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Links between intervertebral disc degeneration and osteoporosis are repeatedly discussed. There is a conclusive explanation as to why osteoporosis can accelerate intervertebral disc degeneration.
The health of our intervertebral discs – as with any other tissue – depends on their blood circulation. However, the nucleus pulposus is the largest avascular tissue formation in our body. So how can it be that its degeneration still depends on blood flow?
The blood supply is the critical part to understand pathogenesis.
As already described in the section on development, the intervertebral disc cannot be considered on its own but only in the structure with the underlying bone (= osteochondral unit). Nutrition is mainly provided via bone tubules through a sinusoidal vascular network on the base and top plates of the vertebral bodies. Another route is via the annulus fibrosus – but this is not pathophysiologically relevant for disc degeneration. After leaving the sinusoidal vascular system, the nutrients pass through the overlying cartilage and then reach the nucleus pulposus. The health of the intervertebral disc can be recognized by the swelling capacity of the proteoglycans produced by the living cells (visible radiographically as disc height).
Vascular diseases such as arteriosclerosis (e.g. caused by smoking or lipometabolic diseases) can lead to reduced blood flow to the vertebral body. The direct connection to degeneration of the intervertebral disc has already been proven. Smokers therefore have a poorer prognosis for disc-related diseases.1Rajesh N, Moudgil-Joshi J, Kaliaperumal C. Smoking and degenerative spinal disease: A systematic review. Brain Spine. 2022 Aug 7;2:100916. doi: 10.1016/j.bas.2022.100916. PMID: 36248118; PMCID: PMC9560562. The reduced blood supply to the osteochondral unit leads to VEGF-induced neovascularization of the intervertebral disc on the one hand, but also to calcification of the cartilaginous endplate on the other. Interestingly, this reaction of the body cannot stop the degeneration. In the long term, the vertebral body remains significantly underperfused. This is probably due to immunological processes.
What does this have to do with osteoporosis?
In osteoporosis, the balance between bone resorption and bone formation is disturbed, resulting in the mechanical performance of the vertebral body being impaired and fractures occurring. The imbalance manifests itself in a decrease in trabecularization in the center of the vertebra and a disordered structure at the edges. This impairs the function of the sinusoidal vascular network with the bone tubules. In a way, the fine nutritional pathways are paved with “concrete”. The consequence is then similar to arteriosclerosis – not enough nutrients reach the osteochondral unit. As with arteriosclerosis, osteoporotic vertebral bodies are also poorly perfused.
In addition, stress peaks and microfractures occur during osteoporotic bone remodeling due to the stiffening of the end plate, which start the calcification cascade in the cartilage. Malnutrition causes the intervertebral disc to lose its swelling capacity and thus its height and buffering effect. As a result, the osteochondral disc area becomes stiffer and the underlying bone becomes softer and softer – a vicious circle.
Therapeutic approaches
Preclinical studies have shown that bisphosphonates can slow down this process, but the effect could not be demonstrated when teriparatide was administered.