[Juvenile periodontitis patients taking gu chi gao].
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BACKGROUND: Generalised prepubertal periodontitis is a rare entity that is usually a consequence of severe systemic diseases. Chronic granulomatous disease is one of the extremely rare inherited immunodeficiency diseases, which predisposes the patient to recurrent severe bacterial and fungal infections. AIM: The purpose of this report is to describe a 5-year old male patient suffering from prepubertal periodontitis associated with chronic granulomatous disease, who was referred to the Department of Periodontology for treatment of severe gingival inflammation. METHODS: A detailed past history was obtained and thorough clinical and laboratory examinations were performed. RESULTS: Medical tests revealed the only immunodeficiency sign as the extremely low burst test result. The patient was diagnosed as having an autosomal recessive (AR) form of chronic granulomatous disease. He was put on prophylactic treatment with trimethoprim-sulfamethoxazole (TMP-SMX) and also a periodontal maintenance regimen with regular 1-month intervals. CONCLUSION: This case report emphasises the importance of the differential diagnosis of severe immunodeficiency in the background of prepubertal periodontitis.
A 5-year-old boy presented with persistent generalized gingival inflammation. Clinical and radiographic examination supplemented by immunological and microbiological investigation led to a diagnosis of localized prepubertal periodontitis. The child was subsequently monitored for 3 years and despite treatment there was continued bone loss related to his primary teeth. This case highlights the need for liaison between specialists in paediatric dentistry, periodontology, immunology and microbiology in order to diagnose prepubertal periodontitis and to establish a rational basis for treatment to prevent progression to juvenile periodontitis.
Localized prepubertal periodontitis has been described as a host-defect mediated form of bacterially induced periodontitis, with an early onset and rapid progression around a few teeth in children prior to puberty. To further our understanding of the etiology of this disease, we have examined the microbiological components of subgingival dental plaque in 9 children with localized prepubertal periodontitis to determine if patterns of putative pathogens existed, and have compared these results with those obtained from 4 children with no periodontitis. Subgingival plaque samples were plated onto a selective medium for Actinobacillus actinomycetemcomitans and onto a non-selective medium for anaerobes, and the predominant cultivable microbiota of 2 sites per child was determined. The subgingival microbiota of children with localized prepubertal periodontitis clearly differs from non-diseased children in the detection of high levels of several suspected pathogens, including A. actinomycetemcomitans, Bacteroides intermedius, Eikenella corrodens, and Capnocytophaga sputigena. These putative pathogens were found in various combinations. These findings suggest that localized prepubertal periodontitis is associated with specific subgingival bacteria which are generally not found in children without periodontitis.
An 11-year-old boy with clinical and radiological features of prepubertal periodontitis is presented. He had a history of recurrent upper respiratory tract infections and otitis media. Neutrophil chemotaxis was significantly reduced compared to normal. Total T- and B-lymphocyte numbers were not altered. T-lymphocyte subsets studied with monoclonal antibodies revealed that both T-helper and T-suppressor cell populations were reduced with a normal TH/TS ratio of 1.8. No significant changes were observed in the serum IgG, IgA and IgM values. Serum C3c and C4 levels were found to be elevated. These findings may contribute to the pathogenesis of prepubertal periodontitis.
This study investigates bacterial invasion of the soft tissue walls of deep pockets from cases with adult (AP) and juvenile periodontitis (JP). Transmission electron microscopy was used to examine pocket soft tissue walls removed from extracted teeth from 5 patients with AP and 2 patients with JP. Bacteria were sparse throughout the epithelium and connective tissue, regardless of the level of tissue breakdown. However many inflammatory cells were seen, and these did appear to be located in regions of marked collagen loss. Accumulations of large numbers of bacteria were extremely rare and found only on the epithelial surface or in artefactual spaces within the deeper tissues. The findings indicate that the tissue destruction associated with periodontitis is not directly related to bacterial invasion. The sparse organisms within the pocket tissues probably result from passive entry rather than an invasive action. Under these circumstances, it would seem reasonable to suggest that bacterial metabolic products rather than the micro-organisms themselves penetrate the tissues in periodontitis.