Knee Osteoarthritis (PDF)

Degenerative Joint Diseases Knee Osteoarthritis BY Dina Othman Shokri  Objectives At the end of this lecture, the student will be able to: I. Overview  Knee anatomy  Definition  Pathophysiolo...

Degenerative Joint Diseases Knee Osteoarthritis BY Dina Othman Shokri  Objectives At the end of this lecture, the student will be able to: I. Overview  Knee anatomy  Definition  Pathophysiology,  Etiology , Classification  Risk Factors II. Identify the clinical manifestation of knee osteoarthritis III. Diagnosis of Knee OA IV. Know how to apply a successful patient management.  Osteoarthritis (OA) Osteoarthritis is a painful, chronic joint disorder that primarily affects not only the knees but also hands, hips and spine. The intensity of the symptoms vary for each individual and usually progress slowly. OA is the most common disease of the joints worldwide, with the knee being the most commonly affected joint in the body. It mainly affects people over the age of 45 years old. OA can lead to pain and loss of function, but not everyone with radiographic findings of knee OA will be symptomatic: In one study only 15% of patients with radiographic findings of knee OA were symptomatic. OA affects nearly 6% of all adults. Women are more commonly affected than men. Roughly 13% of women and 10% of men 60 years and older have symptomatic knee osteoarthritis. Among those older than 70 years of age, the prevalence rises to as high as 40%. Knee osteoarthritis (OA), also known as degenerative joint disease, is typically the result of wear and tear and progressive loss of articular cartilage. Osteoarthritis predominantly involves the weight- bearing joints, including the knees, hips, cervical and lumbosacral spine, and feet. More correctly called osteoarthrosis because it is not inflammatory condition. It is a degenerative joint disease involving the different structures of the joint. The degradation of joints, including articular cartilage and subchondral bone. But also ligaments, the capsule and the synovial membrane degenerate. It never by reversed.  Pathogenesis of OA The pathogenesis of knee OA have been linked to biomechanical and biochemical changes in the cartilage of the knee joint. The cartilage ensures that the bone surfaces can move painless with low friction to each other. In OA, the cartilage decreases in thickness and quality, it becomes thinner and softer, cracks may occur and it will eventually crumble off. Cartilage that has been damaged, cannot recover. Finally the cartilage will disappear. The cartilaginous tissue is not the only one involved. Given its lack of vasculature and innervation, the cartilage, by itself is not capable of producing inflammation or pain at least on early stages of the disease. Hence, the source of pain is mainly derived from changes to the non-cartilaginous components of the joint, like the joint capsule (degenerated and inflamed), synovium (synovial effusion), subchondral bone (the bone will expand and spurs (osteophytes), ligaments (laxity of the ligaments), and peri-articular muscles (muscle atrophy). Common sources of pain near the knee are anserine bursitis and iliotibial band syndrome. Most of these are not visualized by the x-ray, and the severity of x-ray changes in OA correlates poorly with pain severity.  Normal Knee Joint Degenerative Begins Degeneration Progresses OA can occur in either or both of the articulations of the knee (Tibiofemoral joint, Patellofemoral joint). In the knee joint, these changes affect are greater in the medial tibiofemoral and the patellofemoral joint with the lateral tibiofemoral joint less severely affected. A affects the medial compartment of the knee, and as the bone wears away medially a varus or “bowlegged” appearance develops. Much less frequently patients develop lateral compartment OA that results in a valgus or “knock-kneed” deformity.  Etiology and Classification OA is classified into two groups according to its etiology: 1- Primary (idiopathic or non-traumatic): It is OA without obvious causes. It affect mostly elderly people especially women in post-menopausal period. It is related to aging process. As water content decreases due to reduction of proteoglycans content, cartilage becomes less resilient and becomes more susceptible to injury. There is a hereditary (genetic) factor in primary OA. 2-Secondary OA Secondary to other causes (usually due to trauma or mechanical misalignment). a- Trauma A-Intra-articular fracture (If it isn't properly reduced and fixed------articular cartilage become irregular ----friction force increase). B-Extra –articular fracture (If they are malunited-----maldistrubtion of load on joint surface). b-Repeated minor trauma: or stress usually a result of some types of occupation or sports. c-Infection: as pyogenic arthiritis d-Inflamations: as gout and RA e-Deformities: as genu varum /coxa valga------maldistrubtion of load on joint surface. f-Metabolic disorders: e.g. rickets  Risk Factors 1-Obesity: Increases pressure on the knees. Every pound of weight you gain adds 3 to 4 pounds of extra weight on your knees. Obesity also increases circulating level of chemical substances such as leptin, C-reactive protein, and other pro-inflammatory cytokine that may promote cartilage matrix degeneration. 