osteoarthritis lecture to gps
DESCRIPTION
a 2 hour presentation on non-operative management of osteoarthrits, looking at current concepts in exercise and physical therapyTRANSCRIPT
Cameron Bulluss Advanced Physiotherapy and Injury
Prevention 335 Hillsborough Rd Warners Bay
Physiotherapy Management of Osteoarthritis
Presenter
Presentation Notes
8 physios 200 new patients per month Approximately 20% of these present with osteoarthritis of the hip, knee or spine
Physio Facts 12000 registered Physios in Australia 1200 of these have a formally recognised specialty Musculoskeletal Sports Neurology
Advanced Physiotherapy Warners Bay
8 full-time Physios
220 new patients per month, half of these from g.p.s and specialists
Patients range over 10, with average of 46
Most common reason to seek a visit with us is for an OA knee
20 % of our patients present with symptomatic OA
Physio provider for Newcastle Jets Soccer
Osteoarthritis The most common musculoskeletal disorder The leading cause of pain an disability in the community
Presenter
Presentation Notes
Osteoarthritis is the most common joint disorder and there is evidence that a majority of individuals over the age of 65 have radiographic and or clinical evidence of OA. Not all radiological OA is associated with clinical symptoms and not all symptomatic OA produces disability. Arthritis is self reported by 15% Australians. A US study in 2005 predicted a doubling of the prevalance of this disease by 2020. Centers for Disease Control and Prevention (CDC).Arthritis prevalence and activity limitations—United States, 1990. MMWR Morb Mortal Wkly Rep 1994; 43:433–8. It is the most common musculoskeletal disorder affecting Australians, and is the leading cause of pain and disability in the community and the prominent condition leading to replacement surgery of the hip and knee. The most frequent sites affected are the hands, knees, hips and spine. In most common in the hand and second most common in the knees. The sites of involvement in the hand are the first carpometacarpal joint and interphalangeal joints. Importantly the symptoms are often associated with significant functional impairment, as well as signs and symptoms of inflammation, including pain, stiffness and loss of mobility.
Age and Gender
Joint Replacement Trend
Common Sites
41%
30%
19%
Presenter
Presentation Notes
Ann Rheum Dis 1991;50:8-13 doi:10.1136/ard.50.1.8 Research Article Study of 500 patients with limb joint osteoarthritis. I. Analysis by age, sex, and distribution of symptomatic joint sites. Rheumatology Unit, Bristol Royal Infirmary. Abstract Five hundred subjects with symptomatic limb joint osteoarthritis, who had been referred to a rheumatologist, were enrolled into a continuing study. They comprised 342 women (mean age 65.3) and 158 men (mean age 59.7), with a mean symptom duration of 15.4 years at entry. Only 31 patients (6%) had symptomatic osteoarthritis of one joint alone; however, in a further 205 (41%) the disease was limited to one site. One hundred and eighty two (36.4%) had two sites affected and 82 (16.4%) three or more sites of symptomatic osteoarthritis. Of 847 affected joints the most commonly involved were 349 (41.2%) knees, 254 (30%) hands, and 161 (19%) hips. Hip disease stood out as a separate entity, often occurring alone, and having a stronger male preponderance and different associations than osteoarthritis at other joint sites. Knee and hand disease were significantly associated in women. Obesity, hypertension, and Heberden's nodes were common. The number of sites affected, as well as the distribution, was strongly related to age as well as sex, suggesting that polyarticular osteoarthritis arises from slow acquisition of new joint sites in a non-random distribution. 'Generalised' osteoarthritis did not emerge as a distinct entity
Definition- Clinical definitions
- Radiological definitions
- Anatomical definitions
- All vary and none appear to encompass all aspect of the disease
- These even vary between body parts
Presenter
Presentation Notes
Brandt KD, Dieppe P, Radin EL. Etiopathogenesis of osteoarthritis. Rheum Dis Clin North Am 2008; 34:531–59 [review]. None of these defintions are in complete agreement nor perfectly characterise this disorder
Definition “The synovial joint is an organ, and OA represents failure of
that organ and can be initiated by abnormalities arising in any of its constituent tissues. “ (Brandt 2008)
Presenter
Presentation Notes
Brandt KD, Dieppe P, Radin EL. Etiopathogenesis of osteoarthritis. Rheum Dis Clin North Am 2008; 34:531–59 [review].
These abnormalities are in Articular Cartilage Bone Synovium Periarticular Soft Tissues Muscles Nerves
Presenter
Presentation Notes
The common abnormalites of the synovial joint we encounter are those related to: The articular cartilge. This is not the direct cause of symptoms in OA because it is aneural. It also has very limited regenerative capacity and can not be altered with treatment. However if it is injured or degenerates it leaves the subchondral bone exposed to more stress and can be a source of synovial irritation. The subchondral bone, synovium and periarticular soft tissues are all richly innervated and changes to the subchondral bone (oedema and cysts) in particular is most likely to contribute to symptoms
Articular Cartliage Exposes sub-chondral bone Irritation of synovium via
debris Alteration of joint
alignment No pain directly possible as
it is aneural
Presenter
Presentation Notes
The articular cartilge. This is not the direct cause of symptoms in OA because it is aneural. It also has very limited regenerative capacity and can not be altered with treatment. However if it is injured or degenerates it leaves the subchondral bone exposed to more stress and can be a source of synovial irritation. Source of symptoms secondary to Debris in joint affecting synovium Changes in joint alignment causing increased stress on subchondral bone and periarticular soft tissues The aging process contribute to OA pathogenesis in several ways. The first relates to the influence of the aging process on the structural organisation and material properties of the cartilage extracellular matrix. Chondrocyte apoptosis and the effects of synovial inflammation which dysregulate chondrocyte function
The Bony Changes We See Are Increased density of subchondral plate Bone necrosis Bone cysts Bone oedema Sclerosis Osteophytes
Presenter
Presentation Notes
Subchondral Bone There is a continuing debate as to whether the earliest changes of OA take place within the subchondral bone. There is evidence that the first changes detectable in OA are thickening of an increased density of the subchondral bone plate raising he suggestion that this might be the initial event leading to the characteristic cartilage changes of OA by interfering with the flow of nutrients into the articular cartilage from the adjacent bone marrow. There is no doubt that in most cases of OA there is a generalised anabolic effect in bone. The normal balance between osteoblastic and osteoclastic activity is lost with a subsequent subchondral bone sclerosis and osteophyte formation. In addition at the junction of the articular hyaline cartilage and adjacent subchondral bone, in the region of the so-called tidemark, there is remnant of calcified cartilage. Subchondral Bone Periarticular bone changes associated with OA can be segregated into distinct patterns based on the anatomic location and pathogenic mechanisms. These alterations include progressive increase in subchondral plate thickness; alterations in the architecture of subchondral trabecular bone; formation of new bone at the joint margins (osteophytes); development of subchondral bone cysts; and advancement of the tidemark associated with vascular invasion of