Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/57872
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dc.contributor.authorKinane, D.-
dc.contributor.authorBartold, P.-
dc.date.issued2007-
dc.identifier.citationPeriodontology 2000, 2007; 43(1):278-293-
dc.identifier.issn0906-6713-
dc.identifier.issn1600-0757-
dc.identifier.urihttp://hdl.handle.net/2440/57872-
dc.description.abstractThe purpose of this chapter was to outline the etiology, pathogenesis, and tissue changes resulting from periodontal disease in a manner that is clinically relevant to practitioners of periodontics and general dentistry. Thus, we reviewed several processes involved in periodontal pathogenesis and tissue destruction and healing and to discuss the concept of susceptibility and risk of disease. It is clear that there are different forms of periodontitis, different rates of susceptibility to these forms, different responses, different genetics and risk factors at play and different modifiers of these diseases, and variations in healing and tissue destruction. In terms of what are the most relevant of these aspects for clinicians and which of these factors will impact on clinical judgment, probably the most relevant is the concept of differing subject susceptibility. Humans differ in their susceptibility to both periodontitis and gingivitis. We do not understand the genetics and environmental aspects sufficiently but clearly numerous risk factors, including plaque or oral hygiene modifications, systemic health including diabetes and HIV, socio-economics, stress, obesity, and smoking are all relevant and may interact to render subjects at increased risk of periodontal disease. The healing and regeneration of tissues is a further area of variation we need to consider, as is the concept of diagnosis and which of the multitude of host factors that we can use with utility for assessing periodontal disease presence and progression. Extensive microbiological research tends to indicate specific pathogens but there are a multitude of unknowns, difficult to detect and cultivate microorganisms including viruses and Archaea, which may be crucial in disease causation and exacerbation. Alternatively, it may be that in future we will consider the plaque biofilm as the main agent of disease and thus develop strategies and detection procedures based on dealing with this multi-microorganism conglomeration rather than specific microorganisms per se. Possibly, the most important clinical messages include the fact that systemic modifiers such as smoking and diabetes may adversely affect the disease process, the ability to diagnose disease and the healing following tissue destruction. Also, that aggressive periodontitis is autosomal dominant in its transmission and thus siblings, parents and offspring of affected persons are 50% more likely to have the disease, and that both gingivitis and periodontitis are chronic inflammatory conditions initiated and perpetuated by the microbial plaque biofilm and thus mechanical or chemical antimicrobial therapies will be useful for both conditions. Also, that control of gingivitis is a primary preventive measure for the control of periodontitis. With respect to the extensive immunological, microbiological, and diagnostic and tissue regeneration research efforts, we are unfortunately still some way from elucidating accurately the disease and healing processes but in time we will undoubtedly utilize these to develop better diagnostic and therapeutic management of patients. Copyright © Blackwell Munksgaard 2007.-
dc.description.statementofresponsibilityDenis F. Kinane and P. Mark Bartold-
dc.language.isoen-
dc.publisherMunksgaard Int Publ Ltd-
dc.rightsCopyright Blackwell Munksgaard 2007-
dc.source.urihttp://dx.doi.org/10.1111/j.1600-0757.2006.00169.x-
dc.subjectConnective Tissue-
dc.subjectDental Plaque-
dc.subjectAnimals-
dc.subjectHumans-
dc.subjectBacteria, Anaerobic-
dc.subjectGingivitis-
dc.subjectPeriodontitis-
dc.subjectDiabetes Complications-
dc.subjectDisease Susceptibility-
dc.subjectInflammation Mediators-
dc.subjectRisk Factors-
dc.subjectSmoking-
dc.subjectAntibody Formation-
dc.titleClinical relevance of the host responses of periodontitis-
dc.typeJournal article-
dc.identifier.doi10.1111/j.1600-0757.2006.00169.x-
pubs.publication-statusPublished-
dc.identifier.orcidBartold, P. [0000-0002-5695-3877]-
Appears in Collections:Aurora harvest 5
Dentistry publications

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