Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241113EnglishN2019February7HealthcareEmotional Intelligence: A Analytical Study of Basketball Players English0105Maman PaulEnglishThis study examined the emotional intelligence level among male basketball players. A group of fifty (N=50) male inter-college level basketball players of Guru Nanak Dev University, Amritsar, Punjab were selected for this study. The purposive sampling technique was used to attain the objectives of the study. All the subjects, after having been informed about the objective and protocol of the study, gave their consent and volunteered to participate in this study. They were further divided into (N=10) each playing position i.e. Point guard (n1=10), Shooting guard (n2=10), Small forward (n3=10), Power forward (n4=10) and Center (n5=10). To measure the level of Emotional Intelligence of the subjects, the Emotional Intelligence Scale constructed by Hyde et al. (2001) was administered. One way Analysis of Variance (ANOVA) was employed to find out the intra-group differences. Where F values were found significant, LSD (Least Significant Difference) Post-hoc test was applied to find out the direction and degree of difference. For testing the hypotheses, the level of significance was set at 0.05. Summarizing from the above findings we can say that insignificant differences were found among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) on the sub-variables of Emotional Intelligence. EnglishEmotional Intelligence, BasketballINTRODUCTION Many scientific studies have been made on emotions and affections in recent years. More and more sports psychologists suggest that emotional intelligence could serve important role in different fields of sports. Research has shown psychological skills facilitate athletic performance. Relaxation training, positive thought control, self-regulation, imagery, concentration, energy control, self-monitoring, and goal setting are all traits that have been correlated with athletic performance (Zizzi, Deaner, & Hirschhorn, 2003). Many of these traits reflect emotional intelligence. These same traits have been correlated with work group cohesion, job performance, role conflict, and job satisfaction (Zizzi, Deaner, & Hirschhorn, 2003) Emotional intelligence includes distinguishing and controlling emotions in order to influence one's thoughts and behavior (Bradberry, Greaves, 1953). Emotional intelligence is an essential element of human behavior which acts independently and differently from cognitive intelligence (Bar-on, 2000). Emotional intelligence has its roots in Gardner’s interpersonal and intrapersonal intelligence (Bar-on, 2000). The concept of emotional intelligence has provided a new insight into human intelligence and it represents the emotional, personal, and social dimensions of intelligence which are often more important for daily activities and interpersonal competitions than the conventional, cognitive dimensions of intelligence (Goleman, 1998). In order to prepare better players for this new century in sports, it might be better to include emotional intelligence in lives of players. Sports activity is integral to the all-round development of human personality. Sports bring pleasure due to emotional overtones and outward focus of attention in sports activities (Salovey & Mayer 1990). Emotional overtones of sports life removes boredom of daily routines and adds depths of feeling in coloured life. Outward focus of attention in sport brings not only well mental health but also emotional satisfaction (Sharma, 2016). Mayer and Salovey (2004) defined Emotional Intelligence as, “The capacity to reason with emotion in four areas to perceive emotion, to integrate it in thought, to understand it and to manage it. Petrides et al. (2004) suggested that people with high levels of emotional intelligence have a natural aptitude for emotional perception and can utilize this to move people to respond positively to them. Hein (2000) described emotional intelligence as knowing how to separate healthy feelings from unhealthy ones and how to turn negative feelings into positive ones. This study therefore investigated the applicability of emotional intelligence to male basketball players and further administered a programme of emotional intelligence on the athletes with a view to establishing its effectiveness or otherwise