ARTHRITIS: BENDING THE KNEE

By Olutobi Oduneye

Quite often has arthritis been thought of as affecting the knee, while this is not farfetched as most arthritis complaints involve the knee.
Arthritis can be acute or chronic joint inflammation and co-exists with pain and structural damage. There are over a 100types of arthritis with osteoarthritis/degenerative arthritis which is non-inflammatory arthritis being the most common. Here, advancing age, female sex, joint trauma, and obesity are major contributory factors. 
Inflammatory arthritis can also be infectious (which is rare), immune-related, crystal-induced, or reactive arthritis. Inflammatory arthritis frequently manifests with symptoms such as joint pain, swelling, tenderness and warmth in the joints and sometimes morning stiffness that could span for an hour. 
Crystal-induced arthritis includes gout (deposition of monosodium urate crystals in the joint space) and pseudo-gout (calcium pyrophosphate crystal deposition). It can be caused by impairment of renal uric acid secretion, overproduction of uric acid and overconsumption of purine-rich foods. Major risk factors include male sex, advancing age, alcoholism, chronic kidney disease, and diuretics
 Immune-related arthritis includes rheumatoid arthritis, systemic lupus erythematosus, and others. Reactive arthritis is usually seen after or during an infection elsewhere in the body after which micro-organisms cannot be recovered from the joint.

In assessing arthritis, physical examination is important and the following signs are indicative: tenderness, effusion, swelling, erythema and warmth which are associated with inflammatory arthritis are common in acute and less pronounced in chronic arthritis. Obvious joint deformity and decreased range of motion can also be observed in arthritis. Osteoarthritis differs from inflammatory arthritis in that erythema and warmth are usually lacking.

In assessing arthritis, onset, the number of joints involved, symmetry, distribution, and pattern needs to be considered.
1. Onset: septic, crystalline, and reactive arthritis have acute onset, while osteoarthritis and more often than not – RA – have an insidious onset. 
2. Number of involved joints.
Arthritis can be monoarticular (single joint), oligoarticular (2-4 joints) or polyarticular (several joints). Patients with gout experience monoarthritis especially early in the disease, while non-inflammatory arthritides, rheumatoid arthritis can result in polyarthritis of small joints of hands and wrist.
3. Symmetry: a hallmark of RA is polyarticular symmetrical inflammatory arthritis involving the small joints of hands and feet while other causes include SLE and osteoarthritis
Asymmetrical polyarthritis can be seen in psoriatic arthritis, reactive arthritis, gouts, and osteoarthritis. 
4. Distribution.
Axial or spine involvement is common in osteoarthritis. Axial involvement is not seen in RA. Several patterns on peripheral involvement can give a clue to the diagnosis. RA is typically associated with polyarticular symmetrical inflammatory arthritis involving the small joints of hands and feet. Wrist, ankle and knee involvement is also common. Pain, stiffness and limited range of motion of bilateral shoulders and hips may be seen in RA. 
5. Pattern.
Progressive additive pattern with the ongoing involvement of more joints can be seen in RA, psoriatic arthritis and polyarticular osteoarthritis. A migratory pattern where arthritis moves from one joint to another with complete resolution in the previously involved joint can be seen in rheumatic fever. An intermittent pattern can be seen in gout and pseudogout with complete resolution of symptoms in the previously involved joints. 
Other clinical features that can assist narrowing the differential diagnosis include family history and the age of onset with osteoarthritis more common in the older population while inflammatory arthritides more common in younger adults. It is also important to closely evaluate the neighbouring joints to rule out referred pain.

EVALUATION
In inflammatory arthritis, the ESR and CRP are elevated, thrombocytosis, anaemia of chronic disease. Here, the duration of stiffness is prolonged, and it improves with activity. While in osteoarthritis, stiffness is shorter in duration, and exacerbated by activity; furthermore, inflammatory markers are absent. When evaluating a patient with joint pain, clinicians should first find out whether the patient is having articular or nonarticular symptoms. If the complaints are articular, find out the duration. If less than 6 weeks, it is classified as acute and can be gout. It is deemed chronic if it has lasted for more than 6 weeks.
Needle-shaped yellow crystals are seen in gouty arthritis. If the cause mentioned above does not explain arthritis and the person meets the criteria for a typical autoimmune disease, then arthritis can be attributed to the autoimmune disease. Elevation of rheumatoid factor and anti-citrullinated protein antibody, elevated ESR and CRP are indicative of rheumatoid arthritis.

TREATMENT
In the management of osteoarthritis, limiting the pain and improving the function of the joints should be the aim. Both pharmacological and non-pharmacological approaches can be employed for optimum care. Physical therapy, acupuncture, bracing, exercises and weight reduction which are examples of non-pharmacological approaches are necessary post-operatively to optimize patient outcomes, while the pharmacologic management involves topical and oral medications. First-line medications include NSAIDs, topical capsaicin, and duloxetine. In some cases, Corticosteroids can be injected directly into the joint when both non-pharmacological and pharmacological management fails. Opioids should be avoided while surgical replacement of the affected joint(s) is reserved for refractory symptoms. The early use of biologics and disease-modifying anti-rheumatic drugs (DMARDs) is more effective than treatment with glucocorticoids and NSAIDs. There has to be dose adjustment and regular monitoring of symptoms. Traditional or conventional DMARD include methotrexate, leflunomide, sulfasalazine, hydroxychloroquine. Biologic DMARDs include TNF (tumour necrosis factor): Adalimumab, Etanercept, Infliximab, Golilumab, Certolizumab, and non-TNF inhibitors: Tocilizumab (Interleukin-6 inhibitor), Abatacept (inhibits T-cell costimulation), Rituximab (anti-B cell).
In gouty arthritis, when flare-ups occur, it can be quite debilitating and painful. The use of anti-inflammatory medications provides substantial relief and should be initiated within 24 hours in an acute gouty flare. These include oral corticosteroids, NSAIDs such as indomethacin or high-dose naproxen, or colchicine. In the resolutions of symptoms associated with gout, the goal is to ensure a decrease in the serum uric acid levels which then decreases the intra-articular uric acid thereby alleviating the symptoms.