Abstract
Adolescent idiopathic scoliosis (AIS) is a poorly understood deformity of the thoracolumbar spine which affects the intervertebral discs (IVDs) and the articular facet joints. The knowledge concerning facet joints in this context is very limited, although facet joint degeneration is a known contributor of back pain. In this study, a comprehensive investigation was performed to characterize the facet joint chondrocytes and extracellular matrix within the scoliotic spine. Surgically removed articular facet joint tissues were collected from patients undergoing spinal corrective surgery for AIS deformities, while non‐scoliotic articular facet joint tissues were obtained from cadaveric organ donors. Alterations in cartilage tissue structure were evaluated histologically with safranin‐O fast green and a modified OARSI grading scale. Pro‐inflammatory cytokines, matrix‐degrading proteases, and fragmented matrix molecules associated with cartilage degradation were analyzed by immunohistochemistry and western blotting. Safranin‐O fast green staining revealed that young scoliotic facet joints show clear signs of degeneration with substantial proteoglycan loss, similar to osteoarthritis (OA). The proteoglycan levels were significantly lower than in healthy asymptomatic non‐scoliotic control individuals. In comparison to controls, scoliotic articular facets showed increased cell density, increased expression of the proliferation marker Ki‐67, and higher expression of MMP‐3, MMP‐13, and IL‐1β. Expression and fragmentation of the small leucine‐rich proteins (SLRPs) chondroadherin, decorin, biglycan, lumican, and fibromodulin were analyzed with western blot. Chondroadherin and decorin were fragmented in cartilage from patients with a curve greater than 70°, whereas biglycan and fibromodulin did not show curve‐related fragmentation. AIS facet joint cartilage shows hallmarks of OA including proteoglycan loss, overexpression of pro‐inflammatory mediators, increased synthesis of matrix‐degrading proteases and fragmentation of SLRPs. As with patients with age‐related OA, the premature joint degeneration seen in scoliotic patients is likely to contribute to the pain perceived in some individuals.
Highlights
Adolescent idiopathic scoliosis (AIS) is a structural deformity which manifests as a gradually increasing curvature and rotation of the spine.[1]
Articular facet joints in AIS patients demonstrated multiple signs of tissue deterioration which occurs in the form of proteoglycan loss, increased cellular proliferation, overexpression of matrix metalloproteases (MMP)-3, −13, and IL-1ß
As the articular cartilage matures after epiphyseal closure around 20 years of age, its proteoglycan content decreases, and the tissue slowly degrades with aging, a process that is strongly enhanced in OA.[24]
Summary
Adolescent idiopathic scoliosis (AIS) is a structural deformity which manifests as a gradually increasing curvature and rotation of the spine.[1]. ABBREVIATIONS: AIS, adolescent idiopathic scoliosis; IVD, intervertebral discs; MMP, matrix metalloproteases; OA, osteoarthritis; SLRP, small leucine-rich proteins progresses as impairment in spinal function and impaired breathing due to reduced area for lungs to expand.[2] There is a worldwide prevalence of 3% of children aged 10-16 years who suffer from AIS,[3] and currently there are two treatment options: (1) bracing if the curve is below a 50 Cobb angle (major curve angle) and (2) spinal fusion with instrumentation when the curvature is greater than a 50 Cobb angle.[2] the treatment options are highly beneficial for managing progression, the long-term effects on patient’s quality of life are still unclear.[4] Our underlying hypothesis is that abnormal curvature of the scoliotic spine results in degenerative changes and increased secretion of cytokines and proteases in facet joints, as reported in osteoarthritis
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