Lower back pain is a condition which will affect the majority of us in our lifetimes. According to the World Health Organisation, lower back pain is a leading cause of disability, interfering with quality of life and work performance. It is the most common reason for medical appointments, and the biggest cause of absence from work in most parts of the world. It can be due to a specific injury such as a strain or a slipped disc. However, particularly as we age, it can arise without any injury. In many cases, the origins and mechanisms of lower back pain are unclear, and standard NHS advice of painkillers, hot and cold compression and physical therapy are not always effective.
The spine consists of a series of small joints, each one made up of a small bony vertebra, a disc, and a layer of soft tissue called a cartilage endplate. The cartilage endplates cushion the vertebrae, protecting them and acting as shock absorbers. In young people, these endplates should be soft and firm. New scientific studies suggest that lower back pain may be caused by the cartilage endplates within the spine becoming hardened and porous as we age.
In a series of studies conducted by scientists at the Johns Hopkins University involving 12 month-old mice (the equivalent of 70-80 year old humans), their cartilage endplates were found to have hardened into porous bone-like structures. Normal soft cartilage does not usually have nerves or blood vessels. However, these bony structures in the aged mice were found to provide spaces to allow pain-sensing nerve fibres to penetrate throughout the vertebrae.
The porous bone-like structure is created by osteoclasts – a type of specialised cell which removes old bone and replaces it with new bone material. A further experiment conducted to test the relationship between osteoclasts and nerve fibres involved fluorescent tagging and analysis under a microscope. The osteoclasts and nerve fibres were shown to appear in the same areas of vertebrae, leading the scientists to infer that the cells were responsible for generating abnormal nerve fibre growth. A particular molecule produced by osteoclasts, netrin-1, was thought to be the cause.
A theory was formulated that by preventing osteoclasts from forming, this would in turn prevent the spread of abnormal nerve fibre growth. To test this theory, the scientists conducted a new study, this time using mice which had been genetically engineered to lack the specific gene coding for osteoclast formation. Testing showed that these mice did not have porous hardened endplates. Following further testing, it also became evident that they had fewer pain-sensing nerves in their endplates compared to normal mice carrying the osteoclast-producing gene.
Their findings were published in December 2019 in Nature Communications (Ni, S, Ling, Z, Wang, X et al. Sensory innervation in porous endplates by Netrin-1 from osteoclasts mediates PGE2-induced spinal hypersensitivity in mice).
The hope is that by understanding how lower back pain develops, this could lead the way to more effective pain treatments, for example treatments which target abnormal nerve growth in the spine. Though by no means offering a solution, this research represents a helpful step in the right direction for the millions of people worldwide who suffer from this condition.