Naslov
Pathways of pain and possibility of personilized therapy in osteoarthritis

Autori
Grazio, Simeon

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, stručni

Izvornik
Fizikana i rehabilitacijska medicina / Grazio, Simeon - Zagreb : Hrvatsko društvo za fizikalnu i rehabilitacijsku medicinu (HDFRM), 2012, 20-22

Skup
5. hrvatski kongres fizikalne i rehabilitacijske medicine

Mjesto i datum
Zagreb, Hrvatska, 10.05.2012. - 13.05.2012

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Nije recenziran

Ključne riječi
nema dostupnih podataka

Sažetak
Osteoarthritis (OA) is the most common joint disorder worldwide and is a major cause of chronic disability in older adults. It is now recognised as a disease of the whole joint, characterised by variable inflammation of the synovium and changes in subchondral bone. Pain is the most prominent symptom and has a significant impact on the function and quality of life of people with OA. However, the conditions under which pain occurs, as well as pathogenesis of OA, in general are presently ill-defined. Pain can be classified according to different pathophysiological pathways, including but not confined to nociceptive, inflammatory and neuropathic, while in the past decade neuroplasticity has emerged as an important component of the pain sensation in OA. Very recently, sympathetic and sensory nerves were both found to be present within vascular channels in articular cartilage, as well as within the subchondral bone marrow and within the marrow cavities in OA. Although commonly described as a non- inflammatory disease synovial inflammation is increasingly recognised as contributing to the symptoms and progressionin OA. The prevailing theory is that cartilage degradation leads to the release of cytokines and other pro- inflammatory mediators into the joint, which triggers a cycle of self-propagation whereby more inflammatory mediators are released from synovial cells and also from activated leucocytes and macrophages. In recent years it has been recognised that apart from mechanical loading adipose tissue may act as an endocrine organ, releasing several proinflammatory mediators and adipokines in blood that may participate in cartilage alteration in obese patients. Besides obesity, other works have suggested that systemic factors may play a role in OA such as IL-1 beta and IL-6. Inflammatory cascade may exacerbate joint damage in OA and also activates and sensitises nerves in the synovial tissue, leading to increased pain (peripheral sensitisation). One factor suggested to be important in the spreading of pain is the status of the descending pain control. Central sensitisation at the spinal or cortical level adds significantly to the pain hypersensitivity observed in OA. Pain localisation from musculoskeletal structures is poor, and it is difficult to differentiate pain arising from tendons, ligaments and bones as well as from joints and their capsules. Clinically the first manifestation of sensitisation is localised tenderness and/or hyperalgesia, including at palpating the muscles or joints, while later on in some patients, a local pain problem develops into widespread pain and a comorbid pain conditions. Moreover, a clear distinction between spread of pain and referred pain is not possible.Peripheral and central pain mechanisms may be the reason for the often observed discrepancy between joint damage and clinical pain intensity. Besides, physical activity, psychological factors and health status may have an influence on the joint pain experienced by an individual. In the absence of effective preventive strategies and causative treatment, a major focus of OA management is pain relief. Combination therapies are widely used to treat pain in OA, as is the case in all other pain conditions. Multiple modalities of non- pharmacological, pharmacological and surgical therapy for OA exist and several reviews and guidelines on the management of OA have been published, included Croatian guidelines (published in 2010.). Nowdays the vast majority of OA-related pharmacological treatments target the periphery. As the degree of spreading sensitisation is correlated with the level of clinical pain it is highly important to dampen the local nociceptive activity at an early stage. The importance of inflammation in OA joint pain is supported by the analgesic efficacy NSAIDs. These drugs act on local pain and inflammation but also affect central pain mechanisms – either directly or indirectly. But, they fail to more fully address central pain sensitization, which can be one reason for inadequate pain relief in some patients. Opioid analgesics act centrally and might be efficacious treatment for patients with a strong central contribution to the pain experience. There is also some evidence for use of duloxetine and other antidepressants in the treatment of OA-related pain with greater central contributions to pain. Pharmaceutical industry invests massively in finding new and more effective compounds for managing OA. For example, as bone and cartilage are closely interrelated, interventions affecting pain related to bone turnover and/or targeting both bone and cartilage may be relevant for treatment of OA. Given the complexity of mechanisms leading to the development of OA and to its associated pain, the goals of long-term OA management are necessarily individualised, addressing patient function, quality of life and pain relief. Treatment of central pain sensitivity is an area with great promise for improving pain management in at least a subset of patients with OA. Therefore, additional research is needed to both identify patients with stronger central component of OA-related pain and to explore the existing and new pharmacological and nonpharmacological strategies to identify and successfully treat these patients. Combinations of different interventions and oncoming tretaments may offer the optimal potential for therapeutic success.

Izvorni jezik
Engleski

Znanstvena područja
Kliničke medicinske znanosti

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