Size and geometry of apical sesamoid fracture fragments as a determinant of prognosis in Thoroughbred racehorses.

REASON FOR PERFORMING STUDY: Analysis was performed to examine a method for refining the preoperative prognosis for horses that had surgery to remove apical fractures of the proximal sesamoid bones (PSBs). OBJECTIVES: To determine if: 1) there was a difference in size or configuration of apical fractures between the different anatomical locations of the PSBs, which have been shown to affect the prognosis; and 2) the size or configuration could predict the prognosis for racehorses with these fractures. METHODS: The study included 110 weanlings and yearlings and 56 training racehorses that underwent surgery to remove apical PSB fractures. Radiographs of the fractures were used for measurement of the abaxial and axial proportion and the abaxial to axial ratio, and race records were used to determine average earnings per start (AEPS) and total post operative starts. Analysis of variance and regression statistics were used to compare the fragment sizes between the specific PSBs on each of the limbs and compare size and configuration of the fractures to prognosis. RESULTS: There was a significantly larger abaxial to axial ratio (more transverse fracture) for the forelimb medial sesamoids than for all other sesamoids in untrained racehorses (P = 0.03). There were no other significant differences in size. There was no relationship between fracture size or configuration and AEPS nor total post operative starts. CONCLUSIONS: Apical fractures in weanlings and yearlings tend to be more transverse in the forelimb medial PSBs than the other PSBs. Apical fracture size and geometry does not determine prognosis for apical sesamoid fractures. POTENTIAL RELEVANCE: Horses that undergo surgery to remove larger apical fractures of the PSBs do not have a worse outcome than those horses with smaller fractures.

Cytokine and catabolic enzyme expression in synovium, synovial fluid and articular cartilage of naturally osteoarthritic equine carpi.

REASONS FOR PERFORMING STUDY: Understanding the expression of catabolic and anabolic genes during osteoarthritis progression should help to identify the major mediators of the disease. OBJECTIVE: To compare the cytokine and anabolic marker concentrations in synovium, synovial fluid and cartilage between normal and osteoarthritic joints. METHODS: Carpi from horses age 2-11 years were used. Tissues were harvested at the time of surgery or euthanasia, and RNA was isolated for RT-PCR analysis. Tumour necrosis factor alpha (TNFα), interleukin-1beta (IL-1ß), aggrecanase 1 (ADAMTS-4), aggrecanase 2 (ADAMTS-5), matrix metalloproteinase-13 (MMP-13), interleukin 17 (IL-17) and collagen type I alpha 1(Col-1) expression were determined in synovium. TNFα, IL-1ß, ADAMTS-4, ADAMTS-5, MMP-13, IL-17, collagen type IIB (Col-2B), and aggrecan expression were determined in cartilage. TNFα concentration in the synovial fluid was determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Expression of TNFα, ADAMTS-5 and MMP-13 was significantly increased in synovial tissue from OA joints. Synovial membrane IL-1ß abundance showed only moderate elevations in OA, without reaching significant levels. Cytokine expression was increased significantly in OA cartilage samples, particularly TNFα, IL-1ß, ADAMTS-4 and MMP-13; and collagen type I expression was significantly increased in synovial tissues from OA groups. Collagen type II message was diminished in mild and moderate stages of OA, but rebounded to significant elevations in severely degenerate joints. Conversely, aggrecan levels significantly declined in cartilage from all OA groups. Synovial fluid TNFα peptide concentration was significantly increased in severe OA cases. CONCLUSION: TNFα was increased in all degrees of equine OA, and was abundantly expressed in synovial membrane and cartilage. IL-1ß was overexpressed in OA cartilage, but not to a significant extent in synovium. POTENTIAL RELEVANCE: Control of TNFα should be considered further as a target in the treatment of OA. ADAMTS-4 may be the primary aggrecanase causing cartilage breakdown in OA.