Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study describes the histologic characteristics of root surfaces of primary teeth from children with prepubertal periodontitis (PP). Fifteen primary teeth from 4 children with PP, and 2 control primary teeth from 2 healthy children were examined. Light microscopy revealed normal root surfaces in the control teeth. In contrast, the PP specimens revealed bacteria inside dentin tubules or covering cementum, a cuticle, or resorbed dentin; normal, wider than normal, or hypoplastic cementum; resorption lacunae with various depths; aplastic root resorption; alternate resorption and repair; and active repair. No cementoclasts were found in the resorption lacunae. Scanning electron microscopy revealed intrabony and suprabony root areas, and a "plaque free zone" (PFZ). Colonies of filaments were evident at the cemento-enamel junction (CEJ). The suprabony root surfaces had resorption lacunae, isolated short rods, calculus, colonies of filaments, or colonies composed by an heterogeneous bacterial population. The coronal boundary of the PFZ was the border of a sheet-like structure, which included isolated rods or filaments. At the PFZ, isolated filaments and rods, and a fibril matrix were evident. The apical boundary of the PFZ consisted of bundles of soft tissue remnants or the insertion of the periodontal fibers. The intrabony surfaces were mostly covered by soft tissue, which included isolated filaments and short rods. Resorption lacunae with or without soft tissue were also evident in this area. Crystals of calcium oxalate dihydrate and erythrocytes in distinct forms were found at various root areas. The present findings are different from those previously reported for hypophosphatasia specimens.
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PMID:Root surface characteristics of primary teeth from children with prepubertal periodontitis. 957 20

The enamel-renal syndrome of amelogenesis imperfecta (AI) and nephrocalcinosis, and the amelogenesis imperfecta-gingival fibromatosis syndrome have both been associated with mutations in FAM20A. We report on two unrelated Thai patients with three novel and one previously reported mutations in FAM20A with findings suggesting both disorders, including hypoplastic AI, gingival fibromatosis, unerupted teeth, aggressive periodontitis, and nephrocalcinosis/nephrolithiasis. Additional findings consisted of a supernumerary premolar, localized aggressive periodontitis, thin alveolar bone, vitamin D deficiency-associated hyperparathyroidism, and heterotopic calcification in other tissues, including lungs, dental pulp, gingiva, dental follicles, and periodontal tissues, and early cessation of limited menstruation. Greater promotory activity of urine on calcium oxalate crystal growth compared to controls may help to explain the pathogenesis, and suggest that FAM20A mutations can contribute to nephrocalcinosis/nephrolithiasis. Our findings expand the phenotypic spectrum of FAM20A mutations. Since both of our patients and a large number of previously reported cases had all the important features of both syndromes, including AI, renal anomalies, and gingival fibromatosis, we are convinced that these two disorders actually are the same entity. The name of enamel-renal-gingival syndrome is suggested.
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PMID:Enamel-renal-gingival syndrome and FAM20A mutations. 2425 79