**4. Sources of nociception in a joint**

210 Biomedical Science, Engineering and Technology

0.5–0.7 per 1000. The annual costs attributable to knee OA are immense. There is therefore a

A brief review of the basic anatomy of a typical synovial joint is presented here to help understand the mechanisms involved in OA-induced damages of the involved joint that

burden on health from both morbidity and cost. OA is a complex disorder with multiple risk factors.

**2.1 Risk factors for OA**  1. Age > 50 years

5. Injury to the joint

8. Peripheral neuropathy

**3 Anatomy of a joint** 

Fig. 1. A typical synovial joint

2. Crystals in joint fluid or cartilage 3. High bone mineral density 4. History of immobilisation

6. Joint hypermobility or instability 7. Obesity (weight-bearing joints)

9. Prolonged occupational or sports stress

culminate in pain and other symptoms of OA.

Pain is defined as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage". Pain, as generally acknowledged, is mainly a signal that the body has been injured.

The term "nociception" was coined by the Nobel Laureate Sherrington to designate a physiological sensory phenomenon. "Nociception" is derived from "nocere", the Latin word for "to hurt". Nociceptors are peripheral sensory organs that are activated when nociceptive stimuli cause tissue damage. These nociceptors are unspecialised, naked nerve endings found close to small blood vessels and mast cells. The functional nociceptive unit is therefore made up of the structural triad of capillary, nociceptor and mast cell. This is the unit that is sensitive to tissue damage. There are also a rich supply of myelinated and unmyelinated fibres innervating the joint capsule, ligaments subchondral bone, periosteum and menisci.

In the anatomy of the joint described above, the cartilage does not contain blood vessels but derives its nutrients from the synovium. The subchondral bone, periosteum, synovium, ligaments, and the joint capsule contain nerve endings that could be the source of nociceptive stimuli in OA. Irritation of the periostal as a result of remodelling, denuded bone, compression of soft tissue by osteophytes, microfractures of the subchondral bone, effusion and spasm of surrounding muscles has been shown to contribute to the pain that may be felt by patients with OA. So in effect the bone in the periosteum and bone marrow is richly innervated with nociceptive fibres and represents a potential source of nociceptive pain in patients with OA.