the calcified cartilage. Of these lesions that which has the most supportive evidence for a role in symptom genesis is the bone marrow lesion (Fig. 3). Lesions in the bone marrow play an integral if not pivotal role in the symptoms that emanate from knee OA and its structural progression. Bone marrow lesions were found in 272 (77.5%) of 351 persons withpainful knees compared with 15 (30%) of 50 persons with no knee pain (P <.001). Large lesions were present almost exclusively in persons with knee pain (35.9% versus 2%; P <.001). After adjustment for severity of radiographic disease, effusion, age, and gender, all lesions and in particular large lesions remained associated with the occurrence of knee pain. More recently their relation to pain severity and incident pain was also demonstrated. Other bone-related causes of pain include periostitis associated with osteophyte formation, subchondral microfractures, bone attrition, and bone angina caused by decreased blood flow and elevated intra-osseous pressure It is believed that instability causes osteophyte formation but the exact mechanism is still unknown. The net effect of osteophyte formation is to increase stability by increasing the size of the articuling surface. Bone Necrosis Normally the subchondral bone is protected from load by the overlying cartilage. Eburnated bone is not protected in this way and is prone to local pressure necrosis. This affects both the bone and the underlying marrow, so that the marrow can not repair by stimulation of marrow stem cells. These areas of necrosis are usually very small. Bone Cysts Bone cysts or geodes are a feature of advanced OA. They form as a consequence of synovial fluid entering the bone marrow. Unlike cartilage, bone is naturally permeated by narrow channels either in the form of Haversian systems or the canaliculi linking osteocyte lacunae. These channels make convenient routes for synovial fluid to be forced under pressure from the joint cavity into the marrow. Once in the marrow the synovial fluid elicits a bipolar reaction with osteoclastic bone destruction and osteoblastic bone deposition. Ultimately this leads to the formation of a cyst within the bone, containing fibrous or myxoid tissue and lined by sclerotic bone and fibrous tissue.
Subchondral Bone Much of the pain comes from the subchondral bone (Hunter 2009
Rad Clin North America 2009 (539 -531)
Presenter
Presentation Notes
From Insights from the imaging. Rad Clin North America 2009 (539 -531)
Diagnosis Clinical Examination is crucial Imaging can be used to confirm the diagnosis and exclude
other pathology X-Rays provide further information but are notoriously
insensitive MRI provides greater insight subchondral bone marrow lesions, synovitis subarticular bone attrition Articular cartilage damage
Presenter
Presentation Notes
The presence and severity of OA is typically classified using the Kellgren and Lawrence grading system, a system that is heavily dependent on the osteophytes for classification of disease (Table 1). This system suffers from limitations based on invalid assumptions by mixing distinct constructs (osteophytes, joint space narrowing, subchondral sclerosis, subchondral bone shape changes, cysts, and so forth) into one scale. Further, the scale is not linear and the use of Kellgren and Lawrence grade progression as a measure of disease progression should best be avoided. Understanding the radiographic method of disease definition becomes important when one considers that osteophytes, typically the first feature identified on radiographs, are not necessarily a deleterious finding and may represent an effort on the part of the joint to promote stability. They are important, however, if they represent a source of symptoms, and yet most of the epidemiologic research in OA is based on the presence of self-reported OA or radiographic osteophytes and not on symptomatic OA, defined as the concomitant presence of pain and radiographic features. It is the presence of symptomatic OA that is important clinically, not simply the radiographic identification of osteophyte formation or self-reported OA (where misclassification is even more problematic than the commonly used radiographic OA definition). In addition, marked osteoarthritic damage must be present to detect characteristic changes with conventional radiographs, and they are not sensitive diagnostic tests. Bearing in mind that radiographs are notoriously insensitive to the earliest pathologic features of OA the absence of radiographic findings should not be interpreted as confirming the absence of symptomatic disease. Conversely the presence of positive radiographic findings does not guarantee that an osteoarthritic joint is also the active source of the patient’s current knee or hip symptoms where other sources of pain may be contributing. There is a significant discordance between radiographically diagnosed OA and knee pain. Although radiographic evidence of joint damage predisposes to joint pain, it is clear that the severity of joint damage on radiographs bears little resemblence to the pain that is experienced. MRI imaging which shows subchondral bone marrow lesions, synovitis, subarticular bone attrition. The hyaline articular cartilage is aneural and avascular so can not be a direct source of symptoms. It is most likely however responsible for exposing the subchondral bone to stress, syovial fluid, vascular congestion, and to provoking a syovitis. A recent analysis confirmed most beliefs that it is likely that changes in the subchondral bone and synovial activation-effusion predominate.
Knee x-ray useful additional view A clear x-ray does not exclude osteoarthritis Knee X-rays should include Rosenberg view if looking for
OA
Erect PA view at 45 degrees flexion
Activity modification and strengthening
Weight Reduction
Psychological
Pharmaceutical
Keys to Management
Activity modification and exercise
Weight Reduction
Psychological
Pharmaceutical
Keys to Management
Keys to ManagementWeight Reduction
• For every 2 units of BMI increase there is a 36% increase in the risk of developing knee OA
Presenter
Presentation Notes
Obesity: There is large body of evidence that identifies obesity as a risk factor for developing OA of the knee, particularly in women. Obesity is associated with the development of disability and the radiological progression of OA once established. It was generally agreed that obesity was brought about by inactivity brought about by painful joints. However well designed epidemiological studies now show that the risk begins as early as the third decade in life. For every 2 units of body mass index gain (equivalent to about 5 kg), the risk of OA of the knee is increased by 36%. Conversely for every 5 kg decrease in body weight during the preceeding 10 years the risk of OA of the knee declines by more than 50%. People in the upper BMI quartile (>30 ) have a 20 fold risk of developing bilateral OA of the knee. Furthermore, if weight loss may prevent the onset of OA, the loss of body fat is more closely related to symptomatic benefit than is the loss of body weight. Local fat depots may play an important role in disease and symptoms genesis. Among these tissues, the synovium and infrapatellar fat pad seem to produce large amounts of adipokines. Until recently, the fat pad, which is an extra-synovial but an intra-articular tissue, had been neglected. This adipose tissue, however, is able to release growth factors, cytokines, and adipokines. Because obese individuals have higher concentrations of inflammatory markers, inflammation may contribute to functional limitation and disease progression in those with OA.85 Besides direct effects on the joint, inflammatory mediators can affect muscle function and lower the pain threshold.
