To determine if fatigue microdamage is associated with fragmented medial coronoid process (FMCP).
Thirty-eight dogs were admitted for subtotal coronoid ostectomy as treatment for FMCP. Surgical specimens of medial coronoid process (MCP) were retrieved from treated dogs. Normal MCP were collected from 5 age- and breed-matched dogs and 2 age-matched research beagles that were euthanatized for reasons other than elbow disease.
MCP specimens from affected elbows were classified into 4 groups based on disease severity. Specimens were bulk-stained for microdamage using 1% basic fuchsin, embedded in polymethylmethacrylate and sectioned at 130 microm. Specimens were evaluated using epifluorescent microscopy (425-440 excitation, 475 nm barrier filter) for diffuse damage (D.DX), osteocyte loss, and porosity. Cartilage thickness was evaluated using bright field microscopy. Qualitative observations were also made.
MCP specimens from affected elbows had increased D.Dx, increased osteocyte loss, and greater porosity than normal groups. Specimens classified as severe FMCP (Classes 3, 4) had the most fatigue microdamage. Some Class 1 specimens, defined as having no visible fissuring of the articular cartilage (AC), had large microcracks in trabecular bone
Accumulation of subchondral fatigue microdamage, is associated with MCP fragmentation. Fissuring occurs in the subchondral bone before gross fibrillation of articular cartilage develops.
Accumulation of fatigue microdamage in the MCP is important in the pathogenesis of FMCP. The underlying cause of this microdamage accumulation must be identified before treatment plans that will prevent further osteoarthritis of the elbow joint can be designed.