A 'benign' condition masquerading as arthritis.

A 9 year-old boy presented with a 3-week history of low-grade fever, on and off, and additive arthritis of the lower limb joints with no overt antecedent trauma. Investigations for juvenile idiopathic arthritis (JIA), reactive and tuberculous arthritis were normal. He was started on anti-inflammatory drugs as for seronegative oligoarticular JIA. Since arthritis persisted despite treatment, MRI of the left knee joint was planned prior to an aspiration/synovial biopsy. MRI revealed a partial tear of the anterior cruciate ligament with a significant effusion. On careful re-examination, at this point, he was found to have generalised hypermobility with a Beighton score of 9/9. This had been missed initially, leading to a delay in diagnosis and management. He was managed with careful physiotherapy and lifestyle modification. The left knee effusion resolved within a month. This case is being reported in order to highlight the fact that joint hypermobility syndrome can be misdiagnosed as arthritis.

Prevalence pattern of dental caries in the primary dentition among school children.

The purpose of the study was to assess the pattern of prevalence of dental caries in the primary dentition among 5 year old children. The area of study was urban Pondicherry and the study population consisted of 1009 school children of both sexes (527 boys and 482 girls). A simple random sampling method was used to select the schools. Dental caries was assessed by the Dentition status and Treatment Need (WHO 1997). Statistical analysis was done using the Proportion test. The prevalence of caries was 44.4% among the study population, being higher in the boys (P < 0.05); In Mandibular arch in both the sexes (boys P < 0.05, girls P < 0.01); in posterior teeth (both sex wise & arch wise). Comparison of caries among anterior teeth (Boys vs Girls) [corrected] and posterior teeth (upper vs. lower) revealed higher caries prevalence in Maxillary anterior teeth (P < 0.001) and Mandibular posterior teeth (P < 0.001). In both the sexes and arches, primary second molars showed higher caries prevalence.

Evidence for mechanistic alterations of Ca2+ homeostasis in Type 2 diabetes mellitus.

Altered cytosolic Ca2+ is implicated in the aetiology of many diseases including diabetes but there are few studies on the mechanism(s) of the altered Ca2+ regulation. Using human lymphocytes, we studied cytosolic calcium (Cai) and various Ca2+ transport mechanisms in subjects with Type 2 diabetes mellitus and control subjects. Ca2+-specific fluorescent probes (Fura-2 and Fluo-3) were used to monitor the Ca2+ signals. Thapsigargin, a potent and specific inhibitor of the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA), was used to study Ca2+-store dependent Ca2+ fluxes. Significant (P<0.05) elevation of basal Ca, levels was observed in lymphocytes from diabetic subjects. Cai levels were positively correlated with fasting plasma glucose and HbA1c. There was also a significant (P<0.05) reduction in plasma membrane calcium (PMCA) ATPase activity in diabetic subjects compared to controls. Cells from Type 2 diabetics exhibited an increased Ca2+ influx (as measured both by Fluo-3 fluorescence and 45Ca assays) as a consequence of thapsigargin-mediated Ca2+ store depletion. Upon addition of Mn2+ (a surrogate of Ca2+), the fura-2 fluorescence decayed in an exponential fashion and the rate and extent of this decline was steeper and greater in cells from type 2 diabetic patients. There was also a significant (P<0.05) difference in the Na+/Ca2+ exchange activity in Type 2 diabetic patients, both under resting conditions and after challenging the cells with thapsigargin, when the internal store Ca2+ sequestration was circumvented. Pharmacological activation of protein kinase C (PKC) in cells from patients resulted in only partial inhibition of Ca2+ entry. We conclude that cellular Ca2+ accumulation in cells from Type 2 diabetes results from (a) reduction in PMCA ATPase activity, (b) modulation of Na+/Ca2+ exchange and (3) increased Ca2+ influx across the plasma membrane.