The periodontal diseases are highly prevalent and can affect up to 90% of the worldwide population. Gingivitis, the mildest form of periodontal disease, is caused by the bacterial biofilm (dental plaque) that accumulates on teeth adjacent to the gingiva (gums). However, gingivitis does not affect the underlying supporting structures of the teeth and is reversible. Periodontitis results in loss of connective tissue and bone support and is a major cause of tooth loss in adults. In addition to pathogenic microorganisms in the biofilm, genetic and environmental factors, especially tobacco use, contribute to the cause of these diseases. Genetic, dermatological, haematological, granulomatous, immunosuppressive, and neoplastic disorders can also have periodontal manifestations. Common forms of periodontal disease have been associated with adverse pregnancy outcomes, cardiovascular disease, stroke, pulmonary disease, and diabetes, but the causal relations have not been established. Prevention and treatment are aimed at controlling the bacterial biofilm and other risk factors, arresting progressive disease, and restoring lost tooth support.

Gingivitis and periodontitis are among the most common diseases known to man. Although bacterial plaque is generally accepted as the primary etiologic agent, little information is available concerning the influence that host genetic factors have on these diseases. The purpose of the present study was to examine the relative contribution of environmental and host genetic factors to clinical measures of periodontal disease through the study of both reared-together twins and monozygous twins reared apart. Probing depth, clinical attachment loss, gingivitis, and plaque were assessed from the Ramfjord teeth in 110 pairs of adult twins (mean age 40.3 years), including 63 monozygous and 33 dizygous twin pairs reared together and 14 monozygous twin pairs reared apart. Bootstrap sampling was used to estimate and provide confidence limits of between-pair and within-pair variances, intraclass correlations and heritability. Based on ratios of within-pair variances or heritability estimates, a significant (P less than 0.05) genetic component was identified for gingivitis, probing depth, attachment loss and plaque. Heritability estimates indicated that between 38% to 82% of the population variance for these periodontal measures of disease may be attributed to genetic factors. While there is general agreement that bacteria are important in the pathogenesis of the periodontal diseases, future etiologic studies should consider the role of host genetic influences.

Many well designed clinical studies have established the effectiveness of periodontal therapy. Surgical procedures have been shown to be effective in treating periodontitis when followed by appropriate maintenance care. Scaling and root planing alone have recently been compared to scaling and root planing plus soft tissue surgery in several longitudinal trials. A review of the literature indicates several important findings including a loss of clinical attachment following flap procedures for shallow (1-3 mm) pockets and no clinically significant loss after scaling and root planing. These studies also generally report either a gain or maintenance of attachment level for both procedures in deeper pockets (greater than or equal to 4 mm). For these pockets, neither procedure has been shown to be uniformly superior with respect to attachment gain. All reports indicate that both treatment methods result in pocket reduction. However, the literature also indicates that scaling and root planing combined with a flap procedure results in greater initial pocket reduction than does scaling and root planing alone. This difference in degree of pocket reduction between procedures tends to decrease beyond 1-2 years. It has been shown that both treatment methods result in sustained decreases in gingivitis, plaque and calculus and neither procedure appears to be superior with respect to these parameters. Additional data from the study at the University of Minnesota indicate that similar results are maintained up to 61/2 years following active therapy. Pocket depth did not change for shallow (1-3 mm) pockets treated by either scaling and root planing alone or scaling and root planing followed by a modified Widman flap. For pockets 4-6 mm, both treatment procedures resulted in equally effective sustained pocket reduction. Deep pockets (greater than or equal to 7 mm) were initially reduced more by the flap procedure. After 2 years, no consistent difference between treatment methods was found in degree of pocket reduction. However, as compared to baseline, pocket reduction was sustained to 61/2 years with the flap and only 3 years with scaling and root planing alone. After 61/2 years, sustained attachment loss in shallow (1-3 mm) pockets was found after the modified Widman flap. Scaling and root planing alone in these shallow pockets did not result in sustained attachment loss. For pockets initially 4-6 mm in depth, attachment level was maintained by both procedures but scaling and root planing resulted in greater gain in attachment as compared to the flap at all time intervals.(ABSTRACT TRUNCATED AT 400 WORDS)