Table 1.
Model type | Reported histology | Reported behaviors |
---|---|---|
Surgical | Cartilage lesions, cartilage thinning, osteophyte formation, loss of proteoglycan staining, synovitis40,89,90 | Mechanical allodynia, altered gait, changes in static weight bearing and other behaviors20,22,55,71,91,92 |
Tibial overload and noninvasive ACL rupture | Cartilage fibrillation and clefts, proteoglycan loss, subchondral bone sclerosis93 | No behavioral data available to date |
Mechanical loading | Cartilage thinning, subchondral bone sclerosis, osteophyte formation (at higher loads), cartilage lesions, meniscal ossification, synovial hyperplasia, synovial fibrosis94 | No behavioral data available to date |
Chemical (MIA and collagenase) | Osteophyte formation (certain models), cartilage lesions (certain models), chondrocyte death, cartilage fibrillation, collapse of cartilaginous matrix95,96,89,97 | Thermal and mechanical sensitivity (thermal or mechanical hyperalgesia, mechanical allodynia), altered gait, altered sleep patterns20,96,98 |
Spontaneous/genetic | Cartilage lesions, cartilage fibrillation, focal cell loss, proteoglycan loss, apoptosis of deep zone chondrocytes90,99,100 | Behaviors vary by model, but common behaviors include mechanical allodynia, altered gait, sensorimotor dyscoordination, thermal sensitivity, decreased grip strength100–105 |
High-fat diet/obesity | Cartilage fibrillation, proteoglycan loss, synovitis, focal cell loss, acceleration of histological damage seen when combined with other OA models106,107 | Decreased grip strength (associated with obesity, not OA progression), decreased peak vertical force, mechanical allodynia/hypersensitivity, anxiety-like behavior108 |
OA: osteoarthritis; ACL: anterior cruciate ligament; MIA: monoiodoacetate.