on their sports. MATERIAL AND METHODS SUBJECTS To obtain data, the investigator had selected Fifty (N=50) male inter-college level basketball players of Guru Nanak Dev University, Amritsar, Punjab were selected for this study. They were further divided into (N=10) each playing position i.e. Point guard (n1=10), Shooting guard (n2=10), Small forward (n3=10), Power forward (n4=10) and Center (n5=10). TOOLS To measure the level of Emotional Intelligence of the subjects, the Emotional Intelligence Scale constructed by Hyde et al. (2001) was administered. STATISTICAL ANALYSIS One way Analysis of Variance (ANOVA) was employed to find out the intra-group differences. Where F values were found significant, LSD (Least Significant Difference) Post-hoc test was applied to find out the direction and degree of difference. For testing the hypotheses, the level of significance was set at 0.05. RESULTS It can be seen from table-1 that insignificant differences were found with regard to the sub-parameter Self-Awareness among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) as the P-value (Sig.) .365 was found higher than the 0.05 level of significance (p>0.05). Since F-value was found insignificant, therefore, there is no need to apply Post-hoc test. It can be ascertained from table-2 that insignificant differences were found with regard to the sub-parameter Empathy among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) as the P-value (Sig.) .783 was found higher than the 0.05 level of significance (p>0.05). Since F-value was found insignificant, therefore, there is no need to apply Post-hoc test. It is evident from table-3 that insignificant differences were found with regard to the sub-parameter Self-Motivation among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) as the P-value (Sig.) .527 was found higher than the 0.05 level of significance (p>0.05). Since F-value was found insignificant, therefore, there is no need to apply Post-hoc test. It can be observed from table-4 that insignificant differences were found with regard to the sub-parameter Emotional Stability among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) as the P-value (Sig.) .322 was found higher than the 0.05 level of significance (p>0.05). Since F-value was found insignificant, therefore, there is no need to apply Post-hoc test. It can be seen from table-5 that insignificant differences were found with regard to the sub-parameter Managing Relations among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) as the P-value (Sig.) .045 was found higher than the 0.05 level of significance (p>0.05). Since F-value was found insignificant, therefore, there is no need to apply Post-hoc test. The results of Analysis of Variance (ANOVA) in table-6 that insignificant differences were found with regard to the sub-parameter Integrity among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) as the P-value (Sig.) .234 was found higher than the 0.05 level of significance (p>0.05). Since F-value was found insignificant, therefore, there is no need to apply Post-hoc test. It can be seen from table-7 that insignificant differences were found with regard to the sub-parameter Self-Development among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) as the P-value (Sig.) .877 was found higher than the 0.05 level of significance (p>0.05). Since F-value was found insignificant, therefore, there is no need to apply Post-hoc test. The results of Analysis of Variance (ANOVA) in table-8 that insignificant differences were found with regard to the sub-parameter Value Orientation among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) as the P-value (Sig.) .890 was found higher than the 0.05 level of significance (p>0.05). Since F-value was found insignificant, therefore, there is no need to apply Post-hoc test. It can be seen from table-9 that insignificant differences were found with regard to the sub-parameter Commitment among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) as the P-value (Sig.) .577 was found higher than the 0.05 level of significance (p>0.05). Since F-value was found insignificant, therefore, there is no need to apply Post-hoc test. It can be seen from table-10 that insignificant differences were found with regard to the sub-parameter Altruistic Behaviour among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) as the P-value (Sig.) .788 was found higher than the 0.05 level of significance (p>0.05). Since F-value was found insignificant, therefore, there is no need to apply Post-hoc test. It can be seen from table-11 that insignificant differences were found with regard to the parameter Emotional Intelligence among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) as the P-value (Sig.) .890 was found higher than the 0.05 level of significance (p>0.05). Since F-value was found insignificant, therefore, there is no need to apply Post-hoc test. CONCLUSION Summarizing from the above findings we can say that insignificant differences were found among basketball players (Point Guard, Shooting Guard, Small Forward, Power Forward and Center) on the sub-variables of Emotional Intelligence. PRACTICAL APPLICATION The study will be considerably helpful to comprehend the Emotional Intelligence level existing among male basketball players. The sports psychologists and coaches working with these areas will drive benefit from the findings of the present research and they can integrate Emotional Intelligence variables in their training schedule from the very initial stages. Englishhttp://ijcrr.com/abstract.php?article_id=2579http://ijcrr.com/article_html.php?did=2579Bar-On, R. (2000). Emotional and social intelligence: Insights from the Emotional Quotient Inventory, Handbook of emotional intelligence. Bradberry, T., Greaves, J. (1953). Test of Emotional intelligence. Goleman, D. (1998). Working with Emotional Intelligence. Bantam, New York. Goleman, D. (1999). The Human Task of a Project Leader. PM Network Journal, 13, 38-41. Hanin, Y. L. (2000). IZOF-based emotions-profiling: Step-wise procedures and forms. In Y. L. Hanin (Ed.), Emotions in sport, 303–313. Champaign, IL: Human Kinetics. Hyde, A., Pethe, S., & Dhar, U. (2001). Publication Manual for Emotional Intelligence Scale. National Psychological Corporation, 4/230. Kacheri Ghat, Agra, India. Mayer, J. D., Salovey, P., & Caruso, D. R. (2004). Emotional Intelligence: Theory, Finding and Implication. Psycho Enquiry, 15, 197-215. Petrides, K.V., A. Furnham & G.N. Martin. (2004). Social Psychol. 144, 149-162. Salovey, P., & Mayer, J. D. (1990). Emotional Intelligence. Imagination, Cognition and Personality, 9, 185-211. Sharma. M. (2016). A Study of Emotional Intelligence of Players and Non-Players. IOSR Journal of Humanities and Social Science, 21, 4, 16-19. Zizzi, J. S., Deaner, H., & Hirschhorn, D. (2003). The Relationship between Emotional Intelligence and Performance among College Baseball Players. Journal of Applied Sport Psychology, 15, 262-269.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241113EnglishN2019February7HealthcareA Study on Effects of HbA1c Levels on Nerve Conduction Velocity in Type 2 Diabetes Mellitus Patients English0608Abeer MasoodEnglish S. Aijaz A. RizviEnglish Sheelu S. SiddiqiEnglish Md ZiauddinEnglishAim: Diabetes mellitus is specifically a condition of hyperglycemia, insulin resistance, and relative impairment in insulin secretion.It is characterized by micro and macro vascular complications that lead to significant morbidity and mortality. Diabetic peripheral neuropathy is one of the most common long term complications of DM. HbA1c estimation is usually done which is indicative of glycaemic control. Nerve conduction studies (NCS) are electrodiagnostic tests used to evaluate the ability of the electrical conduction of the motor and the sensory nerves. Therefore the effect of HbA1c on the nerve conduction velocity in Type 2 Diabetes Mellitus Patients was studied. Methodology: Total number of 60 subjects (diabetic subjects and the healthy controls) were examined to assess the Diabetic neuropathy. Sensory Nerve conduction velocity (NCV) test was done along with the estimation of HbA1c levels in all the diabetic subjects (HbA1c≥6.5%) and the healthy controls. Results: The analysis showed that the nerve conduction velocity decreased in diabetic patients with apoor glycaemic control in comparison to healthy and diabetic subjects with good glycaemic control. Conclusion: In diabetic subjects there is progressive neuronal involvement which is accelerated by poor glycaemic control leading to development of diabetic neuropathy. Therefore, NCS can be employed for the early detection of neuropathy in diabetic patients. EnglishDiabetes mellitus, Nerve conduction studies, Glycated