Keys to ManagementWeight Reduction
• For every 2 units of BMI increase there is a 36% increase in the risk of developing knee OA
• BMI>30 there is a 20 fold increased risk of knee OA
Presenter
Presentation Notes
Obesity: There is large body of evidence that identifies obesity as a risk factor for developing OA of the knee, particularly in women. Obesity is associated with the development of disability and the radiological progression of OA once established. It was generally agreed that obesity was brought about by inactivity brought about by painful joints. However well designed epidemiological studies now show that the risk begins as early as the third decade in life. For every 2 units of body mass index gain (equivalent to about 5 kg), the risk of OA of the knee is increased by 36%. Conversely for every 5 kg decrease in body weight during the preceeding 10 years the risk of OA of the knee declines by more than 50%. People in the upper BMI quartile (>30 ) have a 20 fold risk of developing bilateral OA of the knee. Furthermore, if weight loss may prevent the onset of OA, the loss of body fat is more closely related to symptomatic benefit than is the loss of body weight. Local fat depots may play an important role in disease and symptoms genesis. Among these tissues, the synovium and infrapatellar fat pad seem to produce large amounts of adipokines. Until recently, the fat pad, which is an extra-synovial but an intra-articular tissue, had been neglected. This adipose tissue, however, is able to release growth factors, cytokines, and adipokines. Because obese individuals have higher concentrations of inflammatory markers, inflammation may contribute to functional limitation and disease progression in those with OA.85 Besides direct effects on the joint, inflammatory mediators can affect muscle function and lower the pain threshold.
Keys to ManagementWeight Reduction• For every 2 units of BMI increase there is a 36% increase in the
risk of developing knee OA• BMI>30 there is a 20 fold increased risk of knee OA• Body fat % perhaps more important than BMI
Inflammatory proteins such as cytokinenes may contribute to sensitisation of nerve endings, tendon and muscle degeneration
Presenter
Presentation Notes
Obesity: There is large body of evidence that identifies obesity as a risk factor for developing OA of the knee, particularly in women. Obesity is associated with the development of disability and the radiological progression of OA once established. It was generally agreed that obesity was brought about by inactivity brought about by painful joints. However well designed epidemiological studies now show that the risk begins as early as the third decade in life. For every 2 units of body mass index gain (equivalent to about 5 kg), the risk of OA of the knee is increased by 36%. Conversely for every 5 kg decrease in body weight during the preceeding 10 years the risk of OA of the knee declines by more than 50%. People in the upper BMI quartile (>30 ) have a 20 fold risk of developing bilateral OA of the knee. Furthermore, if weight loss may prevent the onset of OA, the loss of body fat is more closely related to symptomatic benefit than is the loss of body weight. Local fat depots may play an important role in disease and symptoms genesis. Among these tissues, the synovium and infrapatellar fat pad seem to produce large amounts of adipokines. Until recently, the fat pad, which is an extra-synovial but an intra-articular tissue, had been neglected. This adipose tissue, however, is able to release growth factors, cytokines, and adipokines. Because obese individuals have higher concentrations of inflammatory markers, inflammation may contribute to functional limitation and disease progression in those with OA.85 Besides direct effects on the joint, inflammatory mediators can affect muscle function and lower the pain threshold.
Keys to ManagementWeight Reduction For every 5 kg decrease in body weight during the
preceeding 10 years the risk of OA of the knee declines by more than 50%. (MJA 2004)
Consider the load in the situation where someone 30kg overweight walks down 10 steps
• Impact loading will increase with increased body weight 30 kg overweight will result in over 10 steps 30 x 4 x 10 = 1200 kg extra accumulated load through
Patellofemoral joint
Activity modification and exercise
Weight Reduction
Psychological
Pharmaceutical
Keys to Management
Activity Modification and
Exercise
Weight Reduction
Psychological
Pharmaceutical
Keys to Management
Optimise Loading in Current Activities
Commence Low Intensity Cyclical Exercise
Commence Low Impact Strengthening
Commence Range of Motion Exercises
Activity Modification and Exercise
Optimise Loading in Current Activities
Activity Modification and Exercise
Optimise Loading with Current Activities Reduce Loading if excessive Reduce pressure on subchondral bone Less stress on articular cartilage
Increase Loading if inadequate Improved nutrition of articular cartilage
Change Loading – How? Optimise Activity Selection (exercise and recreational) An understanding is required of the forces involved PFJ 4 -10x body weight in running PFJ 1.5x body weight in walking 3-4x body weight ascending and descending stairs 6x body weight in squatting 4x body weight sit-stand
Loading Changes – examples Replace running with walking Replace walking with low intensity bike Commence weekly hydrotherapy Reduce BMI Reduce hills Improve shoes Walk on grass rather than concrete Provide Supportive Device
Reduce Loading with Bracing
Reducing Load Through the first MTP
Reducing Load with shoes
Brooks Addictions
Reducing Load with a Lateral Heel Wedge
Are foot orthotics efficacious for treating painful medial compartment knee osteoarthritis? A review of the literature R. Marks L. Penton Article first published online: 11 FEB 2004
“These data indicate a strong scientific basis for applying wedged insoles in attempts to reduce osteoarthritic pain of biomechanical origin. Further research to substantiate their efficacy in well-designed clinical trials seems warranted”
American Podiatric Medicine Association Journal
Commence Low Impact
Strengthening
Activity Modification and Exercise
Commence Low Impact Strengthening –Why?
Load Sharing Occurs Between Joints and Muscles
Muscle weakness is likely to be present in knees with symptomatic Osteoarthrits.
