergo phenotypic changes that could enhance their tumorigenic potential, such as exhibition of an increased adhesion to extracellular matrix proteins and resistance to apoptosis. It is believed that this proliferative activity of COX-2 primarily mediated by PGs14 . order to achieve metastases, cancer cells must exhibit a more motile, invasive phenotype, dissociate from neighboring cells within the tumour, invade through extracellular matrix components and intravasate into local blood or lymphatic channels38. Having made their escape from the primary tumour, cancer cells must then extravasate from the blood or lymphatics into the surrounding tissue in order to colonize distant sites. Several lines of evidence indicate that COX2 and the prostaglandins play important roles in aiding these processes – more specifically, PGE2 is thought to promote a more metastatic phenotype in cancer14 . Over-expression of COX-2 can modulate the adhesive properties of cancer cells and increase matrix metalloproteinase activity to promote invasion39. PGE2 promotes cytoskeletal reorganization and increases cancer cell migration and invasion via PI3K signaling. The stimulation of invasion and motility by PGE2 is dependent on the intracellular Src-mediated transactivation of EGFR40. Furthermore, hepatocyte growth factor signaling, which is classically associated with loss of cell-cell contact (or scattering) and invasive growth41, is also transactivated by PGE2 in an EGFR-dependent approach. COX-2, hepatocyte growth factor and β-catenin are co-expressed at the invasive front of tumor specimens42 , suggesting their interplay in tumorigenesis. COX2 has been identified as one of the four key „metastasis progression? genes, which collectively synergize to mediate both tumor development and metastasis to other organs43 . The contribution of COX-2 in carcinogenesis is due to its involvement in several key mechanisms including the conversion of pro-carcinogens to carcinogens as a consequence of arachidonic acid metabolism, stimulation of cell growth, inhibition of apoptosis through p53 suppression and bcl2 induction, stimulation of VEGF and angiogenesis, promotion of invasion and metastasis via matrix metalloproteinases induction and immunosuppression by IL-10 induction36,44. Cox-2 in potentially malignant oral lesions Along with numerous studies in conducted to evaluate the role of COX-2 in oral cancer, few studies have also been carried out to appraise if COX-2 plays a similar role in few of the lesions considered as potentially malignant oral lesions. As depicted in table 2 45-48, COX-2 has been shown to be overexpressed in oral submucous fibrosis (OSMF), oral lichen planus (OLP) and even in oral lichenoid reactions (OLR), as compared to the normal oral mucosa. It is well known that OLP is a chronic inflammatory disease for which the pathogenesis is not fully understood. OLP has autoimmune features and auto immunity has been suggested as a potential cause, whereas WHO has classified OLP as a premalignant condition. Association between chronic inflammation and cancer is known and chronic inflammation is one of the characteristics of OLP47. Increased expression of COX-2 suggests its definite role in OLP. COX-2 has been connected to both malignant development and autoimmunity but as malignant development of OLP is quite rare it was suggested that the increased levels of COX-2 support an autoimmune cause of the disease. As against, Lysitaet al48 suggest that sustained overexpression of COX-2 in the late stage of the disease could play a role in the malignant transformation of some OLP. In case of OSMF, very few studies have been conducted to assess the role of COX-2 in its pathogenesis. Aberrant and persistent tissue inflammations are believed to play an important role on the occurrence of tissue fibrosis. Tsai et al45 in their study demonstrated that COX-2 expression was significantly higher in OSMF specimens and expressed mainly by epithelial cells, endothelial cells, and cells with fibroblast morphology. Simultaneously they also observed the COX-2 expression in cells treated with arecoline and noticed that COX-2 expression was up-regulated as early as half an hour. This indicated that COX-2 expression is an early cellular response and regulated by arecoline at transcriptional level. Cox-2 in odontogenic cysts and tumors of the jaw Limitations in the number of studies related to expression of COX-2 in odontogenic cysts and tumors (table 3)49,50 makes it difficult to understand its exact role in pathogenesis of these lesions. Radicular cyst, being an inflammatory cyst, shows high expression of COX-2 in the lining epithelium, subepithelial fibroblasts, macrophages and endothelial cells, suggesting the role of COX-2 in their pathogenesis. KCOT is a benign neoplasm of odontogenic origin with an occasionally aggressive behavior leading to high recurrence rates. High COX-2 expression in the epithelial lining of KCOT the current knowledge of the role played by COX-2 in tumorigenesis further strengthen the current concept that the KCOT should be regarded as a neoplasm. Furthermore, the multitude of markers known to be overexpressed in KCOTs is suggestive of what could be called a 'network addiction' pattern, rather than a pathological mechanism dependant on a specific activated/suppressed gene, thus explaining its aggressive behavior50 . Cox-2 in salivary gland tumors Salivary gland tumors, most of which are rare benign tumors, represent a histologically heterogenous group with the greatest diversity of morphological and cellular features. Restricted number of studies has been conducted as to evaluate the role of COX-2 in few of the salivary gland tumors (table 4)51-55. Few studies showed no quantitative difference in COX-2 expression in different benign tumors51, while others exhibited considerable overexpression in the same52 . Warthin?s tumor showed COX-2 expression only in the epithelial component, with no expression in the lymphoid components54. These findings support the hypothesis that Warthin's tumors originate from heterotopic ductal epithelial cells of the parotid gland. However, the role of COX-2 expression in the pathogenesis of Warthin's tumors remains to be determined. Likewise, COX-2 expression has also been studied in malignant salivary gland tumors since overexpression of cyclooxygenase (COX)-2 in several human carcinomas suggests that COX-2 is related to carcinogenesis. However, the exact mechanism is still not understood55 . COX-2 in oral reactive lesions Most of the reactive lesions being inflammatory in process, have demonstrated COX-2 overexpression (table 5)56,57. Pulpal inflammation associated with dental caries56 andperiapical granuloma and periapicalcyst57have shown overexpression of COX-2. COX-2 -positive cells were detected in the epithelial cells and inflammatory cells. These studies suggest that COX-2 might play more important roles in the pathogenesis and development of periapical
CONCLUSION
Cyclooxygenase- 2 is chemical mediator that has a low to undetectable expression in normal tissues. It is a crucial element that functions through the production of prostaglandins. This molecule is particularly abundant in activated macrophages and cells at the site of inflammation. Its role in the disease process of various oral lesions is recognized. This mediator is a key factor in many regulatory pathways of the carcinogenic process. Understanding the role of cyclooxygenase -2 in the oral lesions can facilitate the incorporation of treatment protocols that target this molecule.
ACKNOWLEDGEMENT
Authors acknowledge the immense help received from the scholars whose articles have been cited and included in the references of this manuscript. The authors are also grateful to authors/ editor/ Publishers of all those articles, journal and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=834http://ijcrr.com/article_html.php?did=834REFERENCES
1. Vane JR. Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nat New Biology 1991; 231: 232-235.
2. Ferreira SH, Moncada S, Vane JR. Indomethacin and aspirin abolish prostaglandin release from the spleen. Nat New Biology 1971; 231: 237-239.
3. Tamblyn R, Berkson L, Dauphinee WD, Gayton D, Grad R, Huang A, Isaac L, McLeod P, Snell L. Unnecessary prescribing of NSAIDs and the management of NSAIDrelated gastropathy in medical practice. Ann Intern Med. 1997; 127(6): 429-38.
4. Masferrer JL, Zweifel BS, Manning P,T, Hauser SD, Leahy KM, Smith WG, et al. Selective inhibition of inducible cyclooxygenase 2 in vivo is antiinflammatory and nonulcerogenic. ProcNatlAcadSci USA 1994; 91: 3228-3232.
5. Xie W, Chipman JG, Robertson DL, Erikson RL, Simmons DL. Expression of a mitogenresponsive gene encoding prostaglandin synthase is regulated by mRNA splicing. ProcNatlAcadSci USA. 1991; 88: 2692-2696.
6. Meade EA, Smith WL, DeWitt DL. Differential inhibition of prostaglandin endoperoxide synthase (cyclooxygenase) isozymes by aspirin and other non-steroidal anti-inflammatory drugs. J Biol Chem. 1993;268(9):6610-4.
7. Seibert K, Zhang Y, Leahy K, Hauser S, Masferrer J, Perkins W, Lee L, Isakson P. Pharmacological and biochemical demonstration of the role of cyclooxygenase 2 in inflammation and pain. ProcNatlAcadSci U S A. 1994;91(25):12013-7.
8. Svensson CI, Yaksh TL. The spinal phospholipase-cyclooxygenase-prostanoid cascade in nociceptive processing. Annu Rev PharmacolToxicol. 2002;42:553-83.
9. Kirschenbaum A, Liotta DR, Yao S, Liu XH, Klausner AP, Unger P, Shapiro E, Leav I, Levine AC. Immunohistochemical localization of cyclooxygenase-1 and cyclooxygenase-2 in the human foetal and adult male reproductive tracts. J ClinEndocrinolMetab. 2000;85(9):3436-41.
10. Xie WL, Chipman JG, Robertson DL, Erikson RL, Simmons DL. Expression of a mitogenresponsive gene encoding prostaglandin synthase is regulated by mRNA splicing. ProcNatlAcadSci U S A. 1991;88(7):2692-6.
11. Spangler RS. Cyclooxygenase 1 and 2 in rheumatic disease: implications for nonsteroidal anti-inflammatory drug therapy. Semin Arthritis Rheum. 1996;26(1):435-46.
12. Giovannucci E, Rimm EB, Stampfer MJ, Colditz GA, Ascherio A, Willett WC. Aspirin use and the risk for colorectal cancer and adenoma in male health professionals. Ann Intern Med. 1994;121(4):241-6.