haemoglobinINTRODUCTION Diabetes mellitus is specifically a condition involving hyperglycaemia, insulin resistance, and relative impairment in insulin secretion [1]. It has become one of the fastest spreading endocrine disorders, characterized by metabolic abnormalities and with prolonged duration there is ongoing micro and macro vascular complications that can lead to significant morbidity and mortality [2]. In response to insulin resistance, hyperinsulinemia play an important role in the genesis of these abnormalities. The most commonly occurring microvascular complication is “Diabetic neuropathy” (DN) that accounts for around 28% of all the complications seen in diabetics [3]. It is a progressive condition with presence of chronic period of asymptomatic stage [4]. In the asymptomatic stages, it leads to the diabetic foot as the disease process progresses, which proves to be a highly morbid condition that arises from the infection and the ulceration of the foot, ultimately which may lead to amputation [5]. Therefore, identification of neuropathy in diabetics is considered to be important. For preventing DN and other diabetic complications; early identification and good glycaemic control are the essential factors. According to the recommendations of the American Academy of Neurology at least one of the five criteria for diagnosing DN should be present: Symptoms, Signs, electro-diagnostic tests, Quantitative sensory tests and Autonomic testing [6]. Practically, Nerve conduction studies (NCS) are electro-diagnostic tests which are used to evaluate the ability of the electrical conduction of the motor and the sensory nerves. Also, it is a known fact that poor glycaemic control is responsible for early onset of microvasular complications [7]. Glycated haemoglobin (HbA1c) has been established as a marker of glycaemic control and it also provides an indication of the risks that produces onset of microvascular complications [8]. 50% of patients present with symptoms like sensation of numbness, tingling, sharp burning pain. The patients may have a "glove and stocking" distribution of sensory symptoms involvement. Hence, we intended to correlate Nerve conduction studies (NCS) with HbA1c to establish their role in Diabetes. MATERIALS AND METHODS This study was undertaken in the Department of Physiology in collaboration with Rajiv Gandhi Centre for Diabetes and Endocrinology on patients of Type 2 Diabetes Mellitus (T2DM) attending Diabetes clinic at J. N. Medical College, Aligarh Muslim University, India after approval from institutional research and ethical committee. A total number of 60 subjects were included in the study group. The patients of 29-69years of age with a history of diabetes for 5-10 years attending the diabetic OPD were selected. Glycated haemoglobin levels were estimated, depending on the values of HbA1c subjects were divided into 2 Study Groups: Group 1: 30 Type II diabetes mellitus patients with poor glycemic control, of both sexes, of age group 29-69 years. Group 2: 30 Non-diabetic healthy subjects, of both sexes, of age group 29-69 years as a control group. Group 2 was not associated with polyneuropathy, family history of peripheral nerve disease and consumed alcohol or drugs with potential neurotoxic effects. Patients with Type I DM, Type II DM patients on insulin therapy were excluded. A consent was obtained from each participant and procedure was explained. Windows based Computerized EMG/NCV equipment NeuroStim4 in NCV lab in the Department of Physiology was used for electrophysiological analysis using surface electrodes to record the NCV.   Statistical evaluation of the results was performed using the statistical package IBM SPSS22. The data was summarized to test the difference in the mean values between the groups 1 and 2 by using the Student’s (unpaired) t test; p values < 0.05 were taken as the level of significance. Pearson’s correlation was used to correlate between the different parameters. RESULTS DISCUSSION Diabetic neuropathy is a common complication of diabetes mellitus leading to severe morbidity that compromises the quality of life and affects daily routine activities. An intensive treatment of neuropathy at the sub clinical level decreases the risk of neuropathy [9]. One of the important methods for assessing nerve functions in DN is the Nerve conduction studies. In this study, it