It is also likely to be a risk factor for the development and progression of knee osteoarthritis. (Ann Intern Med. 1997
Muscle weakness is probably more important in the pathogenesis of OA than wear and tear (Br J Sports Med 2004)
Presenter
Presentation Notes
Muscle weakness Various studies have investigated the role of muscle strength on joint integrity and some have explored the impact on physical functioning. Sharma and colleagues conducted a 3-year longitudinal cohort study investigating factors contributing to poor physical functioning in 257 patients with knee OA. They found that in addition to such factors as age, reduced absolute quadriceps and hamstrings strength, and poor proprioceptive acuity increased the likelihood of poor physical functioning as measured by the time to perform five repetitions of rising and sitting in a chair. In addition to their exploration in observational studies there is ample evidence from clinical trials demonstrating that muscle-strengthening exercises result in improvements in pain, physical function, and quality of life in people with knee OA. Conclusion: Quadriceps weakness may be present in patients who have osteoarthritis but do not have knee pain or muscle atrophy; this suggests that the weakness may be due to muscle dysfunction. The data are consistent with the possibility that quadriceps weakness is a primary risk factor for knee pain, disability, and progression of joint damage in persons with osteoarthritis of the knee. Br J Sports Med 2004;38:526-535 Muscle dysfunction versus wear and tear as a cause of exercise related OA: an epidemiological update
Low Impact Strengthening – example open chain exercise
Open chain means that the distal part is free to move
Quadriceps Strength Pre-operative quadriceps
strength is a good predictor of functional outcomes 1 year post total knee replacement
Presenter
Presentation Notes
Preoperative quadriceps strength predicts functional ability one year after total knee arthroplasty. Ryan L Mizner, Stephanie C Petterson, Jennifer E Stevens, Michael J Axe, and Lynn Snyder-Mackler + Author Affiliations Department of Physical Therapy, University of Delaware, Newark, 19716, USA. Abstract OBJECTIVE: Quadriceps weakness is common after total knee arthroplasty (TKA) as is longterm disability. We hypothesized that preoperative quadriceps strength would be the best predictor of postoperative functional ability when compared to preoperative pain or knee range of motion (ROM). METHODS: Forty subjects (mean age 63 +/- 8 yrs, body mass index 29.4 kg/m2 +/- 4.2) were tested 2 weeks before and one year after TKA. Quadriceps strength was measured isometrically, pain was quantified using the Medical Outcome Study Short-Form 36 (SF-36) bodily pain subset, and knee flexion range of motion (ROM) was assessed by goniometer. Performance based functional assessment included the Timed Up and Go test (TUG) and a timed Stair Climbing Test (SCT). The Knee Outcome Survey (KOS) and the SF-36 questionnaires were used to quantify perceived function. The ability of preoperative factors to predict postoperative outcomes was analyzed using hierarchical regression. Differences in means before and one year after surgery were analyzed using paired t tests. RESULTS: Significant improvements were found in all functional measures assessed (p < 0.001). Preoperative quadriceps strength accounted for the bulk of the variance in the one-year SCT and the TUG (p < 0.001), but did not achieve significance in predicting one-year questionnaire scores (p > 0.05). Neither preoperative pain nor knee ROM were significant predictors of any functional measure (p > 0.05). CONCLUSION: Preoperative quadriceps strength plays a dominant role in predicting one-year SCT and TUG functional measures, but it is not a good predictor of score on self-report questionnaires. Preoperative bodily pain and knee flexion ROM are poor predictors of all functional outcome measures.
Commence Low Intensity Cyclical
Exercise
Activity Modification and Exercise
Commence Low Intensity Cyclical Exercise - Why Improved nutrition of subchondral bone and articular
cartilage Assist with weight loss Assist with range of motion
Commence Low Intensity Cyclical Exercise - Examples Exercise bike Hydrotherapy Low Impact walking
Bike Set-up is crucial
Commence Range of Motion
Exercises
Activity Modification and Exercise
Commence Range of Motion Exercises – Why? Increasing flexibility of peri-articular soft tissues is likely to
improve functional range of motion 60 degrees knee flexion to walk 80 degrees knee flexion to climb a step 10 degrees ankle dorsiflexion to walk 105 degrees knee flexion to ride a bike
American Academy of Orthopaedic Surgeons – Clinical Guidelines
Clinical GuidelinesRecommendation 1
We suggest patients with symptomatic OA of the knee be encouraged to participate in self-management educational programs such as those conducted by the Arthritis Foundation, and incorporate activity modifications (e.g. walking instead of running; alternative activities) into their lifestyle.
Presenter
Presentation Notes
Patient Education and Lifestyle Modification Recommendation 1 We suggest patients with symptomatic OA of the knee be encouraged to participate in self-management educational programs such as those conducted by the Arthritis Foundation, and incorporate activity modifications (e.g. walking instead of running; alternative activities) into their lifestyle. Level of Evidence: II Grade of Recommendation: B Recommendation 2 Regular contact to promote self-care is an option for patients with symptomatic OA of the knee. Level of Evidence: IV Grade of Recommendation: C Recommendation 3 We recommend patients with symptomatic OA of the knee, who are overweight (as defined by a BMI>25), should be encouraged to lose weight (a minimum of five percent (5%) of body weight) and maintain their weight at a lower level with an appropriate program of dietary modification and exercise. Level of Evidence: I Grade of Recommendation: A (continued on next page) Rehabilitation Recommendation 4 We recommend patients with symptomatic OA of the knee be encouraged to participate in low-impact aerobic fitness exercises. Level of Evidence: I Grade of Recommendation: A Recommendation 5 Range of motion/flexibility exercises are an option for patients with symptomatic OA of the knee. Level of Evidence: V Grade of Recommendation: C Recommendation 6 We suggest quadriceps strengthening for patients with symptomatic OA of the knee. Level of Evidence: II Grade of Recommendation: B Mechanical Interventions Recommendation 7 We suggest patients with symptomatic OA of the knee use patellar taping for short term relief of pain and improvement in function. Level of Evidence: II Grade of Recommendation: B Recommendation 8 We suggest lateral heel wedges not be prescribed for patients with symptomatic medial compartmental OA of the knee. Level of Evidence: II Grade of Recommendation: B Recommendation 9 We are unable to recommend for or against the use of a brace with a valgus directing force for patients with medial uni-compartmental OA of the knee. Level of Evidence: II Grade of Recommendation: Inconclusive Recommendation 10 We are unable to recommend for or against the use of a brace with a varus directing force for patients with lateral uni-compartmental OA of the knee. Level of Evidence: V Grade of Recommendation: Inconclusive (continued on next page) Complementary and Alternative Therapy Recommendation 11 We are unable to recommend for or against the use of acupuncture as an adjunctive therapy for pain relief in patients with symptomatic OA of the knee. Level of