A systemic review of existing serological possibilities to diagnose canine osteoarthritis with a particular focus on extracellular matrix proteoglycans and protein

Abstract

Extra-cellular matrix (ECM) components are important and their stabilization is significant in maintaining normal healthy joint environment. In osteoarthritis (OA), ECM components are altered and indicate disease progression. The joint ECM is composed of proteoglycans (aggrecan, perlecan, inter α-trypsin inhibitor), glycoproteins (fibronectin, lubricin, COMP) and collagen types (most abundantly collagen type II) which represent structural and functional transformation during disease advancement. ECM investigation revealed significant biomarkers of OA that could be used as a diagnostic and therapeutic tool in different canine orthopedic diseases. This review deliberates our current findings of how the components of ECM change at the molecular level during disease progression in canine OA.

Protein biomarkers in serum and urine for determining presence or absence of hip dysplasia in a canine model

“…Alternatively, body fluid proteins are being evaluated for their capabilities in screening for, diagnosing, staging, and monitoring the development and progression of OA in CHD and other joint disorders. To date, OA research using protein biomarkers has primarily focused on breakdown products of articular cartilage in serum and/or synovial fluid . No significant differences were found in CTX‐II concentrations in synovial fluid between controls and dogs affected with OA, while CTX‐II levels in the urine of dysplastic dogs were significantly lower than non‐dysplastic dogs in the present study.…”

“…To date, OA research using protein biomarkers has primarily focused on breakdown products of articular cartilage in serum and/or synovial fluid. 14,23,[32][33][34] No significant differences were found in CTX-II concentrations in synovial fluid between controls and dogs affected with OA, 35 while CTX-II levels in the urine of dysplastic dogs were significantly lower than non-dysplastic dogs in the present study. Another study showed significantly increased levels of TIMP-1, and no significant differences in MMP3 levels in serum and synovial fluid of dogs with CHD compared to non-dysplastic controls.…”

“…Dogs were radiographically categorized as having normal (excellent or good) hips ( n = 49) or having dysplastic (mild, moderate, or severe) hips ( n = 25) based on documented OFA grading scheme . Breed representation for normal hips are: 1 dog‐Border Terrier, German Shorthaired Pointer, Vizsla; 2 dogs‐Beagle, Rottweiler; 3 dogs‐Boykin Spaniel, Corgi, Pyrenean Shepherd; 4 dogs‐Newfoundland; 7 dogs‐German Shepherd Dog; 11 dogs‐Golden Retriever, Labrador Retriever.…”

“…The development of ligament laxity is followed by soft tissue, cartilage, and bone changes occurring due to the forces of movement and weight bearing on the unstable joint. As such, CHD is a common cause of secondary OA in affected dogs, which is a profound health problem in dogs with associated costs of billions of dollars to the pet‐owning households …”

“…As such, CHD is a common cause of secondary OA in affected dogs, which is a profound health problem in dogs with associated costs of billions of dollars to the pet-owning households. [12][13][14] In people, hip dysplasia is recognized as the most common cause of hip OA in women (<40 years) and accounts for 5% to 10% of all total hip replacements in the United States. 6 The dog is an attractive animal model to investigate hip dysplasia and OA in humans as they share remarkable similarities in their clinical expression and pathogenesis, and current diagnostics and treatment options are nearly identical between humans and dogs.…”