13. Eberhart CE, Coffey RJ, Radhika A, Giardiello FM, Ferrenbach S, DuBois RN. Upregulation of cyclooxygenase 2 gene expression in human colorectal adenomas and adenocarcinomas. Gastroenterology. 1994;107(4):1183-8.
14. Tsujii M, DuBois RN. Alterations in cellular adhesion and apoptosis in epithelial cells overexpressing prostaglandin endoperoxide synthase 2. Cell. 1995;83(3):493-501.
15. Tsujii M, Kawano S, Tsuji S, Sawaoka H, Hori M, DuBois RN. Cyclooxygenase regulates angiogenesis induced by colon cancer cells. Cell. 1998;93(5):705-16. Erratum in: Cell 1998;94(2):273.
16. Itoh S, Matsui K, Furuta I, Takano Y. Immunohistochemical study on overexpression of cyclooxygenase-2 in squamous cell carcinoma of the oral cavity: its importance as a prognostic predictor. Oral Oncol. 2003;39:829-35.
17. Li WZ, Ding YQ, Li ZG, Zhang JH. Expression of COX-2 and VEGF-C in squamous cell carcinoma of the tongue and its correlation to lymph node metastasis. Nan Fang Yi Ke Da XueXueBao. 2008;28(2):180- 3.
18. Pandey M, Prakash O, Santhi WS, Soumithran CS, Pillai RM. Overexpression of COX-2 gene in oral cancer is independent of stage of disease and degree of differentiation. Int J Oral Maxillofac Surg. 2008;37(4):379-83.
19. Segawa E, Sakurai K, Kishimoto H, Takaoka K, Noguchi K, Hashitani S, et al. Expression of cyclooxygenase-2 and DNA topoisomerase II alpha in precancerous and cancerous lesions of the oral mucosa. Oral Oncol. 2008;44(7):664-71.
20. Zhang S, Du Y, Tao J, Wu Y, Chen N. Expression of cytosolic phospholipase A2 and cyclooxygenase 2 and their significance in human oral mucosae, dysplasias and squamous cell carcinomas. ORL J OtorhinolaryngolRelat Spec. 2008;70(4):242- 8.
21. Sappayatosok K, Maneerat Y, Swasdison S, Viriyavejakul P, Dhanuthai K, Zwang J, et al. Expression of pro-inflammatory protein, iNOS, VEGF and COX-2 in oral squamous cell carcinoma (OSCC), relationship with angiogenesis and their clinico-pathological correlation. Med Oral Patol Oral Cir Bucal. 2009;14(7):E319-24.
22. Mauro A, Lipari L, Leone A, Tortorici S, Burruano F, Provenzano S, et al. Expression of cyclooxygenase-1 and cyclooxygenase-2 in normal and pathological human oral mucosa. Folia HistochemCytobiol. 2010;48(4):555-63.
23. Wang YH, Wu MW, Yang AK, Zhang WD, Sun J, Liu TR, et al. COX-2 Gene increases tongue cancer cell proliferation and invasion through VEGF-C pathway. Med Oncol. 2011;28Suppl 1:S360-6.
24. Salimi M, Esfahani M, Habibzadeh N, Aslani HR, Amanzadeh A, Esfandiary M, et al. Change in Nicotine-Induced VEGF, PGE2 AND COX-2 Expression Following COX Inhibition in Human Oral Squamous Cancer. J Environ PatholToxicolOncol. 2012;31(4):349- 56.
25. Morita Y, Hata K, Nakanishi M, Nishisho T, Yura Y, Yoneda T. Cyclooxygenase-2 promotes tumor lymphangiogenesis and lymph node metastasis in oral squamous cell carcinoma. Int J Oncol. 2012;41(3):885-92.
26. Nagatsuka H, Siar CH, Tsujigiwa H, Naomoto Y, Han PP, Gunduz M, et al. Heparanase and cyclooxygenase-2 gene and protein expressions during progression of oral epithelial dysplasia to carcinoma. Ann DiagnPathol. 2012;16(5):354-61.
27. Rojas IG, Martínez A, Brethauer U, Grez P, Yefi R, Luza S, et al. Actinic cheilitis: epithelial expression of COX-2 and its association with mast cell tryptase and PAR-2. Oral Oncol. 2009;45(3):284-90.
28. Prado SM, Cedrún JL, Rey RL, Villaamil VM, García AA, Ayerbes MV, et al. Evaluation of COX-2, EGFR, and p53 as biomarkers of nondysplastic oral leukoplakias. ExpMolPathol. 2010;89(2):197-203.
29. Grivennikov SI, Greten FR, Karin M. Immunity, inflammation, and cancer. Cell. 2010; 140(6):883-99.
30. Zamarron BF, Chen W. Dual roles of immune cells and their factors in cancer development and progression. Int J Biol Sci. 2011;7(5):651- 8.
31. Sheng H, Shao J, Morrow JD, Beauchamp RD, DuBois RN. Modulation of apoptosis and Bcl-2 expression by prostaglandin E2 in human colon cancer cells. Cancer Res. 1998;58(2):362-6.
32. Leone V, di Palma A, Ricchi P, Acquaviva F, Giannouli M, Di Prisco AM, et al. PGE2 inhibits apoptosis in human adenocarcinoma Caco-2 cell line through Ras-PI3K association and cAMP-dependent kinase A activation. Am J PhysiolGastrointest Liver Physiol. 2007;293(4):G673-81.
33. Pai R, Soreghan B, Szabo IL, Pavelka M, Baatar D, Tarnawski AS. Prostaglandin E2 transactivates EGF receptor: a novel mechanism for promoting colon cancer growth and gastrointestinal hypertrophy. Nat Med. 2002;8(3):289-93.
34. Chan TA, Morin PJ, Vogelstein B, Kinzler KW. Mechanisms underlying nonsteroidalantiinflammatory drug-mediated apoptosis. ProcNatlAcadSci U S A. 1998;95(2):681-6.
35. Wang D, Buchanan FG, Wang H, Dey SK, DuBois RN. Prostaglandin E2 enhances intestinal adenoma growth via activation of the Ras-mitogen-activated protein kinase cascade. Cancer Res. 2005;65(5):1822-9.
36. Hanahan D, Folkman J. Patterns and emerging mechanisms of the angiogenic switch during tumorigenesis. Cell. 1996;86(3):353-64.
37. Dormond O, Foletti A, Paroz C, Rüegg C. NSAIDs inhibit alpha V beta 3 integrinmediated and Cdc42/Rac-dependent endothelial-cell spreading, migration and angiogenesis. Nat Med. 2001;7(9):1041-7.
38. Weinberg RA. Mechanisms of malignant progression. Carcinogenesis. 2008;29(6):1092-5.
39. Tsujii M, Kawano S, DuBois RN. Cyclooxygenase-2 expression in human colon cancer cells increases metastatic potential. ProcNatlAcadSci U S A. 1997;94(7):3336-40.
40. Buchanan FG, Wang D, Bargiacchi F, DuBois RN. Prostaglandin E2 regulates cell migration via the intracellular activation of the epidermal growth factor receptor. J Biol Chem. 2003;278(37):35451-7.
41. Birchmeier C, Birchmeier W, Gherardi E, VandeWoude GF. Met, metastasis, motility and more. Nat Rev Mol Cell Biol. 2003;4(12):915-25
42. Pai R, Nakamura T, Moon WS, Tarnawski AS. Prostaglandins promote colon cancer cell invasion; signalling by cross-talk between two distinct growth factor receptors. FASEB J. 2003;17(12):1640-7.
43. Greenhough A, Smartt JM, Moore AE, Roberts HR, Williams AC, Paraskeva C, et al. The COX-2/PGE2 pathway: key roles in the hallmarks of cancer and adaptation of tumor microenvironment. Carcinogenesis. 2009;30(3):377-86.
44. Danial NN, Korsmeyer SJ. Cell death: critical control points. Cell 2004;116 (2) 205-219.
45. Tsai CH, Chou MY, Chang YC. The upregulation of cyclooxygenase-2 expression in human buccal mucosal fibroblasts by arecoline: a possible role in the pathogenesis of oral submucous fibrosis. J Oral Pathol Med. 2003;32(3):146-53.
46. Danielsson K, Ebrahimi M, Wahlin YB, Nylander K, Boldrup L. Increased levels of COX-2 in oral lichen planus supports an autoimmune cause of the disease. J EurAcadDermatolVenereol. 2012;26(11):1415-9.
47. Cortés-Ramírez DA, Rodríguez-Tojo MJ, Gainza-Cirauqui ML, Martínez-Conde R, Aguirre-Urizar JM. Overexpression of cyclooxygenase-2 as a biomarker in different subtypes of the oral lichenoid disease. Oral Surg Oral Med Oral Pathol Oral RadiolEndod. 2010;110(6):738-43.
48. Lysitsa S, Samson J, Gerber-Wicht C, Lang U, Lombardi T. COX-2 expression in oral lichen planus. Dermatology. 2008;217(2):150-5.
49. Tsai CH, Huang FM, Yang LC, Chou MY, Chang YC. Immunohistochemical localization of cyclooxygenase-2 in radicular cysts. IntEndod J. 2002 Oct;35(10):854-8.
50. Mendes RA, Carvalho JF, van der Waal I. Potential relevance of cyclooxygenase-2 expression in keratocysticodontogenictumours – an immunohistochemical study. J Oral Pathol Med. 2011;40(6):497-503.
51. Lipari L, Mauro A, Gallina S, Tortorici S, Buscemi M, Tete S, Gerbino A. Expression of gelatinases (MMP-2, MMP-9) and cyclooxygenases (COX-1, COX-2) in some benign salivary gland tumors. Int J ImmunopatholPharmacol. 2012;25(1):107-15.
