Table 1.

Common types of OA models and the behaviors reported within these OA phenotypes.

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.