2-Weak muscle, poor knee Stability and abnormal mobility: due to ligamentous laxity or poor mobility and proprioception. 3-Gender: Females are more affected. 4-Repetitive stress injuries: usually a result of the type of occupation and athletics: as in soccer, tennis, or long-distance running. 5-Overuse and underuses: As both cause improper nutrition to the hyaline cartilage.  Clinical presentation 1-Joint pain and stiffness: This is a 'mechanical' type of pain which is generated by activity (Pain when standing up from a chair, pain when going up and down stairs and walking for long distance), decreases with rest. Joint pain which is less in the morning and stronger at the end of the day following activity. Pain with joint palpation or ROM. Gelling phenomenon: Stiffness after periods of inactivity, passes over within minutes (approx 15min.) of using joint again. In OA, morning stiffness lasting no longer than 30 minutes. 2- Swelling (Edema, Effusion): Caused by synovial irritation, edema of the periarticular structures and inflammation of the bursa are among other cause of joint swelling. and lead to enlarged joints. 3-Muscle spasm: As a protective mechanism due to pain (muscle guarding) due to accumulation of metabolites. Spasm could be one of the causes to limit movement. 4-Muscle weakness and atrophy: Due to pain causes muscle inhibition (inability to fully activate the muscle despite trying). Weakness may also occur as a consequence of reductions in physical activity and disuse. Weakness usually occurs to the antigravity muscles, and muscles that oppose spammed muscles. Muscle atrophy causes apparent enlargement of the joint. 5- Loss of ROM and stiffness: Limitation of ROM in later stages of OA (first extension), stiffness due to shortening of the capsule. Adaptive shortening may also occur due to prolonged positioning of the joint in the resting position (flexion for example). 6-Crepitation, deformity and instability: Crepitation: due to flakes of cartilage break off and move freely inside the joint leading to joint locking, deformity due to unequal load distribution and muscle imbalance and instability due to ligaments stretch and muscle weakness. 7-Antalgic gait: Painful gait, short stance duration on affected leg relative to the swing phase, longer step on affected side, shorter step on sound or least affected leg. Diagnosis of OA: Clinical findings (joint pain) +Radiologic findings(osteophytes)  Imaging X ray is the routine radiograph for OA diagnosis, arthroscopy, CT and MRI may be done for patients before surgery. X-Ray and MRI of the arthritis joint may show some or all of the following: 1-Softening,fabrillation and loss of articular cartilage. 2-Narrowed joint space. 3-Sclerosis and eburnation (Increased bone density) of the subchondral bone. 4-Formation of osteophytes 5-Subchondral cysts, Irritation and hypertrophy of synovial membrane causing joint effusion. The joint capsule undergoes degeneration and adaptive shortening (MRI) Knee X ray Knee MRI Differential diagnosisc  Management Of Knee OA It has been found that the optimal management of OA requires a combination of non pharmacological and pharmacological modalities. 1-Medical treatment: A-NSAIDS: Used to relieve pain and inflammation for more advanced cases, however, it has side effects. B-Intra-articular injections of corticosteroids. C-Topical and injectable medications. D-Glucosamine and hyaluronic acids: Acts as a lubricant and shock absorbing, helps rebuild cartilage. 2-Surgical Treatment (when conservative treatment failed): Osteotomy: Performed to change bone alignment and alter load on joint surface and correct deformities. High tibial corrective osteotomy Arthroscopy for debridement and lavage (cleaning ) of the joint. Arthroplasty: Joint replacement can relieve pain and restore loss of function for patients with advanced disease. Uni-Condylar/Compartmental Arthroplasty Total Knee Arthroplasty  Conservative Treatment Options The primary treatment for OA knee conservatively is exercise therapy within physiotherapy.Physiotherapy normally involves Patient education Exercise therapy Activity modification Advice on weight loss Knee bracing The first-line treatment for all patients with symptomatic knee osteoarthritis includes patient education and physiotherapy. A combination of supervised exercises and a home exercise program have been shown to have the best results. These benefits are lost after 6 months if the exercises are stopped. Weight loss is valuable in all stages of knee OA. It is indicated in patients with symptomatic OA with a body mass index greater than 25. The best recommendation to achieve weight loss is with diet control and low-impact aerobic exercise. Knee bracing in OA can be used. Offloading-type braces which shift the load away from the involved knee compartment. This can be effective when there is a valgus or varus deformity.  