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Osteoclast activation in inflammatory periodontal diseases
Author(s) -
Wiebe SH,
Hafezi M,
Sandhu HS,
Sims SM,
Dixon SJ
Publication year - 1996
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/j.1601-0825.1996.tb00218.x
Subject(s) - osteoclast , periodontitis , bone resorption , proinflammatory cytokine , tumor necrosis factor alpha , inflammation , immunology , neutrophil extracellular traps , lipopolysaccharide , microbiology and biotechnology , dental alveolus , chemistry , cancer research , biology , medicine , endocrinology , dentistry , receptor , biochemistry
OBJECTIVE: In this paper, we review the mechanisms thought to be involved in the activation of osteoclasts in periodontitis. SUMMARY Osteoclasts are regulated by both microbial and host factors. Some factors act directly on cells of the osteoclast lineage, whereas others act indirectly through other cell types in the bone environment. The pro‐inflammatory cytokines (interleukins I and 6, tumor necrosis factors) have been implicated in the stimulation of osteoclastic resorption. The roles of the immunoregul‐atory cytokines (interleukins 2 and 4, interferon γ) are less clear, but decreased levels of these factors may contribute to periodontitis. A number of lipid mediators may be involved in stimulation of bone resorption. These include bacterial lipopolysaccharide and host‐derived platelet‐activating factor and prostaglandins. More recently, reactive oxygen intermediates and extracellular nucleo‐tides, both present at sites of inflammation, have been investigated as possible modulators of osteoclast activity. The potential use of antiresorptive therapies in periodontitis is reviewed. CONCLUSIONS: A wide range of host and bacterial factors contribute to the loss of alveolar bone in periodontitis. However, much remains to be understood about the complex mechanisms through which these factors regulate osteoclast activity. Further studies at the cellular and molecular level will lead to a better understanding of these processes and perhaps suggest new approaches for periodontal therapy.