Evidence: I Grade of Recommendation: Inconclusive Recommendation 12 We recommend glucosamine and/or chondroitin sulfate or hydrochloride not be prescribed for patients with symptomatic OA of the knee. Level of Evidence: I Grade of Recommendation: A Pain Relievers Recommendation 13 We suggest patients with symptomatic OA of the knee receive one of the following analgesics for pain unless there are contraindications to this treatment: Acetaminophen [not to exceed 4 grams per day] Non-steroidal anti inflammatory drugs (NSAIDs) Level of Evidence: II Grade of Recommendation: B Recommendation 14 We suggest patients with symptomatic OA of the knee and increased GI risk (Age >= 60 years, comorbid medical conditions, history of peptic ulcer disease, history of GI bleeding, concurrent corticosteroids and/or concomitant use of anticoagulants) receive one of the following analgesics for pain: Acetaminophen [not to exceed 4 grams per day] Topical NSAIDs Nonselective oral NSAIDs plus gastro-protective agent Cyclooxygenase-2 inhibitors Level of Evidence: II Grade of Recommendation: B (continued on next page) Intra-Articular Injections Recommendation 15 We suggest intra-articular corticosteroids for short-term pain relief for patients with symptomatic OA of the knee. Level of Evidence: II Grade of Recommendation: B Recommendation 16 We cannot recommend for or against the use of intra-articular hyaluronic acid for patients with mild to moderate symptomatic OA of the knee. Level of Evidence: I and II Grade of Recommendation: Inconclusive Needle Lavage Recommendation 17 We suggest that needle lavage not be used for patients with symptomatic OA of the knee. Level of Evidence: I and II Grade of Recommendation: B Surgical Intervention Recommendation 18 We recommend against performing arthroscopy with debridement or lavage in patients with a primary diagnosis of symptomatic OA of the knee. Level of Evidence: I and II Grade of Recommendation: A Recommendation 19 Arthroscopic partial meniscectomy or loose body removal is an option in patients with symptomatic OA of the knee who also have primary signs and symptoms of a torn meniscus and/or a loose body. Level of Evidence: V Grade of Recommendation: C Recommendation 20 We cannot recommend for or against an osteotomy of the tibial tubercle for patients with isolated symptomatic patello-femoral osteoarthritis. Level of Evidence: V Grade of Recommendation: Inconclusive (continued on next page) Recommendation 21 Realignment osteotomy is an option in active patients with symptomatic unicompartmental OA of the knee with malalignment. Level of Evidence: IV and V Grade of Recommendation: C Recommendation 22 We suggest against using a free-floating interpositional device for patients with symptomatic unicompartmental OA of the knee. Level of Evidence: IV Grade of Recommendation: B
Recommendation 3 We recommend patients with symptomatic OA of the knee, who are overweight (as defined by a BMI>25), should be encouraged to lose weight (a minimum of five percent (5%) of body weight) and maintain their weight at a lower level with an appropriate program of dietary modification and exercise
Recommendation 4 We recommend patients with symptomatic OA of the knee be encouraged to participate in low-impact aerobic fitness exercises.
Recommendation 5 Range of motion/flexibility exercises are an option for patients with symptomatic OA of the knee.
Recommendation 6 We suggest quadriceps strengthening for patients with symptomatic OA of the knee.
Recommendation 9 We are unable to recommend for or against the use of a brace
with a valgus directing force for patients with medial uni-compartmental OA of the knee.
Grade of Recommendation: Inconclusive Recommendation 10 We are unable to recommend for or against the use of a brace
with a varus directing force for patients with lateral uni-compartmental OA of the knee.
Grade of Recommendation: Inconclusive
Clinical TrialsEffects of tai chi exercise on pain, balance, muscle strength, and perceived difficulties in physical functioning in older women with osteoarthritis: a randomized clinical trial. The Journal of Rheumatology
CONCLUSION: Older women with OA were able to safely perform the 12 forms of Sun-style tai chi exercise for 12 weeks, and this was effective in improving their arthritic symptoms, balance, and physical functioning
Effect of therapeutic exercise for hip osteoarthritis pain: results of a meta-analysis Source: Arthritis and Rheumatism 2008 Method: systematic review
CONCLUSION: Therapeutic exercise, especially with an element of strengthening, is an efficacious treatment for hip OA
Presenter
Presentation Notes
Effects of tai chi exercise on pain, balance, muscle strength, and perceived difficulties in physical functioning in older women with osteoarthritis: a randomized clinical trial. Rhayun Song, Eun-Ok Lee, Paul Lam, and Sang-Cheol Bae. The Journal of Rheumatology vol 30 no 9 2039-2044 CONCLUSION: Older women with OA were able to safely perform the 12 forms of Sun-style tai chi exercise for 12 weeks, and this was effective in improving their arthritic symptoms, balance, and physical functioning. A longitudinal study with a larger sample size is now needed to confirm the potential use of tai chi exercise in arthritis management. Author/Association: Hernandez-Molina G, Reichenbach S, Zhang B, Lavalley M, Felson DT Title: Effect of therapeutic exercise for hip osteoarthritis pain: results of a meta-analysis Source: Arthritis and Rheumatism 2008 Sep 15;59(9):1221-1228 Method: systematic review Method Score: This is a systematic review. Systematic reviews are not rated. Abstract: OBJECTIVE: Recommendations for lower extremity osteoarthritis (OA) and exercise have been primarily based on knee studies. To provide more targeted recommendations for the hip, we gathered evidence for the efficacy of exercise for hip OA from randomized controlled trials. CONCLUSION: Therapeutic exercise, especially with an element of strengthening, is an efficacious treatment for hip OA Physiotherapy and Knee OA Physiotherapy and Hip OA Physiotherapy and Spinal OA
Exercise variables - Loading Generally low
Exercise Variable – Repetitions or Time- Generally high- 15 mins on an exercise bike at 60 RPM=900 knee flexion –
extensions between 5 and 105 degrees
Exercise Variable - Frequency Minimum 3 times per week
Exercise Variable – Trial period 8 weeks is usually required
Resources
Useful Websites www.aaos.org www.arthritisaustralia.com.au
Questions Acknowledgements – Jess Fidler
OA Changes to the Synovium Hyperplasia Fibrosis Thickening Lymphocytic infiltration Inflammation
Presenter
Presentation Notes
Synovitis and Effusion The synovial reaction in OA includes synovial hyperplasia; fibrosis; thickening of synovial capsule; activated synoviocytes; and in some cases lymphocytic infiltrate (B and T cells and plasma cells).56 The site of infiltration of the synovium is of obvious relevance because one of the most densely innervated structures of the joint is the white adipose tissue of the fat pad, which also shows evidence of inflammation and can act as a rich source of inflammatory adipokines. Synovial causes of pain include irritation of sensory nerve endings within the synovium from osteophytes and synovial inflammation that is caused, at least in part, by the release of prostaglandins, leukotrienes, proteinases, neuropeptides, and cytokines. Synovitis and effusion are frequently present in OA and correlate with pain and other clinical outcomes (Fig. 4).41 Synovial thickening aroundthe infrapatellar fat pad using noncontrast MR imaging has been shown on biopsy to represent mild chronic synovitis.
