Effects of Tetracycline on Cartilage Degradation and Matrix Metalloproteinase Activity/Expression

Baragi, Vijaykumar M.; Jonat, Carsten; Renkiewicz, Richard R.; Qiu, Lihua; Man, Chiu Fai

doi:10.1177/08959374980120012301

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Tetracyclines1

Gene Therapy1

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1999

2011

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Cited by 4 publications

(2 citation statements)

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“…They are reported to inhibit activity and expression of MMPs that are implicated in cartilage degradation associated with OA [87][88][89][90][91]. Both doxycycline and minocycline have also been shown to inhibit the production of nitric oxide synthase, which is up regulated in OA cartilage [92].…”

Section: Tetracyclinesmentioning

confidence: 99%

Concept of Comprehensive Treatment for Osteoarthritis (OA)

Baragi¹

2005

CMCIEMA

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Section: Tetracyclinesmentioning

confidence: 99%

Concept of Comprehensive Treatment for Osteoarthritis (OA)

Baragi¹

2005

CMCIEMA

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“…IL-I has catabolic effects on cartilage, including the generation of synovial inflammation and up-regulation of matrix metalloproteinases and prostaglandin expression (131)(132)(133)(134)(135)(136). Soluble IL-1 receptor antagonist (IL-1ra) is a naturally occurring protein that can inhibit the effects of IL-1 by binding to and preventing IL-1 from interacting with chondrocytes, thereby lowering the effective concentration of IL-1.…”

Section: Gene Therapymentioning

confidence: 99%

Degradation and repair of articular cartilage

Frenkel

Cesare²

1999

Front Biosci

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Approximately 95,000 total knee replacements and 41,000 other surgical procedures to repair cartilaginous defects of the knee are performed annually in the United States (1). The response of normal articular cartilage to injury or arthritic degeneration is often a sub-optimal repair; the biochemical and mechanical properties of the new tissue differ from the native cartilage, resulting in inadequate or altered function. It is believed that the chondrocytes from the surrounding areas, although perhaps capable of some limited migration at the damaged site, are not able to proliferate and produce the macromolecules necessary to create an organized matrix characteristic of normal articular cartilage (2,3). Current therapeutic options for articular cartilage injuries and degeneration have resulted in repair tissue which may be hyaline-like, but does not approximate the durability and function of the normal articular surface. Numerous studies have been performed to increase our understanding of the normal repair process of articular cartilage and its limitations, and to devise methods and materials to regenerate the joint surface.

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