was observed that the nerve conduction velocity progressively decreased from the controls (51.30 ±3.6) to the diabetics with poor glycaemic control (25.32± 12.31). These findings are in accordance with those of previous researchers Bansal et al, 2006 have suggested that the slowing of NCV indicates it is due to the continuous damage occurring to the myelin sheaths and they are also of the opinion that the amplitude decreases with the rising HbA1c levels, thus resulting in the onset and progression of axonopathy [11]. Therefore, the monitoring of diabetic patients with NCS may provide help in predicting the onset of DN. So we draw a conclusion, that the estimation of both NCV and the HbA1c levels in diabetics is helpful in identifying the risk category for DN, which is one of the main causes for severe morbidity among the diabetes. Also Clayton W, Elasy TA et al,2009 showed that the accumulation of sugar products results in a decrease in the synthesis of nerve cell myoinositol, which inhibits Na+/K+ ATPase activity, that is required for normal neuron conduction. Decrease in activity of Na+/K+ ATPase pump results in Na +/K+ retention, oedema, myelin swelling, axoglial dysfunction and nerve degeneration; further leading to cause neuropathy. [12] CONCLUSION The present study showed that both, nerve conduction studies and glycated hemoglobin, are useful modality for detecting diabetic neuropathy. Nerve conduction studies are one of the important methods for diagnosis and evaluation of diabetic sensorimotor polyneuropathy especially for the subclinical neuropathies. Routine nerve conduction studies can be done regularly in diabetic subjects at least on yearly basis. Our study recognises that periodic screening should be carried out in diabetics to prevent long term complications of diabetes. 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. CONFLICTS OF INTEREST:  There is no conflicts of interest. The study was conducted in JN Medical College and Hospital, AMU Aligarh. The study was not funded by any organisation Englishhttp://ijcrr.com/abstract.php?article_id=2580http://ijcrr.com/article_html.php?did=2580  Harris MI. Impaired glucose tolerance in the U.S. population. Diabetes Care 1989 12:464. Zargar AH, Wani AI, Masoodi SR, Laway BA, Bashir MI. Mortality in diabetes mellitus – data from a developing region of the world. Diabetes Res Clin Pract 1999; 43: 67-74. Tesfaye S, Stevens LK, Stephenson JM, Fuller JH, Plater M, Ionescu -Tirgoviste C et al. Prevalence of diabetic peripheral neuropathy and its relation to glycemic control and potential risk factors. The Euro Diab IDDM complications study. Diabetologia 1996; 39: 1377-1384. Perkins BA, Bril V. Diagnosis and management of diabetic neuropathy. Curr Diab Rep 2002; 2: 495–500. Partanen J, Niskanen L, Lehtinen J, Mervaala E, Siitonen O, Uusitupa M. Natural history of peripheral neuropathy in patients with non-insulin dependent diabetes mellitus. N Engl J Med 1995; 333: 89 –94. Consensus statement. Report and recommendations of the San Antonio conference on diabetic neuropathy. American Diabetic Association, American Academy of Neurology. Diabetes Care 1988;11: 592–7. Mayurasakorn K, Somthip N, Caengow S, Chulkarat N, Wanichsuwan M. Glycemic control and microvascular complications among type 2 diabetes at primary care units. J Med Assoc Thai 2009; 92:1094-101. Chandalia HB, Krishnaswamy PR. Glycated hemoglobin. Current Science 2002; 83: 1522-1532. Dahl-Jorgensen K, Brinchmann-Hansen O, Hanssen KF, Ganes T, Kierulf P, Smeland E et al. Effect of near normoglycaemia for two years on progression of early diabetic retinopathy, nephropathy, and neuropathy: The Oslo Study. Br Med J 1986; 293: 1195-1199 The DCCT Research Group: Factors in the development of diabetic neuropathy in feasibility phase of Diabetes Control and Complications Trial (DCCT). Diabetes 1988; 37: 476-481. Bansal V, Kalita J, Misra UK. Diabetic neuropathy. Postgrad Med J 2006; 82: 95-100. [12]Clayton W, Elasy TA. A review of the pathophysiology, classica on and treatment of foot ulcers in diabetic patients. Clinical Diabetes.2009; 27(2): 52-58 

