Osteoimmunological Aspects of Periodontal Diseases
Inflammatory processes in the proximity of bone tissue have been shown to modify bone metabolism. Under homeostatic conditions bone resorption by osteoclasts is closely followed by approximately the same amount of bone formation by osteoblasts, known as t
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Kristina Bertl, Peter Pietschmann, Michael Matejka
11.1 Introduction Inflammatory processes in the proximity of bone tissue have been shown to modify bone metabolism. Under homeostatic conditions bone resorption by osteoclasts is closely followed by approximately the same amount of bone formation by osteoblasts, known as the coupling of bone formation and resorption (Parfitt 1982). Yet, inflammatory cytokines may disturb this delicate equilibrium by enhancing differentiation and activation of osteoclasts. The occurring bone loss can more likely be attributed to increased bone resorption than reduced bone formation and the osteoclasts are considered to be the principal responsible cells (Biancu et al. 1995; Bromley and Woolley 1984). Such inflammatory osteolysis is observed in rheumatoid arthritis, osteomyelitis, bone surrounding a loosened joint prosthesis or marginal and apical periodontitis. Periodontitis is a chronic infectious inflammatory disease. The presence of bacteria in a biofilm on the root surface of the teeth triggers an immune response of the innate as well as of the adaptive immunity. Yet, the biofilm provides a convenient and rather safe environment for the bacteria and thus they are well protected against the host’s defense mechanisms. First clinical signs appear as reversible gingivitis with the typical “cardinal signs of inflammation”: erythema, edema, heat, pain and more or less loss of function. Depending on several influencing factors (e. g. amount of bacteria, type of bacteria or host susceptibility), the equilibrium between the immune system and the bacterial invasion, which is more or less present in gingivitis, might be disturbed. Next, the inflammatory process expands into the proximity of alveolar bone (Fig. 1a, b) where differentiation and activation of osteoclasts is promoted. The resulting uncoupling of bone formation and resorption leads to increased alveolar Dr. Kristina Bertl Bernhard Gottlieb University Clinic of Dentistry, Medical University of Vienna, Division of Periodontology, Sensengasse 2a, 1090 Vienna, Austria [email protected] Pietschmann et al., Principles of Osteoimmunology, Molecular Mechanisms and Clinical Applications; DOI 10.1007/978–3–7091–0520–7, © SpringerWienNewYork 2012
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11 Osteoimmunological Aspects of Periodontal Diseases
Fig. 1 (A) Inflammatory reaction is restricted to gingiva; (B) inflammatory process reaches proximity of the alveolar bone and induces osteoclastogenesis and alveolar bone loss. Modified by Graves et al. (2010) and Schröder and Lindhe (1981). CEJ: cemento enamel junction
bone loss, which is the cardinal sign of periodontitis and might ultimately lead to tooth loss. Consequently, the immune system, which is trying to stop the bacterial invasion, is responsible for the destruction of soft and mineralized periodontal tissue. The presence of the bacteria is “only” required for disease initiation, but not sufficient for development (Graves 2008; Graves et al. 2008). This interaction and communication between imm
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