Physical Therapy Management Assessment: ROM. Tests for Intra-Articular Fluid (The Bulge Test-The Patellar Tap) Muscle Strength. Joint stability. Proprioception Posture. Gait and Function. Psychological status. Aims Of Physical Therapy Treatment: Decrease load on the joint. Decrease pain, inflammation and swelling. Increase mobility and ROM. Improve muscle strength and endurance. Improve joint stability and proprioception. Prevent or minimize deformity formation. improve function and independence in ADL. Improve Gait.  Physical Therapy Management I. To decrease the load 1-Weight reduction Weight increases load on joints. Losing weight directly decrease the load on joint by decrease the joint reaction force during weight bearing and activities. During ambulation, 3 to 5 times the body weight passes through the knee joint, small changes in weight result in large increase in force across the joint. Weight reduction could be achieved either by exercises and/or diet. Weight reductions is highly recommended especially in obese patients in order to maintain the average BMI (18.5 to 25). 2-Walking aids Assistive devices like canes, crutch and walkers to increase the base of support and decrease load. Provide effective unloading of the knee and hip when held contra lateral side. Increase joint stability. Frames or wheeled walkers are preferable for those with bilateral OA. Walking aids is highly recommended. (The cane is held in the hand contralateral to the affected limb and moves together with the affected limb). 3-Braces and orthoses A-Knee brace 1-“Rest” braces: are not advised due to weakening of the quadriceps muscle. N.B. Complete rest is commonly unnecessary; instead relative joint resting by splints or brace is advised (to rest the joint and decrease the load). 2-Corrective braces: used by patients with moderate or severe knee OA. Valgus braces is the most common, it reduces pain and adduction moments, reduce compression of the joint and improve proprioception. However, it is not tolerated by patients, its prolonged use may lead to compartment syndrome, research evidence is weak in its use. It is not recommended as a standard treatment for patients with OA unless patient’s show need for it. B-Foot orthosis Insoles offer great potential as simple, inexpensive treatment strategies for knee OA. Lateral wedge insoles have been advocated for medial compartment OA and medial wedge insoles for lateral compartment OA. Lateral wedge inserts -----By placing the calcaneus in a valgus position, a medial unloading may take place more proximal up the kinematic chain at the knee. Lateral wedge insole If orthosis to be used, lateral foot insert and medial foot arch should be used simultaneously. The two inserts should be different in height so that the net wedge angle is related to the desired amount of knee unloading. It is not standard treatment. 4-Gait retraining During acute episodes of pain, patients could be taught simple biomechanical strategies to reduce knee joint loading. However, these are temporal procedure, prolonged usage of some of these methods may cause muscle tightness, increase energy expenditure during walking and abnormal walking pattern as well as other problem such as low back pain or scoliosis. Thus, these methods are not recommended as treatment procedures except in acute episodes. They mostly reduce ground reaction force on the medial knee and hence reduce pain. Among these strategies A-Increase toe out by voluntarily rotate the feet externally. Out-toeing during walking shifts the ground reaction force vector closer to the knee joint center and thus reduces the GRF moment arm (solid line) to the knee joint center and knee adduction moment. B-Reducing walking velocity is also expected to reduce the GRF and hence joint loading. Thus walking slowly could be an appropriate life style modification. 5-Muscle strengthening to decrease load and impact on joint II. To decrease pain 1-TENS, Interferential. TENS as it has some evidence to show it can help with pain reduction so it is recommended. 2-Ultrasonic: It has an anti-inflammatory effects, and also serves to improve the extensibility of the capsule. Usually used in pulsed mode. There is insufficient evidence to recommend the use of therapeutic ultrasound. 3-Electromagnetic field and laser---- NO clinical benefit. 4-Cryo and thermotherapy: The use of cold therapy is recommended to some extent during acute flare with minor inflammation. The use of heat therapy is not recommended as there is no scientific evidence that heat therapy improve patient symptoms. 