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241113EnglishN2019February7HealthcareDental findings in Fanconi Bickel Syndrome: Case Report English0913Jomaa NermineEnglish Ben Brahim MeriamEnglish Bourguiba EmnaEnglish Jemmali BadiaaEnglishIntroduction: Fanconi-Bickel syndrome is an extremely rare disorder characterized by glycogen accumulation and generalized dysfunction of renal proximal tubules. It was first described by Fanconi and Bickel in 1949. This disease is caused by a defective monosaccharide transporter Glut2. Polyuria, metabolic acidosis, recurrent episodes of severe hypoglycemia, growth retardation, hepatomegaly, and rickets or osteomalacy are clinical consequences of this disease. However, a little information describing the dental and the orofacial signs and symptoms of this abnormality are available. Thus, the aim of this paper was to present the orofacial manifestations and dental management in a girl with Fanconi’s syndrome. Case Report: In this paper, we report a dental findings in a case of 8-year-old girl with the Fanconi-Bickel syndrome who was referred to the Oral Medicine Department of La Rabta hospital (Tunisia). She suffered from many oral manifestations includes delayed development of dentition, opaque areas (hypocalcification), rapidly progressive periodontal disease and premature loss of temporary teeth, as well as general abnormalities. Conclusion: Through this observation, we conclude that the knowledge of craniofacial features and various dental abnormalities helps dentist to discover underlying systemic disease or syndrome. Thus reducing the morbidity of disease and improving the quality of life. Also, this case makes us thinking that an oral evaluation should be performed in all patients with Fanconi Bickel Syndrome. EnglishFanconi-Bickel syndrome, Hypophosphatemic rickets, Delayed eruption, Taurodontism, Premature lossIntroduction Fanconi-Bickel syndrome is an extremely rare disorder characterized by the accumulation of a substance called glycogen in different parts of the body.[1] It was first described by Fanconi and Bickel in 1949.[2]Until now, the prevalence is unknown but less than 200 cases have been described in the literature.[1]The mutations in Glut2 is incriminated in the development of this syndrome.[3] The gene for the glucose transporter protein 2 is expressed in liver, pancreas, intestine and kidney.[3] While, The Fanconi-Bickel syndrome can be referred as idiopathic, sporadic, or primary when no identifiable secondary cause is recognized.[4] As regards the mode of transmission, autosomal dominant, recessive, or X-linked trait were reported. [4,5] This disorder is characterized by hepatorenal glycogen accumulation and general dysfunction of renal proximal tubules.[3] Different to other types of glycogen storage disease caused by enzymatic defects of glycogenolysis, Fanconi-Bickel syndrome caused by a defective monosaccharide transporter, Glut2, in cell membranes of different tissues.[6] The proximal renal tubular dysfunction provoke glycosuria with normal serum glucose levels and urinary loss of bicarbonate, phosphate, potassium, amino acids, and low molecular weight proteins. [7] Polyuria, metabolic acidosis, recurrent episodes of severe hypoglycemia, growth retardation, hepatomegaly, and rickets or osteomalacy are clinical consequences of the disease.[7] A brain damage and convulsions which are the result of hypoglycemia are also a consequences of this disease.[8] Besides, a facial and truncal adiposity, hyperlipidemia and bleeding tendency, which is related to impaired platelet function, can be present on the patients. [8] However, a little information describing the dental and the orofacial signs and symptoms of this abnormality are available.[9] In fact, dental findings of Fanconi’s syndrome have been described as a similar to these in hypophosphatemic vitamin D-resistant rickets.[9] Thus, the aim of this paper was to present the orofacial manifestations and dental management in a girl with Fanconi’s syndrome. Case report Medical history A 8-year-old girl with Fanconi-Bickel syndrome whose condition was first diagnosed when she was 20 months of age. She was referred to the Department of Oral Medicine, LA RABTA hospital (Tunisia) for the evaluation of her dental growth and development. The patient was the third child of a healthy parent, without the notion of consanguineous marriage. The other children are healthy also. Physical examination revealed a short stature with a height of 122 cm and weighed about 20 kg, bone deformities, protuberant abdomen and growth retardation. Laboratory revealed hypocalcemia (65 mg/L), hypophosphatemia(14 mg/L), and Hyperlipidemia ( Triglycerides 2.02 g/L). The proximal renal tubular dysfunction is expressed by glucosuria, generalized aminoaciduria, bicarbonate wasting, and hypophosphatemia. Then, laboratory investigations confirmed severe hypophosphatemic rickets. Dental findings The patient was submitted to clinical evaluation and radiographic examination. The intraoral examination revealed a delayed tooth eruption in permanent dentition. The gingiva presented signs of inflammation. Also, the patient presented dental tartar on the left side.