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Minocycline reduces gingival collagenolytic activity during diabetes. Preliminary observations and a proposed new mechanism of action.
TLDR
The data suggests that tetracycline therapy inhibits tissue collagenolytic enzyme activity by a mechanism al least in part unrelated to its antibacterial efficacy, and this mechanism may provide a new therapeutic approach for suppressing excessive collagen resorption which occurs during periodontal disease and which can occur during other pathologic conditions. Expand
Synovial procollagenase activation by human mast cell tryptase dependence upon matrix metalloproteinase 3 activation.
TLDR
The tryptase dependent activation of synoviocyte procollagenase thereby appears to be entirely dependent upon its ability to activate proMMP-3. Expand
Reactive oxygen species activate and tetracyclines inhibit rat osteoblast collagenase
TLDR
Data suggested that tetracyclines reduced available HOCI and thus prevented the hypochlorous acid conversion of the osteoblast proenzyme to active collagenase, which may have therapeutic potential in the treatment of periodontitis and other diseases by several mechanisms that inhibit pathologic collagen breakdown. Expand
Doxycycline inhibits neutrophil (PMN)-type matrix metalloproteinases in human adult periodontitis gingiva.
TLDR
MMPS in inflamed gingival tissue of AP patients, like those in GCF, originate primarily from infiltrating PMNs rather than resident gingivals cells (fibroblasts and epithelial cells) or monocyte/macrophages, and that their pathologically-elevated tissue-degrading activities can be directly inhibited by pharmacologic levels of doxycycline. Expand
Tetracyclines suppress matrix metalloproteinase activity in adjuvant arthritis and in combination with flurbiprofen, ameliorate bone damage.
TLDR
Tetracycline inhibition curves in vitro suggest that the collagenase in this tissue is not of fibroblast origin, and might be useful adjuncts to prevention of tissue damage in chronic inflammatory arthritides. Expand
A Non‐Antimicrobial Tetracycline Inhibits Gingival Matrix Metalloproteinases and Bone Loss in Porphyromonas gingivalis‐induced Periodontitis in Rats a
TLDR
The tetracycline antibiotics, which have long been used as adjuncts in periodontal therapy based on their antimicrobial effectiveness against a variety of suspected periodontopathic microorganisms, are now known to also inhibit pathologically excessive host-derived MMP activity during periodontals and other diseases, although the mechanisms of action are not yet well defined. Expand
Tetracyclines inhibit Porphyromonas gingivalis-induced alveolar bone loss in rats by a non-antimicrobial mechanism.
TLDR
Serum antibody levels were significantly elevated in the 3 infected groups compared to the non-infected controls, indicated that these groups of rats were infected with P. gingivalis. Expand
A combination of a chemically modified doxycycline and a bisphosphonate synergistically inhibits endotoxin-induced periodontal breakdown in rats.
TLDR
A combination of suboptimal CMT-8 and clodronate "normalized" the pathologically elevated levels of MMPs, elastase, and alveolar bone loss, indicating synergistic inhibition of tissue breakdown in this animal model of periodontitis. Expand
Identification and characterization of gelatinases/type IV collagenases in jaw cysts.
TLDR
Western-blot studies suggested that jaw cyst gelatinases were only in part complexed with and thus inhibited by TIMP-1 or TIMP/TIMP-2, suggesting that both MMP-9 and M MP-2 may participate in cyst expansion. Expand
Inhibition of proteolytic, serpinolytic, and progelatinase-b activation activities of periodontopathogens by doxycycline and the non-antimicrobial chemically modified tetracycline derivatives.
TLDR
Data from this study suggest that Doxy and CMTs have the potential to inhibit the periodontopathogenic bacterial proteinases, which contribute to tissue destruction cascades during periodontitis directly and indirectly by triggering the host response. Expand
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