The Lumbar Facet Joint Synovial Fold Intimal Surface Length Decreases During the Onset of Cartilage Degeneration Following Spinal Hypomobility
Authors: Allison Jeffrey M. , McDowell Jacob A. , Merlo John A. , Cramer Gregory D. , Little Joshua W. 
Published: November 2023

Lumbar facet joint degeneration consistent with spinal osteoarthritis (OA) is a prevalent condition and can be associated with dysfunction and low back pain (LBP). Facet joint degeneration is a whole joint disease and involves many tissues that can contribute to pain, including the synovium. The synovium has a critical role in maintaining joint health and is implicated in the pathophysiological processes underlying OA development and progression. We previously found that spinal hypomobility leads to lumbar facet joint degeneration and is associated with early synovial fold (SF) regression from within the joint space (2 weeks post hypomobility) in rats. These microscopic observations of SF regression occur at the same time point of our earliest detected facet joint histopathological changes; implicating the potential contribution of SF pathology to the onset of facet joint degeneration. Here we used morphometric analyses of the SF intimal length at 2 weeks post hypomobility to quantify and confirm our previous findings and help identify the predominant site of SF regression (ventral SF and/or dorsal SF). We hypothesized that the SF intimal surface length would decrease after hypomobility and that his would be most significant in the cephalad regions where early degeneration is the most severe. We used previously reported methods to perform morphometric analysis of the SF intimal surface length to compare linked and time‐matched control rats. Intimal surface length was defined as a line on the surface of the synovium from the synovium‐subchondral bone junction of the inferior articular process to the same junction at the superior articular process. Measurements were performed on brightfield microscopic images (10× objective, Leica DMRB, optronics microfire camera) of sections that represent the cephalad, cephalad‐middle, caudal‐middle, and caudal regions of bilateral L4/5 and L5/6 rat facet joints. All measurements were normalized to the superior articular process joint surface length to account for variations in joint size. The tissues were formalin fixed, decalcified, paraffin embedded, transversely sectioned (45 μm thick), and stained with Ehrlich's hematoxylin and light green. Intra‐ and inter‐rater reliability was acceptable for joint surface (ICC = 0.96 and 0.83) and SF intimal surface length (dorsal SF ICC = 0.88 and 0.81; ventral SF ICC = 0.81 and 0.86). There was a significant decrease in SF intimal length in the ventral SF in the cephalad and cephalad‐middle regions by week 2 following the onset of hypomobility compared to control rats. We also detected a significant decrease in the dorsal SF intimal length in the cephalad region. Additional studies are ongoing to determine the histopathological changes of the SF following hypomobility. This study confirms and extends our previous observations revealing the location and joint region of SF regression. As this model induces articular cartilage histopathological changes that mimic spinal OA features, it may help to determine the role of the synovium in the onset and progression of spinal OA and LBP.

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