Why does an old knee hurt?
Old knees are mostly painful due to a complex problem called the osteoarthritis (OA). It is one of the most common musculoskeletal disorders, which refers to clinical syndrome of joint pain accompanied by varying degrees of functional limitation and reduced quality of life (1). It affects more than one-third of persons of age more than 65 years. It is estimated that about 30 million Americans are currently affected by this disease. Global estimate reveals that more than 100 million people are affected by OA (2).
OA is not just the result of wear and tear of cartilages of the joint but it may also involve the underlying bone and joint covering (synovium). OA affects nearly all joints. Most commonly involved joints are the weight bearing joints ie knee and hip. Small but frequently used joint such as joints of hands are also involved. OA is linked with family, female sex, past trauma, advancing age and obesity (3). OA can be diagnosed clinically by asking the questions on history as well as by physical examination and findings of X-rays are joint space narrowing, erosion of cartilages, formation of extra bones (osteophytes) etc. Many individuals with bad knee in x-ray may remain asymptomatic too.
Pain is the main reason why an individual with OA knee seeks medical attention. The possible factors responsible for pain in OA includes various peripheral (problems within the joints and surrounding structures), neuropathic (problems in the nervous system) and central mechanisms (changes in the brain and thought processes) (3). The inflammatory or nociceptive or peripheral pain arises from potential tissue damage from the damaged cartilages and joints resulting in peripheral sensitization of nociceptors (pain receptors) which is known as primary hyperalgesia. Whereas neuropathic pain arises from the damage to the nervous system (either central or peripheral). Damage to the nerve fibers supplying knee accounts for development of neuropathic pain in OA (1). Sensory testing can be of importance for the diagnosis of neuropathic pain, although it should always be combined with diagnostic procedures confirming the nervous system lesion or disease. Neuropathic pain is of appropriate anatomical origin and may be described as burning, shooting or pricking type. Some of the features that may be associated with neuropathic pain among individuals with OA may be hyperaesthesia, hypoesthesia, hyperalgesia, hypoalgesia, allodynia, paraesthesia, dysesthesia, etc (4).
Another mechanism of pain ie central pain including central sensitization (CS) in OA occurs due to activation of neurons by nociceptive stimuli which becomes hyper-responsive by further long term stimulus resulting in secondary hyperalgesia. In contrast with neuropathic pain, CS is characterized by widespread and diffused nature of pain and lacks history of damage to the nervous system (5). CS is more of abnormal processing of the peripheral input in the higher center and reveals the fact that “pain is in brain”. Various sensory testing measures including quantitative sensory testing (QST) can be used for assessing CS among individuals with OA. Experts also believe that peripheral sensitization plays an important role in the development and maintenance of CS. CS is the result of excess nociceptive ascending input (more pain stimulus goes to the brain) and reduced inhibitory input (reduction of the pain by the brain is lacking) (1).
As we discussed earlier, the pain in the OA could be due to cartilage damage and changes in the bone as seen in the radiograph. However, the radiographic findings do not really correlate with the pain in OA. It means that those who have “bad knee” as visible in the X-ray may not necessarily have bad pain or more pain. These people can remain painless. At the same time, individuals who have normal knees on X-ray can have severe pain. Also, it is noted that the degree of sensitization in individuals with OA correlates with clinical pain reports but not with radiographic findings (6).
Old knees (OA knee) are painful for various reasons ie peripheral, central and neuropathic. Identification of these syndromes is essential for accurate management of the problem. Clinicians treat the pain in OA based on these syndromes but not on the basis of how the knees appear in the x-ray. Keeping in mind the mechanisms of pain in the OA will guide the clinicians in better management of this complex problem.
1. F. Salaffi AC, M. Carotti. The sources of pain in osteoarthritis: a pathophysiological review. 2014;66 57-71.
2. K S. Osteoarthritis: diagnosis and treatment. Am Fam Physician. 2012 Nov 15.
3. Dimitroulas T, Duarte RV, Behura A, Kitas GD, Raphael JH. Neuropathic pain in osteoarthritis: A review of pathophysiological mechanisms and implications for treatment Seminars in Arthritis and Rheumatism. 2014.
4. Nijs J, Apeldoorn A, Hallegraeff H, Clark J, Smeets R, Malfliet A, et al. Low Back Pain: Guidelines for the Clinical Classification of Predominant Neuropathic,Nociceptive, or Central Sensitization Pain. Pain physician. 2015;18:E333-E46.
5. Nijs J, Torres-Cueco R, Wilgen PV, Girbés EL. Applying Modern Pain Neuroscience in Clinical Practice: Criteria for the Classification of Central Sensitization Pain. Pain physician. 2014:447-57.
6. Finan PH, Buenaver LF. American College of Rheumatology Discordance Between Pain and Radiographic Severity in Knee Osteoarthritis Findings From Quantitative Sensory Testing of Central Sensitization. ARTHRITIS & RHEUMATISM. February 2013; 65.