52. Cho NP, Han HS, Soh Y, Son HJ. Overexpression of cyclooxygenase-2 correlates with cytoplasmic HuR expression in salivary mucoepidermoid carcinoma but not in pleomorphic adenoma. J Oral Pathol Med. 2007;36(5):297-303.
53. Katori H, Nozawa A, Tsukuda M. Increased expression of cyclooxygenase-2 and Ki-67 are associated with malignant transformation of pleomorphic adenoma. AurisNasus Larynx. 2007;34(1):79-84.
54. Loy AH, Putti TC, Tan LK. Cyclooxygenase-2 expression in Warthin'stumour. J Laryngol Otol. 2005;119(7):515-8.
55. Sakurai K, Urade M, Noguchi K, Kishimoto H, Ishibashi M, Yasoshima H, Yamamoto T, Kubota A. Increased expression of cyclooxygenase-2 in human salivary gland tumors. Pathol Int. 2001;51(10):762-9
56. Lundy FT, About I, Curtis TM, McGahon MK, Linden GJ, Irwin CR, El Karim IA. PAR-2 regulates dental pulp inflammation associated with caries. J Dent Res. 2010;89(7):684-8.
57. Lin SK, Kok SH, Kuo MY, Wang TJ, Wang JT, Yeh FT, Hsiao M, Lan WH, Hong CY. Sequential expressions of MMP-1, TIMP-1, IL-6, and COX-2 genes in induced periapical lesions in rats. Eur J Oral Sci. 2002; 110(3):246-53.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241612EnglishN2014June23HealthcareCULTURAL PRACTICES ASSOCIATED WITH FEEDING AMONG UNDERFIVECHILDREN IN A RURAL AREA: A CROSS SECTIONAL STUDY
English4348Vijayashree MathadEnglish Shivprasad SEnglishIntroduction: Cultural practices associated with faulty feedingamong underfive is one of the major problems, which is exaggerated by discarding of colostrums, giving of prelacteal feeds and wrong weaning practices. Objective: To assess the cultural practices associated with feeding among under fives. Material and Method: This cross sectional study was conducted in Kakati-A sub centre, under Primary Health Centre Vantamuri of Belgaum district. The sample size was 290. Data collection was done using pre-designed and pre-tested questionnaire.
EnglishUnder fivechildren, Culturalpractices, Rural area, Breast feeding, Weaning.INTRODUCTION
Cultural practices regarding rearing of underfive children plays a vital role in the growth and development of underfive children. Various myths associated with culture like discarding of colostrums, giving prelacteal feeds, improper weaning foods has serious implecation on the health status of underfive children. Proper feeding practices which includes early initiation of breast feed, avoiding prelacteal feeds and exclusive breast feeding for 6 months and timely weaning are important determinants of growth and development of under five children.1 Exclusive breast feeding protects the child from various infections like gastrointestinal and respiratory tract and also promotes Cognitive and immunological growth. Weaning prior to 6 months may lead to infectious diseases like diarrhea due to inadequate hygiene and the food introduced in developing countries are of concern due to its low energy and nutrient intake.2 Breast-feeding lowers thefrequency and duration of acute respiratory infection and diarrhea ininfants under six months of ageand delayed weaning leads to growth deficiency.3, 4, 5 Optimal under five child feeding practices and appropriate complementary feeding prevents 6% of mortality among under five children.6 According to World Health Organisation (WHO) and systematic review from the Bellagio Child Survival Study Group about1.3 million child deaths could be prevented by 6 months of exclusive breast feeding and continued breast feeding for 1 year and improved complementary feeding. Consequences of faulty feeding practices are poverty reduction and poor socioeconomic development.7, 8 According to the United Nations declaration “the child shall enjoy special protection and shall be given opportunities and facilities by law and order and by means to enable him to develop physically and mentally in a healthy and normal manner and in a condition of freedom and dignity”. In the millennium declaration of September 2000, member states of the United Nations made a most passionate commitment to address the crippling and multiplying misery that grip many areas of the world. Governments set a date of 2015 by which they would meet the Millennium Development Goals. Among this, the first goal is to eradicate extreme poverty and hunger, which is measured by the prevalence of underweight children. The target is to halve the burden of under nutrition. The next important goal with regards to children is to achieve two third reduction in under 5 mortality and infant mortality by 20159 Proper feeding practices constitute an important component of child rearing along with socio demographic and cultural practices. There is an urgent need for education and promotion of proper feeding practices and child care among mothers of under five children.10 Meager amount of information is available regarding the cuktural practices associated with rearingof under five children in this part of the nation and in our field practice area. Hence the present study was undertaken to evaluate the cultural practices and the socio demographic factors associated among children aged under five in Kakati-A sub centre.
MATERIAL AND METHODS
Source of data The present study was conducted in Kakati-A sub centre, under Primary Health Centre Vantamuri of Belgaum district. It was a cross-sectional study conducted over a period of 10 months from March to December 2010. Eleven Anganwadicentres were providing non-formal pre-school education and rendering other services under Integrated Child Development Service Scheme in the village. A total of 290 underfive children were included in the study. The data was collected by interviewing the caretaker after obtaining the informed consent. Information was collected on socio-demographic variables and feeding practices using pre-designed and pre-tested questionnaire.
DATA ANALYSIS
Data was analyzed and expressed as percentages. Chi-square test was used to evaluate association between socio- demographic variables and cultural practices.
ET The study was approved by the institutional HICAL CONSIDERATIONSethics committee and written informed consent was taken from the parents or caregivers of the child.
RESULTS
Basic information was obtained from290 householdsresiding in rural area of south India aged 0-5 years, 155(53.44%) were male and 135(46.55%) were female children. With regards to age distribution it was observed that in 0-12 months age group 19 (6.55%), in 13-24 months age group were 63 (21.73%), in 25-36 months 62 (21.38%), similarly in 37-48 months 59 (20.34%) and 49-60 months age group were 87 (30.00%). Majority 252 (86.90%) children were Hindus and with regards to socio-economic status, 203 (70.00%) belonged to Classes IV and V according to modified B.G. Prasad’s classification. Maximum 179 (61.94%) of underfive children fathers occupation was coolie and 260 (89.96%) of mothers were housewives. The literacy rate of underfive children fathers and mothers was 95.17% and 92.07% respectively.In context to birth order, 127(43.79%) of the children were of 2nd Birth order, 111(38.27%) of 1st Birth order, and 52 (17.94%) where of 3rd, 4th and 5th Birth order.With regard to type of family 149 (51.38%) of the children belonged to the nuclear family, 98 (33.79%) to three generation family, 38 (13.10%) to joint family and 5 (1.72%) belonged to problem family. Majority 168(58.13%) of the mothers got the information regarding breast feeding practices from health care provider, 61(21.10%) from their mother, 55(19.03%) from their mother in law and 5(1.73%) mothers were self informed or got information from sisters and neighbours. 50(17.30%) mothers discarded the colostrum. The reasons cited were: they felt the colostrum was dirty milk 21(42.00%), told by mother in law 12(24.00%), thought not good for baby 9(18.00%) and told by mother and sister, causes diarrhea, evil spirits milk and toxic for child. Most of them 245(84.78%) practiced demand feeding as compared to time bond feeding. According to feeding practices followed by mothers 141(48.79%) children were breast fed within one hour of birth, 53(18.34%) children were started within 1-6 hours, and others 95(32.76%) started later than 6 hours. Prelacteal feeds which is considered as a major wrong practices by WHO was given by 124 (42.76%) of mothers. The common Pre lacteal feeds given to newborn were honey, sugar water and plain water. Exclusive breastfeeding of 6 months as recommended was not practiced by most of the mother, which included early initiation of top feeding before 6 months by 179(61.72%) mother, mainly during 4th month the top feeds included 101(34.83%) buffalo’s milk, 55(18.97%) cow’s milk, 19(6.55%) cerelac and 4(0.79%) children were given goats milk. And delayed weaning later than 6 months was seen in 87(30.00%) children. Correct feeding practicesincluding initiation of breast feeding, feeding colostrumand not giving prelacteal feeds was significantly associated with socio economic status (pEnglishhttp://ijcrr.com/abstract.php?article_id=835http://ijcrr.com/article_html.php?did=835REFERENCES
1. Teresa G, Juan R, Hortensia M,3 Monterrubio E and Jaime S. Poor Compliance with Appropriate Feeding Practices in Children under 2 y in Mexico Cited from jn.nutrition.org by guest on July 26, 2012
2. Victora C, Smith PG, Vaughan JP, Nobre LC, Lombardi C, Teixeira AM et al. Evidence for protection by breast-feeding against infant deaths from infectious diseases in Brazil. Lancet. 1987 (2) 319–22.
3. Brown K, Black R, Roman G, Kanashiro H.Infantfeeding practices and their relationship with diarrheal and other diseases in Huascar (Lima) Peru. Pediatrics J Nutr. 1997 (127) 436–4.
4. Kramer MS, Chalmers B, Hodnett ED, Sevkovskaya Z, Dzikovich I, Shapiro S, Collet JP, Vanilovich I, Mezen I, et al. Promotion of Breastfeeding Intervention Trial (PROBIT): a randomized trial in the Republic of Belarus. JAMA. 2001 (285) 413–20
5. World Health Organization. Complementary feeding of younger children in developing countries: a review of current scientific knowledge. Geneva: WHO/NUT/98.1; 1998.