OA Changes to Nerves Changes leading to reduced proprioception Loss of mechanoreceptors
Structural changes leading increased pain Disorganisation Truncation
Presenter
Presentation Notes
Another source of joint pain in OA may be from the nerves themselves. Following joint injury in which there is ligamentous rupture, the nerves that reinnervate the healing soft tissues contain an overabundance of algesic chemicals, such as substance P and calcitonin gene-related peptide. An interesting observation of these new nerves was that their overall morphology was abnormal with fibers appearing truncated and disorganized. Because these phenomena are consistent with the innervation profiles described in nerve injury models, injured joints may develop neuropathic pain post-trauma. Indeed, treatment of inflamed joints with the neuropathic pain analgesic gabapentin can also relieve arthritis pain.
Biological Pain Generators in OA
Bone
Periarticularsoft tissues
Synovium
Presenter
Presentation Notes
Local to the joint there are a number of tissues that contain nociceptive fibres and these are likely sources of pain in OA. The subchondral bone, periosteum, periarticular ligaments, periarticular muscle, synovium and joint capsule are all richly innervated and are the likely source of nociception in OA.
Risk Factors for Development of OA Non-Modifiable Age Dysplasia Joint alignment Traumatic injury
Modifiable Muscle strength Activity type and level Obesity Traumatic injury
Risk Factors for the Development and Progression of Osteoarthritis Age Joint dysplasia e.g.
FAI of hip
Presenter
Presentation Notes
Susceptibility to OA may be increased in part by genetic inheritance (a positive family history increases risk), age, ethnicity, diet and female gender. In persons vulnerable to the development of knee OA, factors such as Abnormal joint congruity or dysplasia, Multiple factors have been shown to affect the progression of OA including the presence of polyarticular disease, increasing age, associated intra-articular crystal deposition, obesity, joint instability and or mal-alignment, muscle weakness and peripheral neuropathy. These can be sub-grouped into hereditary factors, mechanical factors and the effects of aging. Hereditary Factors - 60 - 70 % of cases in some body sites (hip and hand) - 40 -50% for the knee Mechanical Factors - Acute or chronic insult - Joint alignment Meniscal injury Obesity Muscle weakness - Clinical studies have shown that persons with radiographic knee osteoarthritis (OA), whether symptomatic or not, have weaker quadriceps muscle strength than those without knee OA. Quadriceps weakness is one of the earliest findings reported in knee OA. It is a better determinant of pain and disability than any radiographic changes. The muscle weakness has been suggested to be caused by disuse atrophy of the muscles due to joint pain3,4. The possible alterations in muscle size have not been studied in OA. In addition to pain related arthrogenous inhibition of muscle functions, reflex inhibition of muscles moving the affected joints is supposed to contribute to muscle weakness in OA3,4,8. This indicates that the reason behind the muscle weakness in OA is not clear Age The primary risk factor The aging process contribute to OA pathogenesis in several ways. The first relates to the influence of the aging process on the structural organisation and material properties of the cartilage extracellular matrix. Chondrocyte apoptosis and the effects of synovial inflammation which dysregulate chondrocyte function Nutritional Factors: such as low antioxidant, vitamin c and vitamin d intake, have been shown in observational studies the be associated with the risk of radiological progression of OA and knee pain. However usind dietary intake of antioxidants or vitamins has not been shown to slow progression or modify symptoms.
Risk Factors for the Development and Progression of Osteoarthritis – malalignment
Presenter
Presentation Notes
Malalignment (valgus or varus), Mechanical factors are the dominant risk factor for structural progression. Varus and valgus malalignment have been shown to increase the risk of subsequent medial and lateral knee OA radiographic progression, respectively. Varus malalignment has been shown to lead to a fourfold amplification of focal medial knee OA progression, whereas valgus malalignment has been shown to predispose to a twofold to fivefold increase in lateral OA progression. In an MR imaging– based study, varus malalignment predicted medial tibial cartilage volume and thickness loss, and tibial and femoral denuded bone increase, after adjusting for other local factors (meniscal damage and extrusion, laxity). Understanding the role alignment plays in OA progression is important because it modulates the effect of standard risk factors for knee OA progression including obesity, quadriceps strength, laxity, and stage of disease.
Risk Factors for the Development and Progression of Osteoarthritis Joint Instability or
Injury Leading to Mechanical, Biochemical
Damage to chondralsurface ACL (50 – 60% greater
risk of osteoarthritis) 1st CMC – UCL rupture Scapholunate
Presenter
Presentation Notes
Meniscus The meniscus has many functions in the knee, including load bearing, shock absorption, stability enhancement, and lubrication. The menisci transmit anywhere from 45% to 60% of the compressive loads in the knee. If the meniscus does not cover the articular surface that it is designed to protect because of change in position, or if a tear leaves it unable to resist axial loading, it does not perform this role. The absence of a functioning meniscus increases peak and average contact stresses in the medial compartment of the knee in a range of 40% to 700%. Knee OA after meniscectomy-meniscal repair is traditionally considered a result of the joint injury that leads to the meniscectomy in the first instance and the increased cartilage contact stress caused by the loss of meniscal tissue. Meniscectomy is often accompanied by the onset of OA because of the high focal stresses imposed on articular cartilage and subchondral bone subsequent to excision of the meniscus. The studies that have explored the relationship between the meniscus and risk of disease progression in OA provide a clear indication of the risk inherent with damage to this vital tissue. Each aspect of meniscal abnormality (whether change in position or damage) (Fig. 5) had a major effect on risk of cartilage loss in OA. The intact and functional meniscus is clearly important to the preservation of joint integrity andprevention of further joint damage. In contrast, the meniscus plays a much smaller role in symptom genesis. An unfortunate consequence of the frequent use of MR imaging in clinical practice is the frequent detection of meniscal tears. Degenerative lesions, described as horizontal cleavages, flap (oblique), or complex tears or meniscal maceration or destruction, are associated with older age and are almost universal in persons with OA. In asymptomatic subjects with a mean age of 65 years, a tear was found in 67% using MR imaging, whereas in patients with symptomatic knee OA, a meniscal tear was found in 91%. In the interests of preserving menisci an important cautionary note: meniscal tears are nearly universal in persons with knee OA and are unlikely to be a cause of increased symptoms. The penchant to remove menisci is to be avoided, unless there are symptoms of locking or extension blockade, at which point surgical treatment often becomes necessary. Meniscal Damage The absence of a functioning meniscus increases peak and average contact stresses in the medial compartment in a range of 40% to 700%. Biswal and colleagues studied 43 subjects anddemonstrated that the 26 subjects who had sustained meniscal tears had a higher average rate of progression of cartilage loss (22%) than thatseen in those who had intact menisci (14.9%;P %.018).
