The lumbar intervertebral disc has a meager innervation. This is concentrated in the perianular connective tissue and the central endplate. Although receptor threshold is more closely related to nociceptive function than innervation density, these findings have important implications for any treatment of discogenic pain.

In adolescent idiopathic scoliosis, neither the presentation with a stable spinal deformity, nor presentation with a severe deformity requiring surgery is associated with melatonin deficiency.

The phenomenon of spinal deformity in the pinealectomized chicken has led researchers to postulate a disturbance of melatonin activity as a potential cause of adolescent idiopathic scoliosis (AIS). More recently, structural differences between curves seen in this model and those seen in scoliosis have been highlighted suggesting the deformities observed are not as similar as first thought. We examined melatonin levels, and the radiological and histological characteristics of scoliosis after pinealectomy in chickens. They underwent pinealectomy (P) at 2 days of age, sham surgery (S) or served as controls (C). Mean melatonin levels were 32.9 pmol/L (P), 175 pmol/L (S) and 227.3 pmol/L (C). Scoliosis developed in 75% of chickens after pinealectomy and 38% after a sham procedure. Nineteen percent of unoperated controls also developed scoliosis. A lower melatonin level was associated with the development of scoliosis (p B 0.001), but exceptions were seen with levels up to 265 pmol/L observed in one case. Most of the curves occurring spontaneously and after sham surgery and almost half after pinealectomy were short angular curves: distinct from those resembling idiopathic scoliosis. These occur over one or two segments and are characterized by marked apical wedging, frequently associated with subluxation or dislocation. The intervertebral joint in the chicken is more like a synovial joint histologically than an intervertebral disc. This study highlights important differences between the chicken and the human, and between their respective spinal deformities. Caution is advised when drawing conclusions regarding the pathogenesis of AIS from this model.