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Background: Pendred syndrome is a rare, inherited, autosomal recessive disorder with an iodine organification defect of thyroxin produced by the thyroid gland. Its clinical features include sensorineural hearing loss, classically congenital and prelingual, and goiter., Methods: This is the first case report of Pendred syndrome in the dental literature with oral findings that include localized extensive attachment loss involving mandibular incisor teeth and idiopathic hypercementosis involving multiple teeth in addition to other oral manifestations, suggesting hypothyroidism-like macroglossia and macrocheilia. Furthermore, serum alkaline phosphatase along with inorganic calcium and phosphate levels were also elevated. Peripheral neutrophil function test suggested a defective function of neutrophils., Results: Management of the case included augmenting thyroxin supplementation, in consultation with an endocrinologist, and extraction of hopeless mandibular central incisors followed by placement of immediate transitional dentures., Conclusion: A comprehensive medical history and systemic and laboratory evaluations should be considered a prerequisite to identify, manage, and report such rare conditions in routine clinical practice.

Background: Osteopontin (OPN), a glycosylated phosphoprotein, is a bone matrix component produced by osteoblasts, osteoclasts, and macrophages as a multifunctional cytokine. OPN anchors osteoclasts to the bone surface, and its absence leads to impaired bone resorption. The aim of the present study was to assess the relation between clinical parameters and concentrations of OPN within gingival crevicular fluid (GCF) from inflamed gingiva and periodontitis sites and, subsequently, after the treatment of periodontitis sites., Methods: A total of 45 subjects were divided into the following three groups based on modified gingival index (MGI) and Ramfjord periodontal disease index (PDI) scores: healthy (group I), gingivitis (group II), and chronic periodontitis (group III). A fourth group consisted of 15 subjects from group III, 6 to 8 weeks after treatment (i.e., scaling and root planing [SRP]). GCF samples collected from each patient were quantified for OPN using the enzymatic immunometric assay. Further, the correlation between OPN levels in situ with clinical parameters was analyzed in all groups and before and after treatment in periodontitis patients., Results: The highest mean OPN concentration in GCF (14.347 microg/ml) was observed in group III, and the lowest mean OPN concentration in GCF (2.522 microg/ml) was observed in group I. Its levels in group III decreased to 8.419 microg/ml after treatment (group IV). Further, GCF OPN levels in all the groups showed a statistically significant positive correlation with clinical attachment loss (P <0.05)., Conclusions: OPN levels increase in GCF from healthy to periodontitis states, and periodontal treatment results in the reduction of OPN levels. The data indicate that OPN may play a key role in, and could be considered a biomarker of, periodontal disease progression.

In the past, various models including the autoimmunity model have been proposed to explain the pathogenesis of periodontal diseases. The aim of this review is to introduce the pathogenic role of anti-neutrophil cytoplasmic autoantibodies (ANCAs) in various autoimmune diseases and compare these conditions with periodontal disease to elucidate common pathogenic mechanisms. Also, a novel model to explain the pathogenesis of periodontal disease based on the concept of ANCA-associated autoimmunity is proposed. This encompasses a wide array of biochemical mediators that range from direct and indirect initiators of ANCA production and eventual release of proinflammatory mediators and free radicals, all of which have been implicated in periodontal tissue destruction in the past. In addition, specific links between the typical ANCA-associated diseases and periodontal disease are discussed. Finally, a new paradigm in the periodontal disease-associated destruction is proposed that includes the currently accepted mechanism, namely, the genetic-microbial-host interactions.