Lumbar Spinal Segmental Hypomobility Induced Osteoarthritis is Associated with Early Regression of Facet Joint Synovial Folds

Abstract

Spinal osteoarthritis of the lumbar facet joints is one of the most prevalent and burdensome causes of low back pain (LBP). This condition involves numerous tissues that can directly or indirectly induce pain (e.g., cartilage, bone, synovium, and capsule). Specifically, pathophysiological and morphological changes to the synovium, a key tissue that maintains the health of the joint articular surface, are reported to contribute to the onset and progression of OA. We have previously reported a novel rat model that uses external spinal linkage to cause lumbar spinal hypomobility and induce OA in lower lumbar facet joints (L4/5 and L5/6). This model may replicate the progression of spinal OA in humans and allow mechanistic studies of facet joint OA induced pain. We have shown that this hypomobility is associated with significant bilateral OA changes including synovial fold (SF) regression from within the joint space by 4‐weeks post linkage. The onset of this SF change is unknown. Here we examined if lower lumbar spinal segmental hypomobility in rats is associated with early onset of SF regression from the joint space in the bilateral L4/5 and L5/6 facet joints. We hypothesized that significant SF regression occurs by 1 week following spinal linkage. Analysis was performed using a histological approach based upon our previously reported methods to test our hypothesis in linked (hypomobile) and time matched control rats at 1, 2, and 4 weeks post linkage. The number of facet joint quadrants with SFs was determined using brightfield microscopy to observe formalin fixed, decalcified, paraffin embedded, Ehrlich's hematoxylin and light green stained 45 μm thick sections of the facet joints. The mean number of quadrants containing SFs was calculated for each group. This approach demonstrated acceptable inter‐ and intra‐rater reliability (κ= 0.82 and κ= 0.77). Statistical analysis was performed using a one way ANOVA with Tukey's multiple comparisons. Significance was defined as p <0.05. When compared with time matched control animals (n=4), linked rats demonstrated significant reductions of the SF along the joint surface at 2 and 4 weeks of hypomobility (n=4). No significant differences were found between control groups or at week 1 following linkage. As the synovium can contribute to the development of OA, it is possible that regression of SF in the facet joint by 2 weeks post linkage may reflect pathophysiological changes that contribute to the induction of articular cartilage and subchondral bone degeneration. Further work is required to support these findings including morphometric and mechanistic approaches to determine the functional role of the synovium in hypomobility induced OA and pain. Collectively, these findings support that lumbar spine segmental hypomobility leads to an early onset of SF regression.