( Fig. 1) Teeth 61, 82 and 54 were exfoliated spontaneously without history of tooth decay or trauma (Fig. 2). Moreover, All erupted teeth showed a normal size and shape. But all temporary teeth are mobile and opaque areas (hypocalcification) showed especially in the 51, 62, 63 and 64. Gingival recession was described in temporary molar.(Fig. 3)   The most significant radiographic finding was the taurodontism of both primary and permanent molars. In addition, the developing of dental germs were normal in number and shape, but this development was delayed. Also, we found poorly defined lamina dura, lack of contrast between enamel and dentin in some teeth, and loss of the bone density in maxilla and mandible.   Treatment Our patient was counseled and educated on the maintenance of good oral hygiene. The patient underwent descaling. Then, fissure sealants were applied to all permanent first molars. A modified removable partial denture was indicated to replace teeth 61 and 54. The removable partial denture did not contain clasp, because this dispositive could damage loose teeth with an increased risk of falling (Fig 6 and 7). However, the maxillary base plate was expanded to vestibular gum in order to make the appliance more stable and retentive.     Discussion Oral manifestations: Fanconi Bickel Syndrome is accompanied by severe growth deficiency and hypophosphatemic rickets, including craniofacial manifestations. Those manifestations were previously reported by Morisaki in 1989, which described a case affected by Fanconi&#39;s syndrome with growth deficiency of craniofacial bones and dental alterations. Family history of this case revealed healthy parents without consanguineous marriage.[10] Oral manifestations of this disease, as seen in the present case, includes delayed development of dentition, opaque areas (hypocalcification), rapidly progressive periodontal disease and premature loss of temporary teeth. Also, the pulp/crown ratio of all molar teeth showed taurodontism, as mentioned by Jorgenson et al. [11] In fact, this dental findings of Fanconi Bickel Syndrome have been described as similar with variable degrees to those in hypophosphatemic vitamin D-resistant rickets, Renal tubular acidosis, and hepatomegaly resulting from glycogen storage disease type XI.[9,12] The renal tubular defect decreases the renal threshold for phosphate. This results in loss of phosphates, sugars and amino acids which leads to a failure of calcium. Thus, hypophosphatemic rickets can be developed. Also, this disorder can be caused by a failure of production of 1,25-dihydroxy vitamin D from its precursor 25-hydroxy vitamin D. This altered vitamin D absorption and metabolism affects the growth and development of calcified tissue in the body, including the dental hard tissue. This syndrome results in hypoplasia and deficient calcification of mineralized structures such as bones and teeth. Mainly, dental enamel is the most mineralized tissue in human body, white opaque areas (hypocalcification) or enamel hypoplasia, has been reported in a child with Fanconi Bickel Syndrome.[10,13,14] Clinical and histologic abnormalities may be seen in the dental hard tissue, essentially when systemic symptoms appear during a period of odontogenesis. [15] Hypophosphatemic rickets are characterized by different skeletal and dental manifestations. Those characteristics are collected in Table 1. [16]   As regards delayed eruption, it is considered one of the symptoms of Fanconi’s syndrome.[9] In fact, delayed dental development, like growth deficiency, is a secondary to disturbed biochemical findings that results from deficient hepatic and renal glucose-6-phosphatase activity.[15] Besides, A chronic metabolic acidosis can be a factor in the formation of the dental disease.