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Knee. 2012 Oct;19(5):680-3. doi: 10.1016/j.knee.2011.12.007. Epub 2012 Jan 31.

Minocycline reduces articular cartilage damage following osteochondral injury.

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  • 1Department of Orthopaedic Surgery, University of California, San Francisco, CA, USA.

Abstract

INTRODUCTION:

Secondary injury pathways activated after chondral and osteochondral injury represent a potential target for therapies designed to minimize articular cartilage loss. The primary objective of this study was to test the potential chondroprotective effects of intra-articular minocycline following osteochondral injury.

METHODS:

In vitro experiments were first performed with rabbit femoral condyles explants using an osteochondral drill injury model. Data from these in vitro experiments showed that minocycline at concentrations of 10-1000 nM decreased chondrocyte apoptosis in a dose-dependent manner. In vivo experiments were then conducted using the same injury model, studying the effects of intra-articular minocycline on chondrocyte apoptosis, chondrocyte cell number, and cartilage thickness.

RESULTS:

Four days after injury, minocycline delivered daily directly into the rabbit knee joints decreased acute chondrocyte apoptosis by 56% compared to controls. Analysis performed six weeks after injury demonstrated superior chondrocyte cell number, cartilage thickness, and cartilage repair in animals receiving short-term (one-week) minocycline treatment compared to controls.

CONCLUSIONS:

These data support a therapeutic approach utilizing drugs like minocycline for the acute treatment of osteochondral injuries.

Published by Elsevier B.V.

PMID:
22297212
[PubMed - indexed for MEDLINE]
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