6. Apurba S, DiptaK,Mukhopadhyay, Tanmay K. Panja, Asit B. Saren, Nirmal K. Mandal, and Akhil B. BiswasInfant- and Young Childfeeding Practices in Bankura District, West Bengal, India J HEALTH POPUL NUTR 2010 Jun;28(3):294-299
7. National Family Health Survey. http://www.nfhsindia.org/data/ka-pre.pdf. (Cited on 24-12-2010).
8. Katiyar GP, Agarwal DK, Tripathi AM, Agarwal KN. Feeding practices in Varanasi district. Indian Pediatrics. 1981; 18(1): 65-70.
9. Bloss E, Wainaina F and Bailey RC. Prevalence and predictors of underweight, stunting and wasting among children aged 5 and under in western Kenya. Journal of Tropical Pediatrics. 2004; 50 (5): 260-270.
10. Dinesh K, N.K. Goel, Poonam C. Mittal and PurnimaMisra Influence of Infant-feeding Practices on Nutritional Status of Under-five Children Indian Journal of Pediatrics, 2006(73) 417-422.
11. . David O, Kirti M,Tumbahangphe,DejShrestha et al. Cross sectional, community based study of care of newborn infants in Nepal. BMJ 2002 (325) 10-63
12. Subba SH, TS Chandrashekhar, Binu VS, Joshi HS4, Rana MS, Dixit SB Infant feeding practices of mothers in an urban area in Nepal Kathmandu University Medical Journal 2007 (5) No. 1. 17, 42-47.
13. Apurba S, Dipta K, Mukhopadhyay, Tanmay K, Panja, Asit B et al. Infant- and Young Child-feeding Practices inBankura District, West Bengal, India.J HEALTH POPUL NUTR 2010 Jun;28(3):294-299
14. Katiyar GP, Agarwal DK, Tripathi AM, Agarwal KN. Feeding practices in Varanasi district. Indian Pediatrics. 1981; 18(1): 65-70.
15. Complementary feeding of young children in developing countries: A review of current scientific knowledge. WHO/NUT/98.1
16. Moffat T. A bio-cultural investigation of the weanling's dilemma in Kathmandu, Nepal: do universal recommendations for weaning practices make sense? - J Biosocial Sciences. 2001; 33(3): 321-38.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241612EnglishN2014June23HealthcareEFFECT OF BODY MASS INDEX ON FOLLICLE STIMULATING HORMONE, LUTEINIZING HORMONE, PROLACTIN AND FASTING BLOOD GLUCOSE LEVELS IN WOMEN WITH POLYCYSTIC OVARIAN SYNDROME
English4955V. RajithaEnglish G. RekhaEnglish K.Y.ManjunathEnglishBackground: Obesity is a modern day scourge which plays havoc on the menstrual life of women in the reproductive age group. Disorders of menstrual cycle affect the women psychologically as well as physically. To estimate the obesity of an individual a cost effective method is to calculate the BMI (Body Mass Index). This is a reliable tool in early detection of Obesity and its associated disorders. In women of the reproductive age group an increased Body Mass Index results in alteration of hormonal levels resulting in altered menstrual cycles. In women with polycystic ovarian syndrome, the hormonal levels are so altered that many cycles are anovulatory. Estimation of Body Mass Index and comparing them with the hormonal levels will provide a fair idea in understanding the disease process. Materials and Methods: The test subjects were 79 apparently healthy women volunteers. They were divided into two groups based on menstrual history. Nineteen subjects were in control group and sixty were in the test group. BMI was calculated for both the groups. Blood levels of FSH, LH and Fasting Blood Glucose was estimated after obtaining consent and withdrawal of blood was done under aseptic precautions. The resultant measurements were subjected to statistical analysis, Results: The mean BMI of the test group was 25.48 Kg/m2and the mean BMI of the control group was 23.07Kg/m2. The Mean FSH levels in test group 7.88 mIU/ml and in the control group it was 8.95mIU/ml. The mean Prolactin levels in the test group were 16.635 ng/ml and in the control group it was 10.35 ng/ml. The mean LH levels in the test group were 6.53mIU/ml and in the control group it was 3.76mIU/ml. The mean fasting blood glucose levels in the test group was 94 mg/dl and in the control group it was 84 mg/dl. Conclusion: It is evident from the present study that the mean hormonal levels of LH and Prolactin and the fasting blood glucose levels are significantly higher in persons with polycystic ovarian syndrome and the FSH levels are lower in persons with polycystic ovarian syndrome which indicates that there could be always increased number of anovulatory cycles in such individuals.
EnglishBody mass index, Follicle stimulating hormone, Luteinizing hormone, Prolactin, Glucose, polycystic ovarian syndrome.INTRODUCTION
Polycystic ovarian syndrome is one of the most common endocrine disorder affecting 5-10% of women in their reproductive age group.1 Polycystic ovarian syndrome is an ill defined symptom complex, imbalance of different hormonal functions which can affect ovarian homeostasis resulting in anovulation which will manifest as Polycystic ovarian syndrome.2According to National Institute of Health in 1990Polycystic ovarian syndrome is defined based on diagnostic criteria such as presence of hyperandrogenism, chronic oligo-anovulation and exclusion of other diseases like prolactinemia, thyroid disorders and non classical adrenalhyperplasia.3 Polycystic ovarian syndrome patients usually over weight, LH: FSH ratio was less than 2 which is significantly higher amongpolycystic ovarian syndrome patients4 . Fifty percent (50%) of polycystic ovarian syndrome women are overweight / obese. Body mass index is a commonly used measure for excess body weight.Body mass index and mean age of menarche were significantly higher in Chinese women.5 The percentage of women affected bypolycystic ovarian syndrome and obesity presenting with glucose intolerance is rather high, ranging from 20 to 49%1 .Dysglycemia is also one of the important factors as most of the polycystic ovarian syndrome cases are prone to Diabetes Mellitus. Obese women with polycystic ovarian syndrome showed insulin resistance and fasting hyper insulinemia.6 Nowadays physicians check fasting blood glucose levels as a factor when diagnosing polycystic ovarian syndrome. Women with polycystic ovary syndrome should undergo fasting plasma glucose test and Glucose Tolerance Test to rule out diabetes mellitus as a factor for anovulatory cycles. A high glucose level indicates insulin resistance, which in turn contributes to central obesity in polycystic ovarian syndrome.7 The present study was performed to correlate Body mass index with LH, FSH, Fasting blood glucose levels and mean age of menarche between apparently normal women and women with polycystic ovarian disease.
MATERIAL AND METHODS
This cross-sectional study was performed on 60 afflicted Polycystic ovarian syndrome women volunteers and 19 control women volunteers from the gynaecology outpatient department of Vinayaka Mission Hospital and J.S.Hospital, Salem, Tamil Nadu, India between March 2013 to March 2014. The ethical clearance was obtained from the Institutional ethics committee of VMKV Medical College for conduct of the study. The control group consisted of apparently normal 19 women and test group consisted of 60 women with polycystic ovarian disease. The following parameters were studied 1. Age of menarche 2. Body Mass Index 3. Follicle stimulating hormone levels 4. Luteinizing hormone levels 5. Prolactin levels 6. Fasting Blood Glucose The Body mass index was calculated using the formula: weight in Kilograms/Height in meters2. According to the Asia–Pacific criteria of Body mass index for obesity subjects were divided into four groups. 8 Group 1: Less than 18.0kg/m2 Group 2: Between 18.1 and 22.9kg/m2 Group 3: Between 23.0 and 24.9 kg/m2 Group 4: Greater than 25 kg/m2 Body mass index (BMI) with body fat as Standard Consensus Statement for Indian population was considered, Normal BMI: 18.0 -22.9kg/m2 , Over weight: 23.0-24.9 kg/m2 , Obesity: ≥25kg/m2 as cut off for BMI.9 Based on above classification of BMI Group 1 is less than normal weight, Group 2 is normal weight, Group 3 is overweight, Group 4 is obese. To analyze FSH, LH, Prolactin and Fasting blood glucose levels around 5ml of blood sample was collected under aseptic conditions. FSH, LH, Prolactin levels were analyzed with the help of“Tosoh AIA360 Analyzer Kit” with fully automated analyzer equipment, Fasting blood glucose levels were analyzed with “BioSystem Kit” with Bio system A-15 fully automated analyzer in both test and control groups. To determine the follicular status of the test and control groups, ultrasonography was performed. Based on the following criteria, the EuropeanSociety of Human Reproduction and Embryology/American Society for Reproductive Medicine in 2003 (Rotterdam PCOS ConsensusWorkshop Group, 200410 the test subjects were selected. Inclusion Criteria for Test subjects 1. Age:17years to 40 years 2. Oligomenorrhoea or Anovulation (Less than eight menstrual cycles in a year).9 3. Clinical and biochemical signs of hyperandrogenism. 4. Polycystic ovaries (presence of 12 or more folliclesin each ovary measuring 2–9 mm in diameter and/or increased ovarian volume of 10 ml) Exclusion Criteria for Test subjects 1. Women below 17 years and above 40 years. 2. Pregnant and Lactating mothers 3. Other etiologies (e.g. congenital adrenal hyperplasia, androgen-secreting tumors and Cushing’s syndrome) 4. Patients using drugs affecting sex hormones and blood glucose levels. Inclusion Criteria for control group 1. Women aged between 17-40 Years 2. Regular menstrual cycles between 21 to 35 days. 3. Normal ovaries Exclusion Criteria for control group 1. Women below 17 years and above 40 years 2. Pregnant and Lactating mothers. Statistical Analysis The resultant parametrical measurements were subjected to statistical analysis to validate the significance of the study using SPSS version 16.
