OA can occur in one or both hips. In this way it differs from RA, which usually occurs in both hips at the same time. Hip OA is a slowly degenerative condition. Supports, such as canes, can also help.
If the condition worsens, steroid injections, other medications, or surgery can help provide relief. Alternative therapies can also help, and new technologies are on the horizon. Like hip OA, knee OA can occur in one or both knees. Age, genetics, and knee injury may all play a role in knee OA. Athletes who concentrate solely on one sport that creates extensive, repetitive motion, such as running or tennis, may be at increased risk of OA.
Likewise, if you pursue only one type of physical activity, this may overuse some muscles and underuse others, causing weakness and instability in the knee joint.
Varying your activities helps to work different muscle groups, allowing all the muscles around your knee to be strengthened. Treatment for knee OA depends on the stage of the condition. Learn about the stages of OA in the knee and how each one is treated. Wearing a brace around your knee can be an excellent nonsurgical treatment for knee OA.
Braces can reduce swelling and pressure. They can also increase stability in your knee by shifting your weight away from the damaged part of your knee. This allows for greater mobility. There are several types of knee braces. Some may be custom fitted for you, and others are available OTC. Your doctor may recommend that you try different kinds of braces for different activities. Find out what the best type of brace for your OA is. Cervical OA is also referred to as neck OA or as cervical spondylosis.
It occurs in both men and women. The cervical spine is located in the neck and contains facet joints. These joints help to maintain flexibility in the spine, allowing for a full range of motion.
When the cartilage around the facet joints starts to wear away, cervical OA results. If it does, symptoms can range from mild to severe and include:. Occasionally, more serious symptoms can occur, such as loss of bladder or bowel control, or loss of balance. Check out the risk factors and treatment options for cervical OA. If you have back pain, you may have spinal osteoarthritis. This condition affects the facet joints located in the lower back and buttocks. Age and spine trauma are both potential factors in spinal OA.
Women are more likely than men to get this condition. People who are overweight, or whose jobs require squatting and sitting, may also be at increased risk. If left untreated, spinal OA can worsen, causing more severe symptoms and disability. Read more about OA of the spine. But other risk factors can be controlled, and managing them can help reduce your risk of OA. If you have diabetes, controlling your blood sugar can also help manage your risk of OA.
See how else you can manage your risk and help prevent OA. The sooner you speak with your doctor, the sooner you can receive a diagnosis, begin treatment, and improve your quality of life.
Left untreated, osteoarthritis can become a serious condition leading to major complications. Grating of the joints is common in people with OA. You might also feel or hear your joints clicking or cracking when you move. People in the early stages of arthritis may notice that moving the affected areas of their bodies is not as easy as it once was.
Joint stiffness and pain can contribute to loss of flexibility, also called loss of range of motion. Range of motion is the extent to which you can move your joints in their normal patterns. For example, fully bending and extending your knee is its range of motion.
If you have arthritis, you might not be able to bend your knee as far. Loss of flexibility is usually a very gradual process. Pain, tenderness, and joint stiffness tend to be limited to very specific times in the early stages of osteoarthritis. You might notice your hips hurt after a game of basketball, or that your back is stiff first thing in the morning.
In the early phase of arthritis, the cartilage between your joints becomes worn and torn as well as inflamed. The wear-and-tear process leads to loss of water in the joint, which causes the cartilage to become hard.
Hardened cartilage makes moving the surrounding joint more difficult. The loss of cartilage is a slow process. Some people have early arthritis symptoms for years before the disease progresses. You and your healthcare provider can create an OA management plan together to relieve arthritis pain. Over-the-counter pain relievers , braces to support the joint, and range-of-motion exercises can help you maintain independence and an active lifestyle. Arthrosis and arthritis are conditions that affect your bones, ligaments, and joints.
Symptoms tend to build over time rather than show up suddenly. They include Pain or aching in a joint during activity, after long activity or at the end of the day. Joint stiffness usually occurs first thing in the morning or after resting. Limited range of motion that may go away after movement.
Clicking or popping sound when a joint bends. Swelling around a joint. Muscle weakness around the joint. Joint instability or buckling as when a knee gives out. OA may affect different parts of the body in different ways. Pain in the groin area or buttocks and sometimes on the inside of the knee or thigh. Bony growths spurs at the edge of joints can cause fingers to become swollen, tender and red, sometimes with pain at the base of the thumb. Pain and tenderness in the big toe, with possible swelling in the ankles or toes.
Obesity, Diabetes and Heart Disease Painful joints, especially in the feet, ankles, knees, hip or back, make it harder to exercise. Falls Research indicates people with OA experience more falls and risk of fracture than those without OA. These tests help to make the diagnosis: Joint aspiration. After numbing the area, a needle is inserted into the joint to pull out fluid.
