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The Lumbar Facet Joint Capsule Thickens Following Spinal Segmental Hypomobility Induced Osteoarthritis
Author(s) -
Benckendorf Adam N.,
Merlo John A.,
Cramer Gregory D.,
Little Joshua W.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1041.4
Subject(s) - medicine , lumbar , osteoarthritis , joint capsule , facet joint , facet (psychology) , articular capsule of the knee joint , capsule , low back pain , anatomy , pathology , surgery , knee joint , psychology , biology , social psychology , botany , alternative medicine , personality , big five personality traits
Low back pain (LBP) is a major medical issue and the primary cause for global disability. One common cause of LBP is osteoarthritis (OA) of the lumbar facet joints. OA involves numerous tissues that can induce pain. In particular, during facet joint OA in humans, the articular capsule thickens in response to mechanical and inflammatory stresses; this thickening is associated with LBP. We have previously reported a novel rat model using external spinal linkage to cause lumbar spinal hypomobility and induce OA the in lower lumbar facet joints (L4/5 and L5/6) that may model the progression of spinal OA in humans. This hypomobility results in significant macroscopic OA changes to the articular cartilage and subchondral bone bilaterally by 8‐weeks post linkage. The onset and progression of articular capsule changes and their relationship with pain behaviors is unexplored in this model. Here we examined if lumbar spinal segmental hypomobility in rats is associated with thickening of the ventral articular capsule (ligamentum flavum, LF) as evidenced by increases in morphometric measurements in the bilateral L5/6 facet joints. We hypothesized that 8 weeks of spinal linkage, a time point of significant facet joint OA, is associated with an increase in articular capsule thickness. We used a histological approach with morphometric analyses based upon previously reported methods to test our hypothesis in linked and time matched control rats. LF thickness measurements were performed on images obtained from a brightfield microscope (10X objective, Leica DMRB, optronics microfire camera) on formalin fixed, decalcified, paraffin embedded, Ehrlich's hematoxylin and light green stained 45 μm thick transverse sections of the bilateral L5/6 facet joints. Morphometric measurements were made (OsiriX Lite software) by drawing a line through the thickest region of the LF, perpendicular to the plane of the ventral LF surface. This morphometric approach demonstrated acceptable reliability (ICC= 0.8656). Statistical analysis was performed using an unpaired t‐test. Compared with control animals (n=4), 8 weeks of hypomobility (n=4) was associated with a significant increase in LF thickness ( p <0.05). The articular capsule thickness increased at a time point previously shown to have significant OA changes, which is consistent with facet joint OA and LF thickening in human subjects. Increases in articular capsule thickness are hypothesized to contribute both to the induction or reflect the ongoing pathological processes of OA (e.g., prolonged inflammation and fibrosis). Further work is required to determine the onset, joint location, and mechanisms underlying these capsule changes. These findings suggest that lumbar spine hypomobility induces LF thickening.