Canine Joint Health, Mobility, Energy & Longevity: 5 Things a 10 year old Labrador Taught Me

The healthy joint is a highly metabolic organ comprised of cartilage, bone, synovium, neural and supportive muscle tissues whose function is critical to mobility and life quality. The healthy joint is characterized by delicately balanced anabolic and catabolic activities. In OA joints, the metabolic balance shifts toward catabolism driven by cytokine cascades and inflammatory mediators.1 Pro-inflammatory cytokines such as interleukin-1 (IL-1 ) and tumor necrosis factor- (TNF- ), produced by chondrocytes and synoviocytes, decrease anabolic activities such as collagen and proteoglycan synthesis and upregulate the production of catabolic enzymes including matrix metalloproteinases (MMP’s).1 These cytokines and other cytokines (IL-8, IL-6, etc) also upregulate the expression of pro-inflammatory enzymes cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) that lead to increased production of prostaglandin E2 (PGE2) and nitric oxide (NO).1 Biomechanical alterations resulting from such factors as joint instability, joint mal-alignment and obesity perpetuate OA and its degradative biochemical pathways. Increasingly, chondrocyte apoptosis and premature senescence are linked to NO and other oxidative injury. It is clear that OA has characteristics of progressive, premature aging of the joint that are mechanically driven and chemically mediated. Inflammatory changes within the synovium are also characteristic of the disease process. Synovitis is typically located adjacent to diseased or damaged cartilage and bone. Regional cartilage destruction may be exacerbated by the release of proteinases and cytokines from the activated synovium. […]