Facet Joint Inferior Articular Process Degeneration Following Lumbar Spinal Hypomobility
Authors: Vahey Bryan T , 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 a primary cause of disability worldwide and a financial burden to the healthcare industry. A potential source of LBP is the lumbar facet joint, a synovial joint comprised of two articular processes (superior, SAP and inferior, IAP) located between adjacent vertebrae. A commonly accepted condition associated with facet joint LBP is the development and progression of degenerative changes consistent with osteoarthritis (i.e., spinal OA); however, this relationship is incompletely understood. We previously reported that a rat model using external lumbar spinal linkage to induce hypomobility results in early lumbar facet joint SAP articular cartilage degeneration that mimics the location, histopathological findings, and progression of human spinal OA. The onset, location, and progression of the IAP histopathological degeneration following external linking are unknown. IAP degeneration in human lumbar spinal OA occurs in the joint margins with the greatest severity in the inferior (caudal) pole. Here we examined the onset and location of facet joint IAP articular cartilage degeneration following induced hypomobility. We hypothesized that hypomobility would result in articular cartilage thinning and loss in the caudal IAP joint margins by 8 weeks. We used a morphometric approach from previously reported methods to test if spinal hypomobility is associated with decreases in the ratio of articular cartilage surface (AS) to total joint surface (JS) length and cartilage area and thickness at 4 and 8 weeks post linkage compared with control rats. Measurements were performed on brightfield microscope images (10X objective, Leica DMRB, optronics microfire camera) of L4/5 and L5/6 facet joint sections from the cephalad, cephalad‐middle, caudal‐middle, and caudal regions. The tissues were formalin fixed, decalcified, paraffin embedded, transversely sectioned (45 μm thick), and stained with Ehrlich's hematoxylin and light green. The JS was divided into 11 equidistant points to measure cartilage thickness and define 10 regions for cartilage area from ventral to dorsal. Intra‐ and inter‐rater reliability was acceptable for JS length (ICC = 0.96 and 0.83), AS length (ICC = 0.89 and 0.78), cartilage thickness (ICC = 0.93 and 0.80) and cartilage area (ICC = 0.97 and 0.77). We found that hypomobility was associated with a significant decrease (p < 0.05) in the AS/JS length ratio at 8 weeks post linkage in the caudal region. Compared to control, linked rats also had significant decreases in cartilage thickness and area in points 10 and 11 and areas 9 and 10, the most dorsolateral aspect of the JS. Our findings suggest that hypomobility results in IAP histopathological changes that mimic the pattern of spinal OA in the IAP. Studies are ongoing to determine the temporospatial progression of this IAP caudal lesion and IAP degeneration in other regions at later time points. Collectively, our work demonstrates that hypomobility induces facet joint degeneration that mimics the histopathological pattern of spinal OA. This hypomobility model may allow mechanistic studies to reveal the relationship between OA and LBP.

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