[17] Dental considerations: Firstly, preventive dental care must be included into the treatment plan. All patients affected by Fanconi&#39;s syndrome need counseling and educating on the importance of maintenance of good oral hygiene. Periodic dental examinations each 3 mouth is obligatory. Also, pit and fissure sealants are indicated when the permanent teeth are erupting. In any case, these patients had a high carious risk, because of the hypocalcification on the one hand and his treatment which based on the providing exogenous glucose on the other hand. In fact, this treatment includes frequent carbohydrate feedings during the day and continuous overnight intragastric infusions of glucose polymers.[18,19] This glucose polymers cause a decrease in plaque pH below the critical pH of 5·5. [20] In addition, in children over 2-years-old the daytime glucose polymer is replaced with uncooked cornstarch that acts as a slow release source of glucose.[20] The caries potential of uncooked cornstarch is less than that of glucose, but, cornstarch has a tendency to adhere to the enamel surface if it is not carefully removed each day. [20] Another point is that premature loss of temporary teeth can be managed by oral rehabilitation in order to facilitate speech, mastication, and esthetics. But, it is very important to be careful about the periodontal state of the teeth and we must not damage them more. Conclusion In conclusion, we reported, in this paper, a dental findings in patient with Fanconi Bickel Syndrome. Multiple missing teeth, mobility opaque areas and delayed eruption are described in this case. They make us thinking that an oral evaluation should be performed in all patients with Fanconi Bickel Syndrome. Moreover, the pediatrician and the dentist have to collaborate during the early ages of the affected individuals. Besides, early diagnosis is essential, since morbidity can be minimized if children are treated before the age of eight months. [21] Finally, the knowledge of craniofacial features and various dental abnormalities helps dentist to identify the underlying systemic disease and cure them well. Acknowledgements 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=2581http://ijcrr.com/article_html.php?did=2581 Glycogen storage disease due to GLUT2 deficiency Available from https://www.orpha.net/consor/cgi-bin/OC_Exp.php?Expert=2088&lng=EN:/ Fanconi G, Bickel H. Die chronische Aminoacidurie (Aminosaeurediabetes oder nephrotischglukosurischer Zwergwuchs) bei der Glykogenoseund der Cystinkrankheit. Helv Pediat Acta. 1949;4:359-396. Santer R, Schneppenheim R, Suter D, Schaub J, Steinmann B, Fanconi-Bickel syndrome – the original patient and his natural history, historical steps leading to the primary defect, and a review of the literature. Eur J Pediatr. 1998; 157(10):783-797. Klootwijk E, Reichold M, Helip-Wooley A et al. Mistargeting of peroxisomal EHHADH and inherited renal Fanconi’s syndrome. N Engl J Med. 2014; 370(2):129-138. Pereira PCB, Miranda DM, Oliveira EA et al. Molecular pathophysiology of renal tubular acidosis. Curr Genomics. 2009; 10(1):51-59. Santer R, Schneppenheim R, Dombrowski A, Gotze H, Steinmann B, Schaub J, Mutations in GLUT2, the gene for the liver-type glucose transporter, in patients with Fanconi Bickel syndrome. Nature Genet. 1997; 17(3):324-326. Drube J, Schiffer E, Mischak H et al. Urinary proteome pattern in children with renal Fanconi syndrome. Nephrol Dial Transplant. 2009; 24(7):2161-2169. Karande S, Kumbhare N, Kulkarni M, Fanconi-Bickel Syndrome. Indian Pediatrics. 2007; 44(3):223-225 Ichijiro M, Keiko A, Shizuo S, Orofacial manifestations in a child with Fanconi’s syndrome. ORAL SURG ORAL MED ORAL PATHOL. 1989; 68(2):171-174. SHIRLENE B, and al, Dental findings in Brazilian patients with Fanconi syndrome. International Journal of Paediatric Dentistry. 2016; 26(1): 77-80. Jorgenson RJ, Salinas CF, Shapiro SD, The prevalence of taurodontism in a select population. J Craniofac Genet Dev Biol. 1982;2(2):125-136. Jagtap s v. and al. review: Hypophosphatemic rickets. Indian journal of endocrinology and metabolism. 2012; 16 (2):177-182. Bata P, Tejani Z, Mars M, X-Linked hypophosphatemia: Dental and histologic findings. J Can Dent Assoc. 2006; 72 (1): 69-72. Tümen and al. Types of Rickets, Dental and Histologic Findings: Review of the Literature. 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