5-Massage therapy: Massage temporary relieve pain, reduce tension and improve circulation, Massage therapy is not recommended as standard treatment. 6-Tapping techniques: Theoretically, tapping stabilizes the joint, alters load distribution, realigning the patella and reduce strain on inflamed tissue. the effectiveness depend on strapping technique and duration of application. It has short-term effect. Knee taping (medial patella glide). 7-Joint Mobilization (grade I, II): Knee mobilization (anterior-posterior) Knee mobilization Patients with symptomatic knee OA may benefit from hip mobilizations (caudal glides-, anterior-posterior glides-posterior-anterior glides- posterior-anterior glides in the FABER position), if they have two or more of the following criteria: (1) hip or groin pain or paresthesia, (2) anterior thigh pain, (3) passive knee flexion less than 122 degrees, (4) passive hip internal rotation less than 17 degrees, and (5) pain with hip distraction. Hip mobilization III.To improve mobility and ROM: 1-Active free ROM exercise within painless ROM.----Help in joint nutrition and washing out of pain metabolites by enhancing the synovial fluid circulation. 2-Joint Mobilization grade III,IV and distraction (anterior, posterior glide). 3-Stretching exercise for tight muscles: (Hip adductors, Hip Flexors, Hamstring, Quadriceps, Calf, Iliotibial band). Calf stretch Hip Flexors stretch Iliotibial band Hamstring stretch stretch IV. To improve muscle strength and endurance: Static and Isometric exercises are preferable to avoid friction between joint surfaces. Open kinetic chain is preferable to closed kinetic chain exercises to limit compression on the joint. However, Closed kinetic chain exercises could be used later on to improve function when the muscle strength is improved. Muscle most commonly need strengthening are antigravity muscles: Gluteus maximus, gluteus medius, quadriceps, calf muscles. Quadriceps weakness has been identified as a potential risk for knee OA, and is closely associated with disability seen in patients, many of resistive training have focused on quadriceps strengthening and stabilization and have shown good clinical benefit. Quadriceps activation failure is a possible neuromuscular mechanism for knee OA. In this case the muscle is not weak so much as but it is not able to contract efficiently. 1-Quadriceps strengthening has been a mainstay of conservative treatment for knee OA because muscle weakness can lead to functional disability. Very strong quadriceps can considerably delay the necessity for surgery. 2-Hip abductor muscle strengthening is of equal importance to strengthening of quadriceps. This is because sufficient hip abductor strength reduces adduction moment by reducing adduction moment arm, because of reducing contra-lateral pelvic drop and stabilizing medial joint loading on the knee. 3-Aerobic exercises (low impact): e.g. high chair stationary bike. Aerobic and cardiovascular exercises such as aerobic walking has been shown to increase strength, improve pain, and cardiovascular condition as well as the overall function. These types of exercises are effective in OA treatment though it is less cost –effective compared to other methods. 4-Aquatic exercise is preferable due to low impact and decreased weight bearing on the joints. It may readily tolerated and less likely to flare symptoms. Is a non-invasive therapeutic intervention that is recommended in international guidelines. Although there is some contradictory evidence hydrotherapy can be useful in cases where pain is too grave to exercise on dry land. Many consider water-based exercises as a good preparation of exercise ashore. V. To improve Proprioception, Functional and gait training: 1-Proprioceptive exercise: Reduced proprioception in older adults may be responsible for the initiation or advancement of knee degeneration. This may be due to a process termed neurogenic acceleration of osteoarthrosis. Neurogenic acceleration is the loss of afferent proprioceptive input combined with joint instability that speeds up the arthritic process. The use of elastic knee bandages was found to increase the proprioceptive ability of joint position sense. This finding indicates that external supports or tape may be useful in giving proprioceptive feedback by allowing the patient to access afferent information from other receptors or to use existing proprioception more efficiently. 2-Balance exercise. 3-Under water walking and closed kinematic chain exercises  Advices to the patient  Lose weight to reduce load on the joints.  Modification of life style and daily routine.  Not to put the joint in extremes of range.  Not to stand, sit or lie in a fixed position for long periods.  Use walkers, crutches or canes during outdoors walking.  Drinking enough amount of water.  Eat healthy food rich in fibers.  Not to be exposed to extreme weather or temperature changes.  Avoid high impact sports & activities as jumping &stair climbing.