Abstract
Periodontal diseases generally progress as plaque biofilm and inflammation-associated destruction of the attachment apparatus. Certain host factors can predispose individuals to these diseases. This paper explores the host immunologic response to periodontal pathogens, which begins with an acute phase of inflammation, and includes an influx of neutrophils and plasma fluid proteins. Chronic inflammation appears to develop when this host response fails to properly resolve. Neutrophil production of excessive oxygen free radicals, as well as impaired neutrophil chemotaxis and phagocytosis, may play a role in the pathogenesis of various forms of periodontal disease (as well as in the pathogenesis of common risk factors such as diabetes and smoking). The genetic etiology of certain immune cell deficiencies may also play a role. Current treatment planning for periodontal disease recognizes the destructive role of chronic inflammatory conditions; resolvins and lipoxins may be a beneficial adjunctive approach to modulating the immune response at the cellular and molecular levels. Concomitant management of plaque biofilm and chronic inflammation may prove to be critical in optimum control of many forms of periodontal disease.
Citation: Dave S, Van Dyke T, Suzuki J. Chronic inflammation in periodontal diseases: immunopathogenesis and treatment.
Grand Rounds Oral-Sys Med. 2007;3:10-17. (Digital version Grand Rounds Oral-Sys Med. 2007;3:10-17a.)
(A complimentary copy of this article may be downloaded at www.thesystemiclink.com.)
Periodontal disease refers to any disease of the supporting structures of the teeth, including the interface of epithelium, connective tissue, and mineralized tissue. Very briefly, the relationship of these supporting structures begins with the tooth, which is made up of a crown (visible in the mouth) and a root (embedded in the jaw bone, also known as alveolar bone or the alveolus). The tooth root is covered in cementum, an avascular mineralized bone-like tissue. Between the root and the alveolus is the periodontal ligament, comprised of parallel collagen fibers embedded in the cementum on one end, in the opposing alveolus on the other end. Thus the tooth is actually suspended within the alveolar bone. Where the tooth transitions from the bone to the oral cavity, the periodontal ligament ends and there is a narrow epithelial cuff attached to the cementum by hemidesmosomes. This epithelial cuff, known as the junctional epithelium, provides both a mechanical and biological barrier between the external environment of the oral cavity and the † internal environment of the body. Near the crown, the cuff sur- ‡ rounds the tooth but is not attached; the space between the cuff and the tooth is called the sulcus. A deepening sulcus indicates conversion from health to disease; however, the hallmark of periodontal disease is the destruction of the periodontal ligament and subsequent loss of alveolar bone. §
Periodontal diseases can be broadly classified as being plaque induced or non-plaque induced. The incidence and severity of plaque-induced periodontal diseases can be modified by an in-
Private Practice Periodontics, Calgary AB, Canada
Professor, Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine; Program Director, Postdoctoral Periodontology; Director, Clinical Research Center, and Associate Director Boston University School of Medicine General Clinical Research Center, Boston, MA
Professor of Microbiology-Immunology, School of Medicine; Professor of Periodontology and Oral Implantology, School of Dentistry; Associate Dean for Graduate Education, Research, and International Affairs; Director, Graduate Periodontology and Oral Implantology; Temple University, Philadelphia, PA
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