RESULTS
The mean age of menarche in both the test group and control group was 13 years. The mean BMI of the test group was 25.48 Kg/m2 . The mean BMI of the control group was 23.07Kg/m2 . The Mean FSH levels in test group 7.88 mIU/ml. The mean FSH levels in the control group was 8.95mIU/ml. The mean Prolactin levels in the test group were 16.635 ng/ml. The mean Prolactin levels in the control group were 10.35 ng/ml. The mean LH levels in the test group were 6.53mIU/ml. The mean LH levels in the control group were 3.76mIU/ml. The mean fasting blood glucose levels in the test group was 94 mg/dl. The mean fasting blood glucose levels in the control group was 84 mg/dl. The cumulative mean of all these parameters is depicted in Table-1. The FSH to LH ratio was in the test group was 1.46 and in the control group it was 3.56 (Table-4). Paired samples “t” test was performed to validate the study and its significance (Table-2). Also comparison of the parameters of test and control groups is depicted in (Table-3).
DISCUSSION
Polycystic ovarian disease can cause either primary or secondary infertility if the primary cause like dyslipidemia, insulin resistance and hyper androgenemic causes remain untreated. 11 In the present study the fasting blood glucose levels in the test group was having marginal increase than the control group which is indicative of a rising insulin resistance. Categorization of obesity should be ethno centric as the body fat percentage varies in ethnic populations and treatment modalities also will change accordingly5 . In our study obese women with polycystic ovaries were more than in the control group. However in a study with a small sample size, the prevalence of polycystic ovaries can be moderate.12 and concomitant presence of obesity will worsen the outcome of a metabolic disorder.13 Luteinizing hormone effect in polycystic ovarian syndrome in patients with an increased body mass index, this mediation of hormonal control is done in the pituitary gland and not in the hypothalamus.14 In the present study, the luteinizing hormone levels were higher than the control group which could be contributing to polycystic ovarian disease. Low levels of follicular stimulating hormone were found in women with polycystic ovaries which suggest that there is anovulation in these women.15 It is evident from the present study that the levels of follicular stimulating hormone are lower in women with polycystic ovarian syndrome than in the control group. In most of the studies hyperprolactinemia was an exclusion criterion for polycystic ovarian disease and in the present study where Prolactin levels were also measured and the Prolactin levels were significantly higher in the test group than the control group which indicates that Prolactin levels will be elevated in women with polycystic ovarian disease. In a study conducted in Bangladesh, it has been concluded that a there is a definitive link between body mass index, insulin resistance with the fertility levels.4 In the present study the authors agree with the findings of the study as the parameters measured and the results obtained from the present study were also similar. CONCLUSION Polycystic ovarian syndrome affected women who are obese will have elevated and abnormal hormonal levels as evident from the present study. The Body Mass Index causes disturbances in the menstrual cycle of women with polycystic ovarian syndrome. Anovulatory cycles of women affected by polycystic ovarian disease will reduce fertility levels. Obese women in the reproductive age group with menstrual cyclic disturbances should undergo hormonal profiling and fasting blood glucose to rule out insulin resistance. Since the sampling size of the present study is modest a larger sample size is being done to categorically validate the above findings. However the results of the study can be taken as guideline when investigating obese women with polycystic ovarian disease.
ACKNOWLEDGEMENTS
The authors sincerely wish to thank the management, administrators and the Professor and Head of the department of Anatomy of Vinayaka Missions Kirupananda Variyar Medical College, Salem for their whole hearted support and permissions to utilize their resources and conduct this study. The authors acknowledge the great help received from the scholars whose articles cited and included in references of this manuscript. The authors are also grateful to authors/editors/publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Authors are grateful to IJCRR editorial board Members and IJCRR team of reviewers who have helped to bring quality to this manuscript.
Englishhttp://ijcrr.com/abstract.php?article_id=836http://ijcrr.com/article_html.php?did=836REFERENCES
1. Dunaif A. Insulin resistance and the polycystic ovary syndrome: Mechanism and implications for pathogenesis. Endocr Rev. 1997;18:774– 800.
2. Stein IF, Leventhal ML. Amenorrhea associated with bilateral polycystic ovaries. Am J Obstet Gynecol. 1935;29:181.
3. Zawadski JK, Dunaif A Diagnostic criteria for Polycystic ovary syndrome: Towards a rational approach. In: Dunaif A, Givens JR, HaseltineF(Eds). Polycystic ovary syndrome. Boston: Blackwell Scientific 1992;377.84
4. Ferdousi Begum., Clinical and Hormonal profile of Polycystic ovary syndrome. South Asian Federation of Obstetrics and Gynecology, May- August 2009;1(2):22-25
5. XiaoliChen,Renmin Ni, Yaqin Mo, Lin Li and Dongzi Yang. Appropriate BMI levels for PCOS patients in Southern China.Human Reproduction, Vol.25,No.5 pp 1295- 1302,2010
6. Dale PO, Tanbo T, Vaaler S, Abyholm T. Body weight ,hyperinsulinemia and gonadotropin levels in the Polycystic ovarian syndrome: evidence in two population Fertility and Sterility. 1992,58(38):487-491
7. McKeigue PM, Shah B, Marmot MG.Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians. Lancet .1991;337:382-6.
8. The World Health Organization Western Pacific Region, the International Association for the Study of Obesity, and the International Obesity TaskForce. The Asia–Pacific Perspective: Redefining Obesity and its Treatment. Melbourne: Health Communications Australia, 2000.
9. Misra A, Chowbey P, Makkar BM, Vikram NK, Chadha D, et al. Consesus statement for diagnosis of obesity, abdominal obesity and the metabolic syndrome for Asian Indians and recommendations for physical activity, medical and surgical management. J Assoc Physicians India. 2009;57:163-70
10. The Rotterdam ESHRE/ASRM-sponsored PCOS Consensus WorkshopGroup. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod 2004; 19:41–47.
11. SunitaJ.Ramanand, Balasaheb B Ghongane, et al. Clinical characteristics of polycystic ovary syndrome in Indian women. Indian J EndocrinolMetab. 2013 Jan-Feb: 17(1): 138- 145.
12. Bulent O. Yildiz, Eric S. Knochenhauer, et al. Impact of Obesity on the Risk for Polycystic Ovary Syndrome. J ClinEndocrinolMetab. Jan 2008; 93(1): 162-168.
13. Barber TM, McCarthy MI, Wass JA, Franks S 2006; Obesity and polycystic ovary syndrome. ClinEndocrinol (Oxf) 65:137-145. [PubMed].
14. Pagan YL, Srouji SS, Jimenez Y, et al. Inverse relationship between luteinizing hormone and body mass index in polycystic ovarian syndrome: investigation of hypothalamic and pituitary contributions. J ClinEndocrinolMetab 2006 Apr; 91(4):1309- 16.
15. Jan Holte, Torbjorn Bergh, et al. The independent effects of polycystic ovary syndrome and obesity on serum concentrations of gonadotrophins and sex steroids in premenopauseal women. Clinical Endocrinology Volume 41, Issue 4, 1994: 473-481.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241612EnglishN2014June23HealthcareCOMPARATIVE STUDY BETWEEN USE OF STAINLESS STEEL ENDERS NAILS AND TITANIUM ELASTIC NAILS FOR TREATMENT OF FRACTURES OF SHAFT FEMUR IN CHILDREN
English5663Ulhas SonarEnglish Milind IngleEnglish M. R. KoichadeEnglish AvinashYelneEnglishObjectives: To compare results of Enders and titanium elastic intramedullary nailing for treatment of fractures of shaft femur in children between 5-15 years. Method: Twenty patients between age group of 5-15 years were treated with stainless steel Enders nailing and twenty patients of same age group were treated with titanium elastic nailing. Results were compared using Flynn etal 2001 criteria. Results: Average operative time was 36.2 minutes for Enders and 34.6minutes for titanium nailing. Average hospital stay was 6.21 days for Enders and 7.4 days titanium nailing. Average union time was 9.44 weeks in Enders and 9.52 weeks in titanium group. Average full weight bearing was achieved after 10.28 weeks in Enders and after 10.21 weeks in titanium group. Average full range of motion was achieved after 9.97weeks in Enders and after 9.50weeks in titanium group. Nail exterioration, nail irritation, superficial infection and asymptomatic lengthening were complications. Sixteen patients of Enders and fifteen of titanium group had excellent result as per Flynn etal2001 criteria. Rest had satisfactory results. There were no poor results. It indicated similar results in both groups. Conclusion: We found no statistically significant difference in outcomes of fractures treated with either method in clinical setting. Both methods have their own advantages and disadvantages.
