Progression of periodontitis and influence of periodontal bacteria on release of inflammatory markers in Swedish adults

Abstract

Periodontitis is a common infectious disease worldwide. An estimated 15-35% of the adult population in industrialized countries suffers from this multifactorial disease. The percentage of people affected by periodontal disease increases with age, reaching a peak at the age of 5060 years. A healthy periodontium is characterized by dense connective tissue with occasional granulocytes and a few layers of junctional epithelia in the gingival sulcus. Shifts in the development and course of periodontal disease depend on bacteria-host interactions. An exaggerated host response that releases pro-inflammatory cytokines gives rise to an inflammatory reaction. Chronic infection and inflammation can result in destruction of periodontal ligament and loss of marginal bone, leading ultimately to dental loss. Oral hygiene control is important in preventing periodontal disease progression. Other lifestylerelated factors, such as smoking, which displays the greatest dose-response impact on periodontitis as an independent risk factor, and obesity, are significantly associated with periodontitis.

The general aim of Studies I-IV was to clarify the level of awareness of periodontal diseases and the progression of periodontitis in a Swedish urban population. In the long-term study of individuals with periodontal disease, the effect of the pathogenic microbiota on the release of inflammatory markers in gingival crevicular fluid (GCF) and in blood was also investigated.

In epidemiological oral health investigations, self-reported oral health questionnaires are used widely because they are rime- and cost-effective, providing detailed information on subjects in a single health examination. In Study I, the specific aim was to determine whether any association exists between self-reporting of periodontal diseases and outcome in a clinical examination and whether any difference is present in awareness of periodontal status between smokers and nonsmokers. The questionnaire was completed by 1655 participants, who were subsequently divided into those who suspected having periodontal disease and those who did not. A significant difference was observed between groups. Individuals who reported having periodontal disease, especially those also reporting movable teeth, were confirmed to have the disease. Smokers were more aware of their periodontal status than nonsmokers.

One characteristic of periodontal disease is the loss of marginal alveolar bone, giving rise to horizontal and sometimes angular defects. In Study II, the aim was to analyze changes in radiographic bone height after 17 years in smokers and nonsmokers with periodontal disease and compare these with clinical assessment outcome. Marginal bone level in this prospective study revealed tooth groups at higher risk for progression of periodontal disease. Maxillary molars were most affected, with second maxillary molars being most frequently lost and having the most marginal bone loss of all teeth. Smokers had more severe marginal bone loss over time.

In Studies III and IV, the objective was to investigate the influence of the periodontal microbiota and combinations of microbiota on inflammatory markers in GCF and blood of individuals with periodontal diseases. Matrix metalloproteinases (MMPs) -8 and -9, elastase, prostaglandin E2, and interleukin-1 beta were detected in GCF.

Demographic data showed significant differences between individuals with periodontitis and controls in smoking, body mass index, family history of atherosclerotic disease, and education. Specific periodontal microorganisms appeared to induce host response, with increased release of MMP-8 and MMP-9 in gingival pockets and MMP-9 in plasma, possibly triggering the upregulation of MMP-9 in blood. The combination of T. forsythensis and P. gingivalis or T. forsythensis and P. nigrescens seemed to promote the release of subgingival inflammatory mediators and to be associated with more severe periodontal disease.