Abstract
Indian Hedgehog (HH) has been shown to be involved in osteoarthritis (OA) in articular joints, where there is evidence that Indian HH blockade could ameliorate OA. It seems to play a prominent role in development of the intervertebral disc (IVD) and in postnatal maintenance. There is little work on IHH in the IVD. Hence the aim of the current study was to investigate the role of Indian Hedgehog in the pathology of facet joint (FJ) OA. 24 patients diagnosed with lumbar intervertebral disk herniation or degenerative spinal stenosis were included. Preoperative magnetic resonance imaging (MRI) and Osteoarthritis Research Society International (OARSI) histopathology grading system was correlated to the mRNA levels of GLI1, PTCH1, and HHIP in the FJs. The Weishaupt grading and OARSI scores showed high positive correlation (r = 0.894) (P < 0.01). MRI Weishaupt grades showed positive correlation with GLI1 (r = 0.491), PTCH1 (r = 0.444), and HHIP (r = 0.654) mRNA levels (P < 0.05 in each case). OARSI scores were also positively correlated with GLI1 (r = 0. 646), PTCH1 (r = 0. 518), and HHIP (r = 0.762) mRNA levels (P < 0.01 in each case). Cumulatively our findings indicate that Indian HH signaling is increased in OA and is perhaps a key component in OA pathogenesis and progression.
Highlights
Facet joint (FJ) osteoarthritis (OA) is an important component of degenerative changes in the lumbar spine, and is a major contributing factor to low back pain[1]
We examined the pathological changes in the FJ OA in humans and analyzed the expression levels of Hh signaling-associated PTCH1, GLI1, and Hh-interacting protein (HHIP)
It was found that the mRNA levels of GLI1, PTCH1, and HHIP are positively associated with the magnetic resonance imaging (MRI) image and pathological scores of the FJs, suggesting a role of the Indian Hh pathway in the development of FJ OA
Summary
Facet joint (FJ) osteoarthritis (OA) is an important component of degenerative changes in the lumbar spine, and is a major contributing factor to low back pain[1]. Patched[1] (PTCH1) and Smoothened (SMO) are two transmembrane receptors that respond to Indian Hh signaling. When Indian Hh is not present, Patched[1] inhibits Smoothened, and represses the downstream gene expression by suppressing the Gli zinc finger transcription factors (GLI1, GLI2, and GLI3)[15,16]. When Indian Hh is present, it binds to Patched and releases Smoothened, activating the Hh signaling pathway and allowing the active Gli transcription factors to enter the nucleus and enhance the transcription level of downstream targets[17]. We examined the pathological changes in the FJ OA in humans and analyzed the expression levels of Hh signaling-associated PTCH1, GLI1, and HHIP. The prospective relationship between the pathology of FJ OA and Hh signaling is discussed
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