The Ligamentum Flavum Thickens During the Advanced Stages of Hypomobility Induced Lumbar Spinal Osteoarthritis

Abstract

Low back pain (LBP) is a primary cause of global disability. The lumbar facet joint is recognized as a clinically relevant pain generator. Pain can occur through the onset and progression of facet joint degeneration consistent with spinal osteoarthritis (OA). OA is now defined as a whole joint disease involving many tissues in addition to the articular cartilage, including the joint capsule. Capsular thickening due to mechanical and inflammatory stress can present clinically as a source of LBP. We have previously examined capsular thickening that occurs during OA, by using a rat model of external spinal linkage to cause lumbar spinal hypomobility and induce degeneration in the lower lumbar facet joints (L4/5 and L5/6). We have shown that this model mimics the location, progression, and histopathological changes of the articular cartilage typically reported in human spinal OA. Additionally, we found that by 8 weeks post linkage this degeneration is associated with significant thickening of the ventral articular capsule (ligamentum flavum, LF) in the cephalad portion of the joint. These articular capsule changes are unexplored at later stages of this model when degeneration is more advanced. Here we used a morphometric approach to examine if spinal hypomobility of the bilateral L4/5 and L5/6 facet joints in rats is associated with LF thickening. We hypothesized that 12 weeks of spinal linkage would be associated with an increase in articular capsule thickness in joint regions undergoing cartilage degeneration. We tested our hypothesis by comparing LF thickness in linked and time matched control rats at 12 weeks post linkage. LF thickness measurements were performed on images obtained from a brightfield microscope (10× objective, Leica DMRB, optronics microfire camera) on formalin fixed, decalcified, paraffin embedded, Ehrlich's hematoxylin and light green stained 45 μm thick sections. Morphometric measurements were made by drawing a line through the thickest region of the LF, perpendicular to the plane of the ventral LF surface. This approach demonstrated acceptable inter‐ and intra‐rater reliability (ICC= 0.94 and 0.99). Twelve weeks of hypomobility was associated with a significant increase in LF thickness (p<0.05) compared with control animals in the cephalad and caudal regions. This agrees with our recent findings that significant degeneration is present in the superior articular process (predominantly cephalad region) and inferior articular process (predominantly caudal region) by week 12. Our findings suggest that advanced cartilage degeneration is associated with LF thickening. These findings require additional study to examine the causes of LF thickening (e.g., prolonged inflammation and fibrosis) to better understand the role of the LF in the pathophysiology of OA and OA induced LBP.Support or Funding InformationNCMIC