EnglishEnders nails, Titanium elastic nails, fractures of shaft femur in childrenINTRODUCTION
Shaft or diaphyseal fractures of the femur are uncommon but significant injuries in children. They constitute less than 2% of all skeletal injuries in children. The commonest causes of femoral shaft fractures are falls and road traffic accidents. For children under walking age, abuse needs to be considered.(1) For generations traction and casting were standard treatment for all femoral shaft fractures in children and femoral fractures ranked high in duration of hospitalization for single diagnosis. Advantages of spica cast include low cost, excellent safety profile and very high rate of good results with acceptable leg length equality, healing time and motion.(2) Operative management is becoming a preferred option because of fact that there is decrease in incidence of malunion, shorter hospital stay, lesser surgical cost, better nursing care and early ambulation.(3) There has been growing trend to widen the indications for surgical treatment as attention has been focused on the difficulty of caring for children in body cast for 2-3 months.(4) The methods included external fixation, compression plating and intramedullary nailing with either rigid or flexible nails.(5) Intramedullary nail fixation has advantages as it is a percutaneous technique which does not damage growth cartilage. It keeps intact the fracture hematoma, maintains stability in three planes and provides opportunity to an early weight bearing giving an early rehabilitation at low cost with a minimal rate of complications.(6) It allows early weight bearing and walking.It aims to develop early bridging callus which contributes to rapid restoration of bone continuity.(7) In addition it requires much less operative time and fluoroscopy time.(8)
MATERIAL AND METHODS
This prospective study is an institutional based comparative study conducted at Indira Gandhi Government Medical College, Nagpur. All surgeries were performed by same surgical team.All patients between 5-15 years age group with closed or uncontaminated grade I compound fracture were included in study.Thorough history taking and clinical examination was done at first visit and patients were admitted after radiological investigations were done. Patients were divided in two groups, one group to be treated with stainless steel Enders nailingand other with titanium elastic nailing. All patients were operated in supine position.After proper preparation medial and lateral incisions were taken. Using awl, 2-2.5 centimeters proximal to physis, entry point was made. Nails were chosen so that each nail should fill at least 40% of canal by thickness. Nail lengths were predetermined on C-arm for Enders nailing. Two nails of similar thickness were bent approximately 25° at 1.5 centimeters from blunt ends. Both nails were passed up to fracture site. Closed reduction was done and whenever required open reduction was done and either of nail was passed in proximal fragment followed by second nail. Nails hammered to their final position. Thorough wound wash was given. Wounds closed in layers. Sterile dressing applied.Sutures were removed on outpatient basis between 10-14th day. Patients were allowed partial weight bearing to full weight bearing at first follow up between 4-8 weeks as per pain tolerance of patients.X-rays were taken at every follow up.Clinically wound related complications and limb length discrepancy was monitored. Results were classified as per criteria described by Flynn et al 2001(11) as depicted in table no 1. Children exceeding the criteria in any category were assigned the worse results.(11)All cases were at least followed for minimum duration of six months.Cases were further followed till the nail removal was done at varying periods.
STATISTICAL METHODS
The descriptive statistics for demographic variables like age, sex were obtained according to two nail types used in the surgery. The mean and standard deviations of diameters were obtained for the two nail types. The significance of difference in the mean nail diameter in both groups was evaluated using t-test for independent samples. Mean duration of surgery of two groups was evaluated for significance of difference using t-test for independent samples. Also, the difference between the mean stay at hospital for two groups of surgeries was determined using t-test for independent samples. The mean time for union, full weight bearing and full range motion between two surgery types was assessed for statistical significance using the above test.
RESULTS
In our study we derived the following results :- Minimum age in our series for Enders nailing group was six years, and for titanium elastic nailing group was also six years. And maximum age for Enders nailing group was thirteen years and for titanium elastic nailing group was fifteen years. An average mean age for Enders nailing group was 9.95years and for titanium elastic nailing group was 9.81years. Average age of male patient for Enders nailing was 10.6 years and for titanium elastic nailing was 9.5 years. Average age of female patients for Enders nailing was 8.3 years and 10.5 years was for titanium elastic nailing. The difference between the mean ages of patients was found statistically insignificant (p > 0.05) between two selected groups of Enders and titanium elastic nailing. It indicates that there was no age bias while selecting patients for treatment as regards to age. In our study overall there was a male preponderance. In our series there were 70% males in Enders nailing group and in titanium elastic nailing group 75% were males and rest were the females. The proportion of males and females selected for the two types of surgeries was statistically insignificant with p > 0.05. This indicated randomization as regards the gender distribution in two surgeries. In our series right side was involved in 42.5 % of patients and in 57.5% of patients left side was involved. In our study side distribution was almost similar in both surgical groups. This indicated randomization as regards the side distribution in two surgeries. In our study low energy injuries which includes fall were more common cause of fracture femur in children than high energy injuries including road traffic accidents. Distribution of mode of trauma was almost similar in two surgical groups indicating randomization regarding distribution of patients considering the mode of trauma. We had one grade I compound fracture which was treated with Enders nailing and rest were closed ones. We had two patients with associated injuries. Both hadipsilateral tibia fracture. One patient was treated with Enders nailing for femur and closed reduction and cast for tibia. Other patient was treated with titanium elastic nailing for fractures of femur as well as tibia. In our series transverse fractures were commonest overall. Oblique fractures were commoner than spiral fractures and comminuted fractures were least common. In our series middle third level fractures were commoner than upper third followed by lower thirdlevel fractures. In our series total operative time required was average 36.2 minutes for Enders nailing and for titanium elastic nailing it was 34.6 minutes. Maximum time required was 42 minutes and minimum was 30 minutes for Enders nail. For titanium elastic nailing maximum time required was 40 minutes and minimum time required was 30 minutes. There was no statistical significant difference in mean duration of surgery between two surgical groups indicating similar results. We had to open the fracture for getting reduction in four cases of Enders nailing and two cases of titanium elastic nailing. In most of the situation open reduction was required due to soft tissue interposition. Average stay at hospital was 6.21 days for patients treated with Enders nailing and 7.4 days for patients treated with titanium elastic nailing. The difference was found to be statistically insignificant with p > 0.05 using t-test for independent samples. On an average union was achieved in 9.44 weeks in Enders nailing group and in 9.52 weeks in titanium elastic nailing group. Union time was similar in both types of treatments. The difference was statistically insignificant (p > 0.05) for ‘Union time’. Our patients were able to bear full weight on an average after 10.28 weeks in Enders nailing group and after 10.21 weeks in titanium elastic nailing group. Out come in terms of time for full weight bearing was similar in both types of treatment. The difference was statistically insignificant (p > 0.05) for time for full weight bearing. Full range of motion was achieved in on an average after 9.97weeks in Enders nailing group and after 9.50weeks in titanium elastic nailing group. Outcome in terms of time for full range of motion was similar in both types of treatments. The difference was statistically insignificant (p > 0.05) for full range of motion. In our series there were no major complications. There was a single case of superficial infection in both groups which resolved with course of antibiotics for few days. There was one case of nail exterioration in titanium elastic nailing group which was asymptomatic and was found incidentally when a patient was called for implant removal. There were three patients in titanium elastic nailing group and two in Enders nailing group who suffered irritation at entry site of nail. All were resolved with course of few days of analgesics. There were four cases of lengthening in Enders nailing group and five cases of lengthening in titanium elastic nailing group. Lengthening was less than one centimeter in all cases and was clinically asymptomatic. In our series in Enders nailing group sixteen patients had excellent results and four patients had satisfactory results. There were no poor results. In titanium elastic nailing group fifteen patients had excellent results and five patients had satisfactory results. There were no poor results. Flynn et al 2001 scoring was almost similar in both surgical groups indicating similar results in both groups. The results of our study are also depicted in the X- ray photographs provided.
DISCUSSION
Goals of treatment of femoral shaft fractures in children and adolescent are achieving bone union with length, alignment and limb’s functional restoration, without losing movements of adjacent joints.(12) Enders and titanium elastic nails are the two types of flexible intramedullary nails used over the years; and both of them are consistently producing good results. (13)Small incision is required for these procedures. They usually require less time and minimal blood loss occur without damaging epiphyseal area. (14) Retrograde fixation is preferred. It has demonstrated significantly less axial range of motion and greater torsional stiffness than antegrade fixation in transverse as well as communited fracture patterns.(15)Normally recommendation for distal third femur fractures is antegrade nail insertion. But study done by Mehlman et al in synthetic models demonstrated that given satisfactory cortical starting points in the distal fragment, retrograde insertion provides greater stability.(16) Even about rotational stability, the study done by Gwyn et al has proved that this method of fixation provides a consistent mean of rotational stability for variety of fracture pattern in a synthetic model.(17)Most of the complications are caused by use of too thin nails, asymmetry of the frame, and malorientation of the implants.(18) Many studies have proven efficacy of both methods in treatment of femoral shaft fractures but very few have discussed about comparison of both methods of fixation. According to Wall EJ et al 2008 the in vitro mechanical studies comparing the two types of nails have demonstrated superior or equal stability in association with the use of titanium nails as compared with stainless steel nail. Biomechanical properties of titanium are often considered to be better than those of stainless steel with regard to biocompatibility, modulus of elasticity, osseointegration, corrosion resistance, and magnetic resonance imaging compatibility.But in clinical setting he has found superior results with use Enders nails as compared with titanium elastic nails in terms of rate of malunion. He hypothesized that the increased flexibility of titanium as compared with stainless steel nails may be responsible for the outcome. He stated that stainless steel nails are stiffer than titanium nails, which may be beneficial for preventing angular malunions following pediatric femoral fractures. (19) But there are some recent studies which have found no difference between clinical outcomes of both procedures. According to study performed by Lohiya et al 2011, there was no difference in results with type of nail used in his series (p = 0.12). Furthermore, he concluded that stainless steel nails produce results similar to titanium nails at considerably lesser price. (20) In another study performed by Kumar et al 2011 in sixty two fractures treated with flexible intramedullary nailing, he did not find any mismatch in the results of fractures stabilized withtitanium elastic nails or with that of Enders nails.(21)
CONCLUSION
We found that flexible intramedullary nailing is effective method of treatment for fractures of shaft of femur in pediatric age group between five to fifteen years with good outcomes and reasonably less complications. Enders nailing and titanium elastic nailing both are effective in treatment of femoral shaft fractures in children. We found no statistically significant difference in outcomes of fractures treated with either method in clinical setting. Both methods have their own advantages. Using titanium elastic nail the insertion of nail and negotiation of fracture was much easier as compared with Enders Nails. But implant removal was difficult compared to Enders nail. On the other hand Enders nail are much cheaper as compared to titanium elastic nail which is important aspect in Indian scenario.
ACKNOWLEDGEMENT
Authors acknowledge the immense help received from scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals, books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=837http://ijcrr.com/article_html.php?did=837REFERENCES
1. Madhuri V, Gahukamble AD, Dutt V, Tharyan P. Interventions for treating femoral shaft fractures in children and adolescents (Protocol). Cochrane Database of Systematic Reviews 2011, Issue 4. Art. No.: CD009076. DOI: 10.1002/14651858.CD009076.
