**6. Treatment: emerging techniques and technologies**

The modes of treatment for OA have always focus on decreasing pain and improving function ranging from information, education, physical therapy and aids, through analgesics, non-steroidal anti-inflammatory drugs and joint injections, and to surgery in which all or part of the joint is replaced with plastic, metal or ceramic implants.

OA is complex in genetics, pathogenesis, monitoring and treatment however, the principal goals of management are:


214 Biomedical Science, Engineering and Technology

• A noxious stimulus causes stimulation of nociceptors (pain receptors) in the receptor

• This firing of primary afferent fibres at the site of tissue injury causes axonal release of substance P (SP). This stimulation leads to activation of cells in the dorsal horn of the spinal cord and transmission of the nerve impulse to the midbrain and cortex. Thus, impulses travelling along first order neuron synapse on second-order neuron in the dorsal horn of the spinal cord. The axon crosses to the contralateral side and ascends to synapse on the third-order neurons. The third-order neurons send fibres

• Transmission of sensory information is modulated (inhibited or potentiated) throughout the nervous system by neurons from the midbrain and spinal cord that

• Peripheral nociceptor sensitisation, which is the transmission of impulses at subnormal threshold, occurs following the release of chemical mediators such as prostagladins and leukotrienes at the site of injury or damage. Continued stimulation by peripheral nociceptors then leads to sensitisation of neurons in the spinal cord.

Tissue injury results in the release of inflammatory mediators such as serotonin, bradykinin, calcitonin gene-related peptide (CGRP) and SP, which lead to nociceptor nerve fibre sensitisation in peripheral tissue. These damaged fibres release inflammatory agents causing a spread of increased sensitivity around the area of tissue damage. This is called primary hyperalgesia. The repeated depolarisation of primary afferent fibres leads to a continuous release of neurotransmitters onto the secondary neurons in the spinal cord, resulting in central sensitisation and secondary hyperalgesia. Peripheral pain sensitisation is a feature of

In addition to peripheral pain sensitisation pain in OA, could also be due to local and central sensitisation of pain, pathways resulting in normal stimuli becoming painful with

Most of the substances involved in inflammation such as proinflammatory cytokines and bradykinins interact with the nociceptive fibres present within the joint and induce hyperalgesia and allodynia seen in patients with chronic inflammatory joint disease like OA. These mechanisms acting in concert could participate in the progression of hyperalgesia to

Chronic pain (CP) is pain that persists for a month beyond the usual course of an acute

to the cerebral cortex where conscious perception of the sensation occurs.

release endogenous opioids, catecholamines and other neurotransmitters.

**5.3 Radiological changes in OA**  • Joint space narrowing

• Osteophytes • Bony cysts

• Subchondral sclerosis

**5.4 Mechanism of pain in OA** 

organ (e.g. joint).

osteoarthritis in the joint.

**5.5 Progression of OA to chronicity** 

chronicity.

**Summary of process of pain perception** 

This is known as central sensitisation.

inflammation being an important feature in the process of OA.

disease or a reasonable time period for an injury to heal.


Despite huge laboratory and clinical research, there are no proven diseases modifying therapies for OA. However, emerging orthopaedic surgical procedures may help to alleviate the attendant pain and functional loss resulting from joint damage in OA. Some of the surgical approaches in the management of OA include

• Arthroscopic approach

	- Autologous Chondrocyte Implantation (ACI)
	- Meniscal Transplantation (MT)
