The specifics of the disease process are obscured by our incomplete understanding of the role of various risk factors. Box 10219, Riyadh 11433, Saudi Arabia. The independent variables used were sociodemographic factors (age, gender, income, education), medical factors (systemic diseases, drugs), behavioral factors (regular dental checkup, smoking), and oral factors (presence of supragingival calculus and plaque). 15 0 obj Objectives. A recent review on the modifiable risk factors concluded that smoking and excess caloric intake contribute to increases in systemic markers of inflammation and can modify gene regulation through a variety of biologic mechanisms [97]. [Correlation between psychosocial factors and periodontal disease--a systematic review of the literature]. Author information: (1)Department of Psychosomatics and Psychotherapy, University Hospital Munster, Domagkstrasse 22, D-48149 Munster, Germany. Conclusions. endobj An understanding of risk factors is essential for clinical practice. x�+�r endobj �26S073QI�r � Sources. endstream endstream A similar finding has been observed even in the elderly population. This aggregation within families strongly suggests a genetic predisposition. Drugs such as anticonvulsants, calcium channel blocking agents, and cyclosporine may induce gingival overgrowth [59]. �*T0T0 Bi������f����� � endobj x�+�r Diabetes as a risk factor for periodontal disease Many authors have described diabetes as a risk factor for periodontal disease. This is important to oral health because low dietary intake of calcium and vitamin C has been associated with periodontal disease [74]. Many works of the literature report familial aggregation of periodontal diseases, but due to different terminology, classification systems, and lack of standardized methods of clinical examination, it is difficult to compare reports directly. Yousef A. AlJehani, "Risk Factors of Periodontal Disease: Review of the Literature", International Journal of Dentistry, vol. The possible relationship between periodontal disease and socioeconomic status was found in several studies [108, 110, 120–122]. One likely candidate is the C-reactive protein (CRP), although this protein is part of the body’s normal response to infection and inflammation. The focused question addressed in this systematic review was whether the scientific evidence is enough to consider stress and psychological factors as risk factors for periodontal disease. teristics, periodontal disease definitions, and techniques used across studies, it was not appropriate to apply statistical methods to estimate the overall pooled risk of periodontal disease in the studies. endobj Some of the recent studies have reported elevated CRP levels among those with periodontitis [142–145]. schneig@mednet.uni-muenster.de endobj This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This outcome is thought to be the effect of biologic mediators of inflammatory processes such as prostaglandins E2 and TNF. Bacteremia from periodontitis and dental disease is known to be the primary cause of infective endocarditis [52]. Review of the literature. Am J Dent 27(2): 63-67. But half of all heart attacks occur among people who do not have high cholesterol. <>stream %���� Data/sources/study selection. This paper aims to review the evidence on the potential roles of modifiable and nonmodifiable risk factors associated with periodontal disease. �26S073QI�r � x�+�r endstream Risk indicators for alveolar bone loss,”, P. Meisel, J. Reifenberger, R. Haase, M. Nauck, C. Bandt, and T. Kocher, “Women are periodontally healthier than men, but why don't they have more teeth than men?”, T. Mundt, C. Schwahn, F. Mack et al., “Risk indicators for missing teeth in working-age pomeranians—an evaluation of high-risk populations,”, G. D. Slade and A. J. Spencer, “Periodontal attachment loss among adults aged 60+ in South Australia,”, J. M. Albandar and A. Kingman, “Gingival recession, gingival bleeding, and dental calculus in adults 30 years of age and older in the United States, 1988–1994,”, G. H. Gilbert, “Racial and socioeconomic disparities in health from population-based research to practice-based research: the example of oral health,”, C. Susin, R. V. Oppermann, O. Haugejorden, and J. M. Albandar, “Tooth loss and associated risk indicators in an adult urban population from south Brazil,”, T. C. Hart, “Genetic considerations of risk in human periodontal disease,”, M. L. Laine, M. A. Farré, M. A. García-González et al., “Risk factors in adult periodontitis: polymorphism in the interleukin-1 gene family,”, B. G. Loos, R. P. John, and M. L. Laine, “Identification of genetic risk factors for periodontitis and possible mechanisms of action,”, N. J. López, L. Jara, and C. Y. Valenzuela, “Association of interleukin-1 polymorphisms with periodontal disease,”, B. S. Michalowicz, “Genetic and heritable risk factors in periodontal disease,”, L. Quappe, L. Jara, and N. J. López, “Association of interleukin-1 polymorphisms with aggressive periodontitis,”, T. Roshna, R. Thomas, K. Nandakumar, and M. Banerjee, “A case-control study on the association of human leukocyte antigen-A*9 and -B*15 alleles with generalized aggressive periodontitis in an Indian population,”, M. J. McDevitt, H. Wang, C. Knobelman et al., “Interleukin-1 genetic association with periodontitis in clinical practice,”, N. W. Johnson, G. S. Griffiths, J. M. A. Wilton et al., “Detection of high-risk groups and individuals for periodontal diseases. It must be borne in mind that familial patterns may reflect exposure to common environmental factors within these families. Chronic periodontitis involves complex interactions between microbial factors and susceptible hosts [91, 92]. Although periodontal disease nosology has changed many times over the timeframe of these reports, most familial reports for periodontitis are for early-onset forms now called aggressive periodontitis [132–139]. 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