Periodontal disease: an overview for physicians.

Periodontitis is now seen as resulting from a complex interplay of bacterial infection and host response, often modified by behavioral factors. There has been a fundamental change in the prevailing periodontal disease model of the 1960s, which suggested that the susceptibility to periodontitis increases with age, and that all individuals are susceptible to severe periodontal disease. More recent research has changed the belief in universal susceptibility to the current view that only some 5-20% of any population suffer from severe generalized periodontitis, and that only moderate disease affects a majority of adults. One major risk factor is smoking, as there is now a clear association between smoking and periodontal disease independent of oral hygiene, age, or any other risk factor. In human periodontitis, there is no simple, direct pathogen-disease link. There are three pathogens that have a strong association with progressive periodontal disease: Actinobacillus actinomycetemcomitans, spirochetes of acute necrotizing gingivitis, and Porphyromonas gingivalis. These pathogens may be the cause of continued loss of periodontal attachment in all periodontal disease classifications despite diligent periodontal therapy. This loss of attachment, or destruction of the periodontal ligament and loss of adjacent supporting bone, is seen in adult periodontitis, as well as in early-onset periodontitis, which affects young persons who otherwise appear healthy. The three forms of early-onset periodontitis are prepubertal periodontitis, localized and generalized juvenile periodontitis, and rapidly progressive periodontitis. They are distinguished from adult periodontitis by the age of onset of the disease, the rapid rate of disease progression, manifestations of defects in host response, and the composition of the subgingival microflora. Prepubertal periodontitis is associated with attachment loss around teeth of the deciduous and/or permanent dentition, and is often associated with severe congenital defects of hematological origin, and alterations in neutrophil chemotaxis function. Periodontitis may also be associated with systemic conditions such as metabolic disorders (diabetes mellitus, female hormonal alterations), drug-induced disorders, hematologic disorders/leukemia, and immune system disorders. These systemic disorders have been documented as capable of affecting the periodontium and/or treatment of periodontal disease. In order to rationally treat and prevent periodontal disease, we need to know the etiologic agents for specific patients, and the mechanism of bacterial pathogenesis in periodontitis. In systemic diseases in which the periodontal tissues are affected as well, early detection and carefully managed therapeutics with the physician and periodontist working together may prove beneficial to the patient's general health and quality of life.

Histological, clinical, and digital subtraction radiographic evaluation of repair of periodontal defects resulting from mechanical perforation of the chamber floor using ePTFE membranes.

The aim of this study was to test the hypothesis that a biocompatible membrane, when placed between the gingiva and cortical bone in teeth with periodontal defects that occurred following mechanical endodontic perforation, would facilitate greater regeneration than in control sites not treated with guided tissue regeneration. One beagle dog with a healthy periodontium was used in the study. The maxillary right first and second molars and the mandibular left first and second molars acted as the experimental group in which furcation perforations were treated by guided tissue regeneration. The maxillary left and mandibular right first and second molars served as the controls in which furcation perforation lesions were only treated by open flap debridement. Clinical, histological, and standardized radiographic evaluation showed significant differences between the test and control groups. In addition, digital subtraction radiography revealed a gain in alveolar bone height and increased density at all experimental sites, and a loss at all control sites. Histological evaluation showed extensive regeneration of both alveolar bone and connective tissue at experimental sites, but none at control sites. The results of this study suggest that the use of guided tissue regeneration in furcation lesions produced by endodontic perforations will result in significant new bone and connective tissue attachment.