Visual Analog Scores before and after Knee BracingPain (mm) 7.9 vs 4.4 Activity level (%) 36 vs 61
References
Presenter
Presentation Notes
Nordesjo LO, Nordgren B, Wigren A, Kolstad K. Isometric strength and endurance in patients with severe rheumatoid arthritis or osteoarthrosis in the knee joints. A comparative study in healthy men and women. Scand J Rheumatol 1983;12:152-6. Ekdahl C, Andersson SI, Svensson B. Muscle function of the lower extremities in rheumatoid arthritis and osteoarthrosis. A descriptive study of patients in a primary health care district. J Clin Epidemiol 1989;42:947-54. O'Reilly S, Jones A, Doherty M. Muscle weakness in osteoarthritis. Curr Opin Rheumatol 1997;9:259-62. Hurley MV. The role of muscle weakness in the pathogenesis of osteoarthritis. Rheum Dis Clin North Am 1999;25:283-98. Hurley MV, Newham DJ. The influence of arthrogenous muscle inhibition on quadriceps rehabilitation of patients with early, unilateral osteoarthritic knees. Br J Rheumatol 1993;32:127-31.
Pathophysiology of Osteoarthritis OA represents abnormalities of any of the constituent tissues
of the synovial joint Breakdown of the dynamic equilibrium between breakdown
and repair Not a degenerative disease in that the cells are normal
Presenter
Presentation Notes
PATHPHYSIOLOGY OF OSTEOARTHRITIS The synovial joint is an organ, and OA represents failure of that organ and can be initiated by abnormalities arising in any of its constituent tissues. The disease occurs when they dynamic equilibrium between tissue breakdown and repair of the synovial tissues is overwhelmed. In OA, inflammatory changes are secondary and are caused by particulate and soluble breakdown of cartilage and bone. OA should not be considered a degenerative disease insofar as the cells are the cartiage and bone are normal and if the inciting breakdown mechanism is reduced can restore the damaged tissue to normal. The joint derangement in OA with subsequent diminished movement and chronic pain is progressive but the course of the disorder is often punctuated by exacerbations and remissions. The presence of small islands of fibrocartilage within the eburnated bone has already been described. These result from damage to the bone, often with exposure of the marrow. The marrow contains mesenchymal stem cells, multipotent cells with the ability to differentiate into any connective tissue. In the environment of OA they develop into small nodules of fibrocartilage. The changes within the osteoarthritic joint are not restricted to the articular cartilage. The disease process also affects the subchondral and marginal bone, and the synovium and the synovial fluid as well as the supporting connective tissue elements. Synovium In OA the synovium is thrown into finger like folds or filli. There is an increase in the number and size of synoviocytes inthe synovial membrane. In many cases, particularly early inthe course of the disease the synovium is inflamed, due to increased blood flow through the synovium and perivascular oedema associated with mast cell infiltrate. As disease advances there is progressive synovial fibrosis. Articular Cartilage An imbalance between matrix synthesis and matrix degeneration causes cartilage loss and inhibits self repair.
The Normal Anatomy of Synovial Joints
Presenter
Presentation Notes
The normal anatomy of synovial joints Synovial joints allow very complex movements by virtue of their structure. The bone ends are not in contact but are covered by hyaline cartilage. Motion between the two cartilages is facilitated by the lubricating action of synovial fluid. Unlike fibrous and cartilaginous joints, in which the stability of the joint comes from the bones being directly attached by the material forming the joint, diarthrodial joints gain their stability from a complex of structures surrounding the joint including the capsule ligaments and muscles. These structures prevent separation of the two bone ends. To give stability, a suitable spacer is required to bring the ligaments and capsule under tension. Cartilage acts as the spacer. This is made possible by its natural tendency to expand. Thus the two opposing forces of the cartilage trying to pull the bone apart and the capsule ligaments and muscle preventing it maintains stability. It follows that should the cartilage reduce in amount or the capsule and ligaments become lax, the joint will become unstable. Instability may lead to an increased risk of developing OA or be a consequence of it.
The Normal Anatomy Synovial Joints –Synovium
Presenter
Presentation Notes
Synovium and Synovial Fluid The space created by the capsule is lined in part by the cartilage over the bone ends and elsewhere by synovium. Synovium is a specialized lining tissue found in a number of sites where there is and interface between solid and liquid connective tissue matrices. It consists of an incomplete surface cell layer of synoviocytes made up of 2 cell populations: fibroblast-derived cells specialised to produce hyaluronans; and macrophoges that phagocytose debris shed from the cartilage and synovium into the synovial fluid. The synovial subintima (the layer of tissue immediately below the synovioctye layer) contains the only blood vessels and nerves within the lining tissues of the joint.
The Normal Anatomy of Synovial Joints – Articular Cartilage
Presenter
Presentation Notes
Articular Cartilage covers the bone ends of synovial joints. It is made up of 2 distinct layers, a relatively thick outer layer consisting of non mineralised cartilage, and a relatively thin inner layer consisting of calcified cartilage at the interface between the cartilage and the cortex-like bone plate on which the cartilage sits, and to which it is attached by collagen fibres. The non-mineralised cartilage has 2 zones. There is a thin outer zone in which the cells are flattened and the collagen fibres are running paralllel toot he srface and the main body of the cartilage in which the chondrocytes are rounded the collagen fibres run at right angels to the surface and the matrix is rich in proteglycans. Chondrocytes usually lead a solitar existence within spaces in the matrix called lacunae. They obtain nutrients and chemical messages by molecular diffusion and load induced bule transport through the extracellular matrix. The lacunae have a complex lining comsisting of a number of specialised molecules including type 4 collagen which effectively surrounds them.