This test will look for infection or crystals in the fluid to help rule out other medical conditions or other forms of arthritis. X-rays can show joint or bone damage or changes related to osteoarthritis. Magnetic resonance imaging MRI gives a better view of cartilage and other parts of the joint.
Medications Pain and anti-inflammatory medicines for osteoarthritis are available as pills, syrups, patches, gels, creams or injectables. They include: Analgesics. These are pain relievers and include acetaminophen and opioids. Acetaminophen is available over the counter OTC ; opioids must be prescribed by a doctor. These are the most commonly used drugs to ease inflammation and pain.
They include aspirin , ibuprofen , naproxen and celecoxib , available either OTC or by prescription. The OTC versions help with pain but not inflammation. These OTC products contain ingredients like capsaicin, menthol and lidocaine that irritate nerve endings, so the painful area feels cold, warm or itchy to take focus away from the actual pain.
These prescription anti-inflammatory medicines work in a similar way to a hormone called cortisol. Platelet-rich plasma PRP. Available from a doctor by injection, this product is intended to help ease pain and inflammation. Other drugs. The antidepressant duloxetine Cymbalta and the anti-seizure drug pregabalin Lyrica are oral medicines that are FDA-approved to treat OA pain.
A good exercise program to fight OA pain and stiffness has four parts: Strengthening exercises build muscles around painful joints and helps to ease the stress on them. Range-of-motion exercise or stretching helps to reduce stiffness and keep joints moving. Aerobic or cardio exercises help improve stamina and energy levels and reduce excess weight. Balance exercises help strengthen small muscles around the knees and ankles and help prevent falls. Talk to a doctor or physical therapist before starting a new exercise program.
Weight Loss Excess weight puts additional force and stress on weight-bearing joints, including the hips, knees, ankles, feet and back, and fat cells promote inflammation.
Physical Therapies and Assistive Devices Physical therapists, occupational therapists and chiropractors can provide: Specific exercises to help stabilize your joints and ease pain.
Information about natural treatments and products that can ease pain. Although much attention has been focused on BMLs, MRI studies of subjects with OA also have a number of other joint changes, which include knee effusions, meniscal lesions, hyaline cartilage loss and synovitis, all at the same time reviewed in [ 30 ].
It is, therefore, not entirely clear as to which lesions come first and whether there is a temporal sequence to the development of lesions that influence pain in OA. These issues have been addressed by the Multicenter Osteoarthritis Study MOST study [ 31 , 32 ], which is a large prospective, longitudinal study to assess the temporal relation between MRI-detected BMLs, full-thickness cartilage loss and subchondral cysts SCs in the same subregion of the knee, for the evaluation of the pathogenesis of SCs in light of SF intrusion and bone contusion theories.
The findings of the MOST study have demonstrated that mensical pathology is strongly associated with incident and enlarging BMLs [ 32 ] and BMLs also predict SC formation in the same region [ 31 ], thereby supporting the bone contusion theory of SC formation. Previous studies have demonstrated that BMLs and full thickness cartilage loss predict SC formation longitudinally [ 33 ].
BMLs appear to represent focal bone remodelling due to overloading, and enlarging BMLs are predictors of pain and progression of cartilage damage in OA [ 34 ]. They are, therefore, potential targets for treatment of pain in OA. Taljanovic et al. This study concluded that the amount of bone marrow oedema in the OA hip, as measured by MRI, correlates with the severity of pain, radiographic findings and microfractures.
Synovitis is an under-appreciated phenomenon in OA, which may explain the perception of pain. Various imaging modalities including US Fig. Roemer et al. The most common sites of detection included the posterior cruciate ligament and the suprapatellar region. For knee pain, synovitis conferred a 9. US scan of the first CMC joint of a subject with OA showing evidence of synovial thickening and increased vascularity on power Doppler imaging.
Recently, functional MRI fMRI studies have been used to investigate how the brain processes noxious stimuli in OA and the cortical location to which perception of pain is mapped Fig. The principles and problems of fMRI are well known [ 42 ], but it is worth highlighting a few points in relation to the experimental difficulties with regard to pain studies by fMRI.
Such studies involve the use of a fast MRI method less than a second per image slice for which the image intensity is sensitive to the variations in magnetic field created in tissue by the presence of paramagnetic deoxyhaemoglobin.
The use of paradigms with reproducible and quantifiable levels of pain stimulus are thus of great importance. As with all fMRI, careful paradigm design on how the pain is delivered and the data analysed and the use of appropriate control measurements are thus essential [ 43 ]. Schematic diagram of central pain-processing pathways implicated in OA pain processing.
Recent work by Baliki et al. These data suggest that painful stimulation in subjects with OA of the knee engages with many brain regions commonly observed in acute pain. Local treatment of the knee with lignocaine resulted in reduction of brain activity detected on fMRI in the regions described previously, suggesting that central activation of the brain mediates pain during OA.