2. Flynn JM, Skaggs DL. Femoral shaft fractures. In :Beaty JH, Kasser JR, editors. Rockwood and Wilkin’s Fractures in children volume four.7th ed. Philadelphia: Lippincott Williams and Wilkins, a Wolter Kluwer business ; 2010. P. 797-841
3. Singh P, Sharma V, Singh H, Wani IH, Gupta R, Gupta N. Treatment of Fractures Of the shaft of the femur in children by Ender`s nails: A prospective study. The Internet Journal of Orthopedic Surgery. 2009;11:1.
4. Khurram B, Humayun BEG. Flexible intramedullary nailing versus external fixation of paediatric femoral fractures. Actaorthop. Bel 2006;72:159-163
5. Vidyadhara S, Rao SK. Global reconstruction of type IIIA open comminuted femoral shaft fracture with segmental bone loss in an 11- year-old girl. Singapore Med J. 2006;47(9):817-9.
6. Ramírez JA, NafarrateEBlNúñez JA, Vallejo J, Campbell O, Peña JC. Arturo Aguirre Madrid Clavoscentromedularesflexibles en el tratamiento de fracturaspediátricas. Revista Mexicana de orthopaediapaediatrica 2004;6: 724-733.
7. Ligier JN, Metaizeau JP, Prévot J, Lascombes P. Elastic stable intramedullary nailing of femoral shaft fractures in children. J Bone Joint Surg Br 1988, 70(1):74-7.
8. Gregory P, Sullivan JA, Hernodon WA. Adolescent femoral shaft fractures: rigid versus flexible nails. Orthopedics 1995; 18:645-649
9. Anglen JO, Choi L. Treatment Options in Pediatric Femoral Shaft Fractures. journal of orthop trauma 2005;19: 724-733
10.Oztürkmen Y, Do?rul C, Balio?lu MB, Karli M. Intramedullary stabilization of pediatric diaphyseal femur fractures with elastic Ender nails. ActaOrthopTraumatolTurc. 2002;36(3):220-7.
11. Shekhar L, Mayanger JC. A clinical study of Ender nails fixation in femoral shaft fractures in children. Indian J Orthop 2006; 40: 35-7.
12. Cunha FM, Figueiredo LA, Coelho LFA, Malheiros DS, Terra DL, Lima CLFA. Femoral shaft fracture in children and adolescent. ActaOrthop Bras.2007; 15(2):80- 83.
13. Hasan Al-Sayed. Titanium Elastic Nail Fixation for Paediatric Femoral Shaft Fractures.Pan Arab J. Orth. Trauma- 2006; 10 (1):7-15.
14. Shiha A, Rifae HH, El-Deen MA. Elastic Stable Intramedullary Nailing of Femoral Shaft Fractures in Children. Pan Arab J. Orth. Trauma- 2004 ;8:11-16.
15. Fricka KB, Mahar AT, Lee SS, Newton PO. Biomechanical analysis of antegrade and retrograde flexible intramedullary nail fixation of pediatric femoral fractures using a synthetic bone model. J PediatrOrthop. 2004 MarApr;24(2):167-71.
16. Mehlman CT, Nemeth NM, Glos DL. Antegrade versus retrograde titanium elastic nail fixation of pediatric distal-third femoralshaft fractures: a mechanical study. J Orthop Trauma. 2006 Oct; 20(9):608-12.
17. Gwyn DT, Olney BW, Dart BR, Czuwala PJ. Rotational control of various pediatric femur fractures stabilized with titanium elastic intramedullary nails. J PediatrOrthop. 2004 Mar-Apr;24(2):172-7.
18. Lascombes P, Haumont T, Journeau P. Use and abuse of flexible intramedullary nailing in children and adolescents. J PediatrOrthop. 2006 Nov-Dec;26(6):827-34.
19. Wall EJ, Jain V, Vora V, Mehlman CT, Crawford AH. Complications of titanium and stainless steel elastic nail fixation of pediatric femoral fractures. J Bone Joint Surg Am. 2008; 90(6):1305-13.
20. Lohiya R, Bachhal V, Khan U, Kumar D, Vijayvargiya V, Sankhala SS. Flexible intramedullary nailing in paediatric femoral fractures. A report of 73 cases. J OrthopSurg Res. 2011;22:64
21. Kumar S, Roy SK, Jha AK, Chatterjee D, Banerjee D, Garg AK. An evaluation of flexible intramedullary nail fixation in femoral shaft fractures in paediatric age group. J Indian Med Assoc.2011;109:416-7.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241612EnglishN2014June23HealthcareAESTHETIC INTERDISCIPLINARY MANAGEMENT OF AGGRESSIVE PERIODONTITIS - A CASE REPORT
English6471Priyanka K. CholanEnglish P. RagaviEnglish P. RajapriyaEnglish Mangaiyarkarasi SubramanianEnglishAggressive periodontitis is a type of periodontal disease and is further classified based on their etiology and pathogenesis as: Localized aggressive periodontitis (LAP) and Generalized aggressive periodontitis (GAP). GAP is characterized by generalized interproximal loss of attachmentinvolving at least three permanent teeth other than firstmolars and incisors. This case report describes the periodontal and the aesthetic management of a patient with generalized aggressive periodontitis.
EnglishAggressive periodontitis, flap surgery, implants, smile correctionINTRODUCTION
Aggressive periodontitis, as the name implies is a type of periodontitis where there is rapid destruction of periodontal ligament and alveolar bone which occurs in otherwise systemically to healthy individuals of a younger age group but older patients maybe rarely involved in it1,2 . Its etiology is highly correlated due to the presence of Aggregatibacteractionmycetemcomitans3 and host response defects and also possibly related to a genetic inheritance4 .Though there is no widely accepted treatment protocol for Generalised Aggressive periodontitis, this article presents the clinical management of the periodontal and esthetic aspects of a patient with aggressive periodontitis and smile designing for the same. Clinical relevance to interdisciplinary dentistry A multidisciplinary approach to provide improved aesthetics and function. A combinational approach by a team of periodontist, endodontist and prosthodontist helped in the periodontal and esthetic management of a patient with aggressive periodontitis. Management included full mouth flap debridement, implant placement and fixed prosthesis and aesthetic management of protruded teeth and facial profile.
CASE REPORT
A 24 year old female patient reported to the Department of Periodontics with the chief complaint of forwardly placed teethwith spacing which has increased over the years and bleeding gums for the past 6-7 years. The patient noticed the flaring of anterior teeth few years before, after which she noticed it to be gradually increasing and associated with intermittent episodes of gingival bleeding. There were no related complaints other than a cosmetic concern from the patient. Her medical history appeared non-contributory, as she was not taking any medication, referred no allergies, and had no history of episodic illness or orofacial trauma. Familial history reveals brother with mobile anterior teeth and periodontally compromised dentition. Clinical oral examination, showedgeneralised gingival recessionassociated with deep periodontal pockets as shown in tables I, II, III and IVwith Millers grade I mobility in 11,12,21,22,26,23,24,36,37,38,47 and Millers grade III mobility in 31,41,32 and 42 (Figure 1). The panoramic X-ray (Figure 2) and full mouth IOPAs revealed generalized moderate to severe bone loss which was a combination of both horizontal and vertical bone loss and the severity of bone loss in correlation to the age of the patient suggested a rapid rate of disease progression. The patient was referred for a complete medicalevaluation to rule out any underlying systemic disease. Her complete blood count was within normal limits, including basal glucose and creatinine levels. Absolute monocyte and neutrophil counts were slightly elevated. Due to the age of the patient, familial history, the severity of bone loss, the lack of a detectable systemic disease and rapid rate of disease progression, the diagnosis of Generalized Aggressive Periodontitis was made.Treatment plan was categorized under the following phases including non-surgical phase, surgical phase, restorative phaseand maintenance phase. The major challenges faced in treating this particular case were, compromised periodontal status with advanced attachment and bone loss, gingival recession, unaesthetic gingival display, proclined upper incisors and spacing between the teeth. The treatment options proposed wereorthognathic surgery, orthodontic treatment, rehabilitation with implants and endodontic treatment. The patient was reluctant for orthodontic treatment and orthognathic surgery, due to the prolonged duration of treatment and major surgery associated fear and anxiety. Hence a full mouth periodontal management with extraction of hopeless prognosis teeth and rehabilitation with implants with aesthetic endodontic correction was planned.
