Onset and Progression of Facet Joint Articular Cartilage Degeneration Following Lumbar Spinal Hypomobility
Authors: Merlo John A. , Lawson Craig , McDowell Jacob A. , Benckendorf Adam N. , Cramer Gregory D. , Little Joshua W. 
Published: November 2023

Low back pain (LBP) is the leading cause of physical disability worldwide and a substantial socioeconomic burden. Osteoarthritis (OA) of the facet joint is a common source of LBP, however, the relationship between spinal OA and LBP is complex and requires further investigation. We previously reported a spine OA rat model that uses external lumbar spinal linkage to induce hypomobility, leading to significant macroscopic facet joint OA changes. This model may replicate human spinal OA progression and allow mechanistic studies of facet joint OA induced pain. Here we examined the onset and progression of L4/5 and L5/6 facet joint articular cartilage degeneration on the superior articular processes (SAP) following linkage. We hypothesized that spinal linkage would result in an early (1–2 weeks post linkage) thinning of articular cartilage that is progressively greater with longer durations. We used a histological approach based upon previously reported methods to test if spinal linkage is associated with decreases in the ratio of articular cartilage surface length (AS) to total joint surface (JS) length and/or regional articular cartilage surface area in linked and time matched control rats (n=3–4 per group) at 1, 2, 4, and 8 weeks post linkage. Measurements (AS, JS, and area) were performed on brightfield microscopy images (10X objective, Leica DMRB, optronics microfire camera) of sections from the mid‐level of L4/5 and L5/6 facet joints. The tissues were formalin fixed, decalcified, paraffin embedded, sectioned (45 μm thick transverse sections), and stained with Ehrlich's hematoxylin and light green. The JS was divided into 11 equidistant points to define 10 regions from ventral to dorsal and calculate articular cartilage area of each region. Intra‐ and inter‐rater reliability was acceptable for JS (ICC = 0.99, ICC = 0.95), AS (ICC = 0.99, ICC = 0.92), and articular cartilage area (ICC = 0.99, ICC = 0.87). Compared to controls, hypomobility was associated with a significant decrease in the AS/JS ratio (one way ANOVA with Tukey's multiple comparisons, p < 0.05) at 2, 4, and 8 weeks post linkage. Linear regression analysis in 1, 2, 4, and 8 week controls demonstrated no relationship with the AS/JS ratio (r2 = 0.09), while in linked rats longer durations predicted more pronounced decreases in the AS/JS ratio (r2 = 0.84). Descriptive regional analysis supported these findings and revealed that linked rats had reduced cartilage surface area (≥25%) in the ventral‐most (1 medial region) and dorsal‐most (3 lateral regions) regions at week 2 compared with controls. Rats with longer linked durations had greater percentage reductions in cartilage area (≥50%) in the same peripheral regions with additional involvement of adjacent regions and expansion toward the center of the joint stemming mostly from the dorsolateral SAP (dorsal regions with ≥25% reduction: week 4 = 4, week 8 = 5). Our findings suggest that hypomobility results in early (by 2 weeks) and progressive cartilage degeneration in the joint periphery, similar to human facet joint OA. The external spinal linking model creates progressive cartilage loss and may be useful in determining the relationship between OA and pain.