Such results also help to disentangle pain responses from anxiety or other emotional, non-painful responses. In the same study, patients who had spontaneous back pain in a cohort of patients with low back pain showed activity by fMRI in the medial prefrontal cortex, with reduced brain activation after treatment with lignocaine [ 44 ].
The regions activated in these studies of OA subjects show patterns in brain regions similar to those in touch-evoked pain allodynia [ 45 ] and acute pain [ 46 ]. Recent work by Gwilym et al. In their study, 20 right-handed subjects with hip OA were compared with 12 right-handed control subjects.
Correlation of high PainDETECT scores was found with higher ratings of hyperalgesia on sensory testing and higher activation in the periaqueductal grey region compared with patients with less neuropathic symptoms and signs. Using this technique, 2D or 3D images of blood flow or metabolic brain processes can be acquired. A variety or radioisotopes e. In tissue, the emitted positron will only travel by up to a few millimetres before encountering an electron and the two particles will annihilate and yield two high-energy photons that travel in opposite directions.
A ring of scintillation detectors around the patient are designed to detect these annihilation pairs in coincidence and so reconstruct an image representing the tissue distribution of the radionuclide. Kulkarni et al. The brain activity of 12 patients with OA was compared in three different states: arthritic knee pain; experimental knee pain pin applied on an occasion when the patients were not experiencing arthritic pain ; and pain free. Measurements of regional cerebral metabolic rate of glucose metabolism rCMR Glu were measured in the three scenarios described.
In a comparison of arthritic vs pain-free conditions, rCMR Glu was bilaterally enhanced in all areas of the brain implicated in pain processing, which included the posterior cingulated cortex, anterior midcingulate cortex, prefrontal cortex, orbitofrontal cortex and primary somatosensory cortex. In addition, unilateral activations were seen in the left thalamus, left periungal cingulated cortex, left amygdala and right supplementary motor area.
In comparison, different regions of activation were observed in arthritic pain vs experimental pain. As the results from this study in Fig. Bilateral activation was observed in the periungal cingulate, anterior midcingulate, posterior midcingulate, subungal cingulated and posterior cingulated, the amygdala and orbitofrontal cortex.
The most statistically significant activations were observed in the anterior cingulated cortex, where the activation spanned from the anterior to the posterior midcingulate region. This study proposed that although arthritic pain and experimental pain activate similar areas of the brain, arthritic pain is also associated with areas of the brain implicated in affect, aversive conditioning and motivation. These findings have important potential implications for the management of patients with long-term OA pain.
The brain imaging studies described above provide deeper insights into the mechanistic processes of treatment effects, and have potential use as an anatomic and functional model for future analgesic drug development.
In this review, we have outlined current understanding of the mechanisms of pain mediation locally in the OA joint based on molecular pathways and imaging studies. A number of features in the OA joint implicated in mediating pain have been outlined and include BMLs, effusions and synovitis. A summary of a logical approach for treatment of pain in OA is illustrated in Fig. Therapeutic options for targeting pain at different levels of the pain-processing pathway. Current treatments for pain continue to be focused on both the use of topical agents including NSAIDs [ 21 ] and capsaicin [ 19 ] and systemic agents including NSAIDs and opiate drugs [ 21 ].
Physical approaches, such as the application of heat or cold packs, transcutaneous electrical nerve stimulation TENS and capsaicin may affect molecular pathways; for example, desensitization of TRPV1 is thought to underlie the paradoxical analgesic effect of capsaicin. The first reports of blockade of a specific molecular target with anti-NGF mAbs in a study of knee OA suggested that although promising analgesic effects were achieved in the short term, significant side effects were an important consideration, including paraesthesia, peripheral neuropathy and worsening arthritis [ 14 ].
There were also worsening rates of joint replacement in the treatment group, questioning whether anti-NGF therapy is viable in OA subjects in the long term. In a patient population with a chronic disease, this approach will need to demonstrate efficacy with minimal side effects in the long term, if it is to be adopted in routine care.
Such results are awaited from ongoing studies of other NGF-directed therapies in development. Therapeutic approaches targeting BMLs may include pharmacological intervention or alteration of loading. Emerging studies have demonstrated the use of bisphosphonates to target pain related to BMLs.
For example, Laslett et al. The authors reported that participants had reduced VAS pain scores at 6 months, but not 12 months post-infusion. There was also a reduction in BML size compared with placebo, which was maintained at 12 months.
It remains to be seen whether such therapies could have a sustained analgesic effect, and whether reduction of BML in the long term could influence structural progression of OA. Data have also emerged that synovitis is a significant factor influencing pain in OA and recent work has proposed use of CSs in reducing such effects [ 39 ]. Evidence has also shown that exacerbations of OA can be associated with a synovial reaction [ 9 ]. Such changes may be amenable to treatment with anti-inflammatory drugs [ 10 ].
In hand OA, Keen et al.
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