CASE DISCUSSION
The periodontal management included supragingival and subgingival scalingand root surface debridementand the patient was motivated for better plaque control. Full mouth disinfection with chlorhexidine gelsupplemented with systemic antimicrobial therapy was followed for a period of 8 days. The patient was recalled after 2 weeks for evaluation of the response to treatment5,6 . Persistent high bacterial counts and the presence of periodontal pathogens at surgery adversely affect clinical attachment level gains, meticulous initial therapy and good oral hygiene are considered to be prerequisites for successful periodontal surgery7 . In the surgical phase,a quadrant-wise full mouth flap debridement (Figure 3)was done with bone grafting in relation to upper and lower molar regions. Extraction of hopeless prognosis teeth 31, 32, 41, 42 were done with immediate implant placement. Life care implants 2.8×10 mmwas placed in relation to 32, 42 region (Figure 4)and temporary crowns were given.A postsurgical evaluation done 3 weeks later showed satisfactory healing and probing depths within normal limits. The patient was put on regular recall appointments for evaluation of the gingival and periodontal status and maintenance therapy. Since the patient was concerned about the esthetic appearance of the anterior teeth, she was advised to undergo aesthetic endodontic management. Targets to be achieved in Aesthetic management include: 1. Correction of labial proclination and spacing, which was done stepwise by targeting the required outcome of diastema closure 2. Reduction of theproclined upper incisors 3. Reduction of excessive incisal exposure 4. Rectification of the smile line8 In order to appropriately execute the treatment plan, proper pre-operative photographs were taken
(Figure 5) and awax mock up was done on the study cast (figure 6).9,10Duplication of the wax mock uphelped in both evaluating the possible treatment outcome and aided in providing the patient an understanding of the probable outcome of the treatment. It also helped in obtaining the template to provide proper temporaries during treatment course 9,11. Due to the excessive proclination, the tooth preparation in upper incisors would result in pulpal exposure which indeed led to the intentional root canal treatment for 11, 12, 21 and 22. The tooth preparation was done for full veneer crown in upper incisors 11, 12, 21 and 22 (figure 6). During the tooth preparation the proclination had to be reduced and the incisal height had to be decreased, so the tooth preparation was done more on the labial aspect. The incisal reduction was done excessively to reduce the crown height and the preparation margins were done above DEJ(dentinoenameljunction) inorder to reduce the excessive incisal exposure. The temporaries were given with the help of the available template for the upper incisors, the treatment outcome was evaluated and the high points, mainly canine recountouring was done for 33 and further adjustments were made on the temporaries. Following this an impression was taken with the temporaries which acted as a guide for the final porcelain fused metal crowns. Since the periodontal status was compromised, the full veneer crownsfor 11, 12, 21 and 22 were done as a single unit which acted as a splint supporting the mobile teeth. The permanent crowns were then luted in place with type 2 GIC (figure 7). This case was followed upto two years to evaluate any relapse or further bone resorption is related to rehabilitation of teeth resulted in full satisfaction.
CONCLUSION
Even though the occurrence of aggressive periodontitis is much lower than the chronic Periodontitis, the management ofaggressive periodontitis is more demanding compared to that of chronic periodontitis because of its strong geneticpredisposition as an unmodifiable risk factor. In the present scenario the key to a wholesome management of aggressive periodontitis lies in the early diagnosis of the disease process, rigorous treatment modalities and scrupulous life- long maintenance therapy.
Englishhttp://ijcrr.com/abstract.php?article_id=838http://ijcrr.com/article_html.php?did=838REFERENCES
1. Armitage G C. Development of a classification system for periodontal diseases and conditions.AnnPeriodontol 1999;4:1-6.
2. American Academy of Periodontology, “Parameter on aggressive periodontitis,” Journal of Periodontology, 2000:71(5): 867– 869.
3. Fine DH, Markowitz K, Furgang D, Fairlie K, Ferrandiz J, Nasri C, et al. Aggregatibacteractinomycetemcomitans and its relationship to initiation of localized aggressive periodontitis: longitudinal cohort study of initially healthy adolescents. J ClinMicrobiol 2007;45:3859-69.
4. Kinane DF, Shiba H, Hart TC. The genetic basis of periodontitis. Periodontol 2000 2005;39:91-117.
5. M. G. Jorgensen and J. Slots, “Practical antimicrobial periodontal therapy,” Compendium of Continuing Education inDentistry, 2000;21(2):111–124.
6. Roshna Tand Nandakumar K. Generalized aggressive periodontitis and its treatment options:case reports and review of the literature. Case reports in medicine October 2012, Article ID 535321.
7. Jung M H, Park J W, Suh J Y and Lee J M. Clinical case report on treatment of generalized aggressive periodontitis. J Periodontal Implant Sci 2010;40:249-253.
8. Goldstein RE. Esthetics in Dentistry.Philadelphia, PA: JB Lippincott Co 1976:7.
9. Davis N C. Smile Design. Dent Clin N Am 2007;51:299-318
10. Bhuvaneswaran M. Principles of smile design.J Conserv Dent 2010;13:225-32
11. Harry F. Albers. Tooth - colored restoratives: Principles and Techniques, Ninth edition.
12. Goldstein RE. Esthetics in Dentistry.Philadelphia, PA: JB Lippincott Co 1976:7.
13. Chalifoux PR. Anterior porcelain veneers, three-quarter crowns, and full crowns. Contemporary Esthetics and Restorative Practice. 1998;2(1):52-61.
14. Kinsel R P, Capoferri D.Full crowns in the esthetic zone.Dental Dialogue 2005; Volume 5(4). 15. Abbott SJ. Metal-ceramic restorations. Adv Dent Res. 2003;17:55-60.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241612EnglishN2014June23HealthcarePLEURAL IMPLANT OF THYMOMA CYTOMORPHOLOGY - A CASE REPORT
English7275Brahmaiah ChariEnglish Vinay H. ShankarEnglish Geetha V. English Chethana S. BabuEnglish Brij Mohan Kumar SinghEnglishThough recurrence of thymoma is rare, yet pleural dissemination has been described by few authors. We present a 37 year old patient who was diagnosed as thymoma WHO classification type B3, stage III on Masoaka staging and underwent complete thymectomy. Two years later she presented with recurrent myasthenic symptoms.On evaluation a pleural nodule was identified .CT guided fine needle aspiration suggested a recurrence.Asrecurrence is rare and no definitiveguidelinesregarding therapy; cytological morphology would be of great help in recognizing recurrence. This would also serve to reduce the requirement of thoracoscopic surgery and its related mortality and morbidity.
EnglishThymoma , FNAC(Fine needle aspiration cytology), WHO-World health organization, CT- Computed TomographyINTRODUCTION
Thymoma is a thymic epithelial neoplasm exhibiting organoid features, accompanied by variable numbers of reactive lymphoid cells.1Cytological diagnosis of thymoma is one of the difficult task encountered in mediastinal lesions,the reason being the rarity of the tumour and the difficulty in getting proper and adequate sampling which is highly dependant on the technical skill of interventional radiologist. Additional characteristic histopathological features that helps in diagnosis of thymoma, such as organotypical differentiation, lobule formation, dilated perivascular spaces can be completely missed in aspiration slides. As there is no standard protocol for the treatment of recurrences, most of the authors in the literature proposed thetreatment that would be multimodal based on evidence based practice.2 Invasive thymoma is characterized by microscopic invasion through fibrous capsule or frank invasion into pericardium, great vessels, and lung. Some thymomasshow multiple implants on pleural and pericardial surfaces.3An invasive thymoma behaves as a malignant tumor despite its benign histologic appearance.A frequent pattern of dissemination of thymoma is by formation of pleural implants.4
CLINICAL FEATURES
A 37 year old female patient was admitted for evaluation of a chest nodule, detected on regular follow up with CT thorax. Past history was significant for myasthenia gravis and thymoma which was diagnosed 2 years earlier. She had undergone a resection of tumour with histopathological diagnosis as thymoma type B3 according to WHO classification 2004. Systemic examination was within normal limits. Her currentCT scan showed non-enhancing soft tissue density, two pleural lesions. One, measuring 3.6x1.4cms in third intercostal space and another noted along minor fissure 8x16mms(Fig A & B).
DISCUSSION
The distinction between benign and invasive thymoma depends on the demonstration of local invasion or extrathymicmetastasis.2Benign or invasive thymomasshow perivascular space rosette-like formation and gland-like formation seen in contrast to thymic carcinoma.3 Keen and Libshitz6 and Zerhouni et al 5 documented 94% and 91% accuracies of invasion to great vessel and/or pericardium, lung, and pleura on thin-section CT scans.Local invasion by thymomacan involve the chest wall, lower neck, pleura, great vessels and pericardium. They may also spread by pleural seeding.7,8 The reason for the appearance of pleural implants, so called ‘droplet metastases’, after many years of the resection of a non-invasive thymoma is not clear.7The 5-year and 10-year survivals in the series of Verley and Hollmann were 85% and 80% for the group with noninvasive thymomas and dropped to 50% and 35% for the group with invasive thymomas.6,7
CONCLUSION
FNA cytology is a rapid and useful technique in confirming the presence of pleural deposits in a thymoma and cell block when available can be used for IHC studies for confirmation and avoid unnecessary thoracic surgeries and its related morbidity
Conflicts of interest – Ni
ACKNOWLEDGEMENT
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=839http://ijcrr.com/article_html.php?did=839REFERENCES
1. WahCheuk , John K, C.Chan. Tumors of lymphoreticular system, The Thymus. In:Diagnostic Histopathology of Tumors . Christopher Flitcher (editor); Third Edition.Church Hill Livingstone Elsevier,China: 1315
2. Lucchi M, Mussi A. Surgical treatment of recurrent thymomas. J Thorac Oncol.2010 Oct;5(10 Suppl 4):S348-51
3. Hao-Chun Hung Tan Lee San-Kan LeeDifferential Diagnosis of Invasive Thymoma and Thymic Carcinoma by CT Findings Chin J Radiol 1999; 24(5):179-184.
4. Suster S, Moran CA. Thymoma classification: current status and future trends. Am J ClinPathol. 2006;125:542-554.
5. Zerhouni EA, Scott WW Jr, Baker RR, Wharam MD, Siegelman SS. Invasive thymoma: diagnosis and evaluation by computed tomography. J Comput Assist Tomogr 1991; 15: 429-433.
6. Keen SJ, Libshitz HI. Thymic lesions: experience with computed tomography in 24 patients. Cancer 1987; 59: 1520-1523
7. Verley JM, Hollmann KH. Thymoma: a comparative study of clinical stages, histologic features and survival in 200 cases. Cancer 1985; 55: 1074-1086
8. Marco Lucchi, Fulvio Basolo and Alfredo Mussi Surgical treatment of pleural recurrence from thymomaEuropean J CardiothoracSurg 2008;33:707-711