Preventative administration of doxycycline has shown to markedly reduce the severity of canine osteoarthritis (OA) in weight-bearing regions of the medial femoral condyle, and therapeutic administration of oral doxycycline has shown to reduce the severity of articular cartilage breakdown in various animal OA models. The disease-modifying effect is attributed to the reduction in levels of active and total collagenase and gelatinase in the articular cartilage of the affected joint.
A prospective, clinical study of 81 dogs with OA secondary to spontaneous cranial cruciate ligament (CCL) rupture concluded that doxycycline inhibits nitric oxide production in dog cartilage with CCL rupture, therefore displaying doxycycline may have a role in the treatment of canine OA. Canines with secondary OA secondary to CCL rupture were randomized into 2 groups before surgery. The Doxy-CCL group (n=35) received 3 to 4mg/kg of oral doxycycline every 24 hours for 7 to 10 days. The CCL group (n=46) did not receive treatment. Synovial fluid, articular cartilage, synovial membrane, and CCL samples were obtained during surgery or immediately following euthanasia from healthy dogs (control group). Total nitric oxide concentrations measured in cartilage were significantly lower in the Doxy-CCL group, but were not different from those measured in the control group.
In another study, 10 healthy adult dogs underwent transection of the left anterior crucial ligament (ACL), which resulted in a significant reduction in bone mass, with increased osteoclastic activity and increased bone formation. Doxycycline treatment did not significantly affect either bone formation or resorption. The author’s concluded that doxycycline offers protection against joint breakdown in this OA model through inhibition of matrix metalloproteinases in articular cartilage, rather than through an affect on subchondral bone.