Cranial cruciate ligament rupture (CCLR) has an increased prevalence in dogs that are overweight. A humoral role for adipose tissue has been postulated as adipocytes synthesize and release adipokines, which can result in inflammation and increased degradation in musculoskeletal tissues. To date, the role of adipokines in CCLR has not yet been clarified.
This study aims to assess gene expression for key adipokines, inflammatory mediators, and cartilage degradation markers in cranial cruciate ligaments (CCLs) from dogs with CCLR, and to determine if these mediators have a relationship with disease.
Twenty-five CCLs samples were collected from dogs with CCLR. Gene expression for adiponectin, leptin, visfatin, MCP-1, TNF-α, IL-6, aggrecan, collagen type I and MMP-13 in CCLs were determined by qRT-PCR. Pearson's correlation was used to determine associations between gene expression of the adipokines and inflammatory mediators studied together with age and bodyweight, whilst Kendall's tau was used for comparisons with body condition score.
The most highly expressed adipokines in CCLs were MCP-1 and visfatin. Leptin was negatively correlated with aggrecan (r = -0.82, p = 0.01). Visfatin was positively correlated with MMP-13 (r = 0.45, p = 0.05) and negatively correlated with body condition score (r = -0.41, p = 0.02). Moreover, IL-6 was positively correlated with collagen type I (r = 0.53, p = 0.02) and negatively correlated with bodyweight (r = -0.52, p = 0.02).
The canine CCL contains cells that can express adipokines. The associations between key adipokines and cartilage markers gene expression, together with clinical measures such as body condition score and bodyweight, suggest that adipokines are possibly involved in CCLR.