Changes to the Articular Cartilage Loss of chondrocytes Matrix degeneration
Presenter
Presentation Notes
Articular Cartilage An imbalance between matrix synthesis and matrix degeneration causes cartilage loss and inhibits self repair. Death of chondrocytes It is affected by age and frequently lasts a lifetime but can be injured or destroyed via a variety of chemical, mechanical or microbiological agents (Newman 1998). Degradation and destruction of the articular cartilage exposes the subchondal bone to stress and can lead to the pain and dysfunction of osteoarthritis.
What Causes the Pain
Pain
Social
Psychological Biological
Presenter
Presentation Notes
The structural determinants of pain and mechanical dysfunction in OA are not well understood, but are believed to involve multiple interactive pathways that are best framed in a biopsychosocial framework.
Physiotherapy and OA Prevention and Management Modifiable Risk Factors Impact Loading Obesity Muscle strength Future injury Attitudes
Non-modifiable Risk Factors Previous Injury Joint Dysplasia Gender Age
Modifiable Risk Factors – Injury Risk ACL incidence reduced by 85 – 90% in several studies by use
of a special preventative program
Presenter
Presentation Notes
The key potentially modifiable risk factors for the development of OA include injury, obesity, and occupational and sporting overuse. In the female sporting population it has been shown that the incidence of ACL injuries can be reduced by approximately 90% with a preventative exercise program Is Physical Activity a Risk Factor for Primary Knee or Hip Replacement Due to Osteoarthritis? A Prospective Cohort Study YUANYUAN WANG, JULIE ANNE SIMPSON, ANITA E. WLUKA, ANDREW J. TEICHTAHL, DALLAS R. ENGLISH, GRAHAM G. GILES, STEPHEN GRAVES and FLAVIA M. CICUTTINI + Author Affiliations From the Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Alfred Hospital, Melbourne; Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of Population Health, University of Melbourne, Carlton; Cancer Epidemiology Centre, The Cancer Council Victoria, Carlton; Baker Heart and Diabetes Research Institute, Melbourne; Department of Orthopaedic Surgery, University of Melbourne, Royal Melbourne Hospital, Melbourne; and the AOA National Joint Replacement Registry; Discipline of Public Health, School of Population Health and Clinical Practice, University of Adelaide, Adelaide, Australia. Y. Wang, MD, PhD, Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Alfred Hospital; J.A. Simpson, PhD, Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of Population Health, University of Melbourne, Cancer Epidemiology Centre, The Cancer Council Victoria; A.E. Wluka, FRACP, PhD, Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Alfred Hospital, Baker Heart and Diabetes Research Institute; A.J. Teichtahl, MBBS (Hons), B. Physio (Hons), Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Alfred Hospital; D.R. English, PhD, Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of Population Health, University of Melbourne, Cancer Epidemiology Centre, The Cancer Council Victoria; G.G. Giles, PhD, Cancer Epidemiology Centre, The Cancer Council Victoria; S. Graves, FRACS, PhD, Department of Orthopaedic Surgery, University of Melbourne, Royal Melbourne Hospital; AOA National Joint Replacement Registry; Discipline of Public Health, School of Population Health and Clinical Practice, University of Adelaide; F. Cicuttini, FRACP, PhD, Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Alfred Hospital. Address correspondence to Prof. F. Cicuttini, Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Alfred Hospital, Melbourne, VIC 3004, Australia. E-mail: [email protected] Abstract Objective. To estimate prospectively any association between measures of physical activity and the risk of either primary knee or hip replacement due to osteoarthritis (OA). Methods. Eligible subjects (n = 39,023) were selected from participants in a prospective cohort study recruited 1990–1994. Primary knee and hip replacement for OA during 2001–2005 was determined by linking the cohort records to the National Joint Replacement Registry. A total physical activity level was computed, incorporating both intensity and frequency for different forms of physical activity obtained by questionnaire at baseline attendance. Results. There was a dose-response relationship between total physical activity level and the risk of primary knee replacement [hazards ratio (HR) 1.04, 95% CI 1.01–1.07 for an increase of 1 level in total physical activity]. Although vigorous activity frequency was associated with an increased risk of primary knee replacement (HR 1.42, 95% CI 1.08–1.86) for 1–2 times/week and HR 1.24 (95% CI 0.90–1.71) for ≥ 3 times/week), the p for trend was marginal (continuous HR 1.08, 95% CI 1.00–1.16, p = 0.05). The frequency of less vigorous activity or walking was not associated with the risk of primary knee replacement, nor was any measure of physical activity associated with the risk of primary hip replacement. Injury: Injury to a joint has long been recognised as a risk factor, and is the most important modifiable risk factor for knee OA in men. Meniscal and cruciate injuries increase the risk of subsequent OA development by 5 – 10 times, with 40 – 60% of long term study participants having OA changes by the age of 20 years. It is said that major injury ages the knee by 30 years. Although surgical repair is widely undertaken and appears to be associated with reduced pain and improved function in the short to medium term, longer studies indicate that this may not be as protective as once thought, with similar proportions of patients going on to develop OA. It has been suggested that the level of proteases released at the time of injury stay elevated and tip the balance of the chondrocyte and articular cartilage towards degeneration rather than repair. Occupational overuse: Occupational overactivity perhaps thought overuse and frequent minor injury has long been recognised as a risk factor for OA. A number of studies have shown a consistent association between hip osteoarthritis an farming in men with agricultural workers who were active for 10 years having double the risk of those working 2 years. Combinations of risk factors: These compound the risk and this is prarticularly evident with the interaction between occupational knee bending and obesity with risk increased 10 – 15 times and between age and injury to the knee. Nutritional Factors: such as low antioxidant, vitamin c and vitamin d intake, have been shown in observational studies the be associated with the risk of radiological progression of OA and knee pain. However using dietary intake of antioxidants or vitamins has not been shown to slow progression or modify symptoms.
Treatment
Presenter
Presentation Notes
· Physical therapy is effective in treatment of OA. Both strengthening and aerobic conditioning exercises reduce pain and improve function. Transcutaneous electrical nerve stimulation (TENS) reduces pain, cryotherapy improves function, and low level laser therapy reduces pain and improves function. · Psychological management using cognitive-behavioral therapy reduces pain, with effects that are maintained through a 6-month follow-up. Ref (IASP)
OA Prevention and Management Some of the symptoms come from changes to the synovium,
bone and nerves Medical treatment
Much of the pathology comes from degeneration in the articular cartilage Irreversible but can be slowed
Much of the pain comes from the subchondral bone Partly reversible
Much of the loss of range comes from either the pain or from the periarticular soft tissues This can be improved with an exercise program