Pathological Alterations of the Lumbar Facet Joint Subchondral Bone and Synovial Fold during Hypomobility Induced Cartilage Degeneration
Authors: Allison Jeffrey M. , Martin August D. , McDowell Jacob A. , Merlo John A. , Lawson Craig , Cramer Gregory D. , Little Joshua W. 
Published: June 2021

Low back pain (LBP) is a leading cause of worldwide disability and socioeconomic burden. Degeneration of the lumbar facet joints (FJ) or spinal osteoarthritis (OA) is one clinically relevant source of LBP. Recent studies suggest that the increased prevalence of OA may be a result of not only overuse of a synovial joint but also less joint movement. A better understanding of how FJ degeneration is induced and progresses may provide the foundation to reveal the underlying mechanisms of spinal OA and LBP.

OA is a whole joint disease involving several tissues. The avascular articular cartilage relies upon adjacent tissues to maintain its homeostasis. Of particular importance is the synovial fluid from the synovium that is largely responsible for nutrient supply and waste removal for the cartilage; this requires appropriate joint movement. When cartilage loses access to synovial fluid, vascular channel ingrowth into cartilage and neovascularization from the subchondral bone can occur to promote degeneration. Less joint movement (hypomobility) could contribute to OA through a similar process. Although previous studies implicated neovascularization in OA induction and progression in other joints, less is known in the FJ. It was reported that during spinal OA there were increased subchondral channels invading the FJ articular cartilage. Here, we used a preclinical rat model of spinal OA to examine lumbar FJ degeneration after hypomobility. Previously, we found that hypomobility in lumbar FJs leads to cartilage degeneration that mimics the location and progression of spinal OA. We also observed that the synovial fold (SF) regressed from the FJ cavity by 2 weeks after hypomobility in the same location as early cartilage degeneration. As synovium pathology can induce subchondral processes to promote degeneration, we examined the onset, location, and progression of subchondral vascular channels after hypomobility. We hypothesized that channels would increase in the cephalad regions of the FJ superior articular process (SAP) by 2 weeks after hypomobility adjacent to cartilage degeneration and SF regression. We performed histological analyses on brightfield microscopic images of sections from the cephalad and cephalad‐middle regions of bilateral L4/5 and L5/6 FJ in hypomobile and control rats at 1, 2, and 4 weeks. The tissues were formalin fixed, decalcified, paraffin embedded, transversely sectioned (45 μm), and stained with Ehrlich's hematoxylin and light green. Intra‐ and inter‐rater reliability was acceptable for channel counts (K = 0.88 & 0.76) and a severity scale of vascular channel ingrowth (Kw = 0.81 & 0.89). Spinal hypomobility was associated with significant increases in vascular channel counts and severity of cartilage invasion in the FJ SAP margins by 2 weeks. In hypomobile rats, we also observed changes to the appearance of blood vessels in the adjacent SF (increased numbers of enlarged & disorganized vessels). These changes correlate with the onset and locations of SAP cartilage degeneration after hypomobility. Our findings mimic spinal OA and suggest a role for the subchondral bone and SF in FJ degeneration.

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.