Periodontics. Fernando Suarez

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       RISKS

       Theodoros Katsaros, DDS, MSD

      DEFINITIONS AND TERMINOLOGY

Risk determinant: A risk factor that cannot be modified (eg, genetic factors, sex, age).²

Risk factor: Environmental, behavioral, or biologic factors that increase the likelihood of developing the disease; identified through longitudinal studies and confirmed to be present before the onset of the disease (eg, smoking, diabetes, pathogenic bacteria).

Risk indicator: A putative risk factor that is correctly identified through cross-sectional study designs.

Risk marker or risk predictor: Characteristics or factors that have the ability to predict individuals at high risk for disease, but are not part of the causal chain.³

      Risk assessment is an essential component of periodontal patient management due to a number of local and systemic factors that can potentially affect the manifestation and progression of the disease. Accounting for these factors is an important step toward the delivery of optimal periodontal care.¹ In this chapter, the main risk factors, risk determinants, risk indicators, and risk markers are reviewed. The association between them and the onset and progression of periodontal disease is discussed, as well as the impact on treatment outcomes. It should be highlighted that this chapter is based on the current knowledge, and if new evidence emerges in the future, some of these factors may be classified under a different category.

      Box 4-1 lists examples of risk factors, risk determinants, risk indicators, and risk markers or predictors for periodontal disease.

BOX 4-1 Classification of the main risk factors, risk determinants, risk indicators, and risk markers for periodontal disease

      Risk Factors

      SMOKING

      Smoking is a well-documented risk factor for periodontal disease. The effects of smoking on the periodontal status can be classified as local and systemic.

      Local effects

      At the local level, smokers demonstrate increased supragingival⁴ as well as subgingival calculus formation.⁵ Additionally, the presence of nicotine has an effect on gingival fibroblasts, demonstrating an increase in gingival mediated collagen degradation. This action is mediated through the activation of matrix metalloproteinases (MMPs) and redistribution of the tissue inhibitors of metalloproteinases (TIMPs) to the cell membrane. Interestingly, this action is enhanced by the presence of Porphyromonas gingivalis.⁶ With regard to the often observed fibrotic clinical appearance of the gingival tissues in smokers, in vitro investigations have demonstrated a possible explanation by the increase in the production of CCN2/CTGF (connective tissue growth factor) protein and consequently Type I collagen production.⁷ The vasoconstriction and fibrosis on the gingival tissues often result in decreased bleeding on probing (BOP) even in the presence of bacterial plaque and calculus.⁸

      Smokers also present with increased radiographic bone loss compared with nonsmokers, and there is a dose-dependent relationship: The odds of heavy smokers having severe bone loss are higher (odds ratio [OR] 7.28) compared with light smokers (OR 3.25).⁹ These detrimental effects are also observed in populations that maintain good levels of oral hygiene. Cross-sectional studies demonstrated that smokers had significantly reduced bone levels compared with nonsmokers, with the observed amount of bone loss occurring in a shorter time frame in smokers.¹⁰ Similar conclusions were obtained when evaluating the bone levels of a different population (Swedish hygienists) through the assessment of bitewing radiographs. Smokers had the highest amount of radiographic bone loss compared with nonsmokers or former smokers.¹¹

      0Van Winkelhoff et al¹² investigated the prevalence and levels of periodontal pathogens in both smokers and nonsmokers who were treated for periodontal disease as well as untreated populations. A higher prevalence of periodontal pathogens was noted in treated and untreated smokers in comparison with the respective nonsmoking populations. Based on these findings, the authors suggested integrating the use of systemic antibiotics in patients who do not exhibit a favorable response to initial treatment.¹² Haffajee and Socransky¹³ performed a similar study, implementing DNA-DNA hybridization. Subjects were divided based on two criteria: (1) according to their smoking habits in current smokers, former smokers, and nonsmokers; (2) according to their periodontal status in periodontally healthy, well-maintained, and periodontitis patients. Current smokers had larger proportions of sites colonized by periodontal pathogens.¹³ Zambon et al¹⁴ came to similar conclusions after conducting a large cross-sectional study using immunofluorescence. Tannerella forsythia and Aggregatibacter actinomycemetcomitans were more likely to be identified in the subgingival microflora of smokers. Furthermore, there was a dose-dependent relationship between the СКАЧАТЬ