Osteoarthritis of the Knee in the Active Adult: A Primary Care . Ppt Powerpoint Presentation slides Anonymous Medical Slideshow THE KNEE IN PRIMARY CARE

Osteoarthritis of the Knee in the Active Adult: A Primary Care .

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Slide 1 :

Osteoarthritis of the Knee in the Active Adult: A Primary Care Sports Medicine Approach Francis G. O’Connor, MD, MPH Department of Military and Emergency Medicine Medical Director, Consortium for Health and Military Performance Uniformed Services University of the Health Sciences

Slide 2 :

Clinical Questions? What is the definition of osteoarthritis? Are there guidelines available to assist with diagnosis and management? What’s constitutes a good diagnostic assessment? Does weight loss really make a difference? Do oral meds (Tylenol, NSAIDs, steroids) help or hurt? What about the role of steroid injections? What about braces, and heel wedges? Are the chondroprotective agents, glucosamine and intra-articular hyaluronic acid indicated, if at all? What’s the role of exercise as a treatment? and as a cause? Who needs to see an orthopedic surgeon, and when? Matt Foley, Motivational Speaker

Slide 3 :

Objectives Review the Definition and Epidemiology of Osteoarthritis Review the Diagnostic Criteria for Osteoarthritis of the Knee Discuss the Evaluation of the Active Adult with Knee Osteoarthritis Discuss the Management of the Active Adult with Knee Osteoarthritis Matt Foley, Motivational Speaker

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Case Presentation Tom is a 51 y/o male, retired Army Colonel, with a diagnosis of right knee osteoarthritis. History of being a collegiate wrestler, as well as a recreational runner with completion of seven marathons. History of right knee trauma 30 yrs ago. Currently with difficulty walking 18 holes of golf. Imaging with mild joint line narrowing and subchondral sclerosis No meniscal tear by MRI Mild to moderate tibia varum

Slide 5 :

Case Presentation A former classmate is recommending a high tibial osteotomy and autologous cartilage transplant implantation. He wants your advice on what might be effective non-operatively prior to considering a surgical intervention. Most importantly…he’s your golf partner!

Slide 6 :

What’s the Epidemiology and Definition of Osteoarthritis?

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Epidemiology Osteoarthritis is the most common form of arthritis in the United States. Radiographic evidence of osteoarthritis is present in the majority of people over age 65; 80% of those over 75. Approximately 11% of those over 65 have symptomatic osteoarthritis of the knee.

Slide 8 :

Definition of Osteoarthritis “Osteoarthritis (OA) is a degenerative joint disease, occurring primarily in older persons, characterized by erosion of the articular cartilage, hypertrophy of bone at the margins (i.e., osteophytes), subchondral sclerosis, and a range of biochemical and morphologic alterations of the synovial membrane and joint capsule. Pathologic changes in the late stages of OA include softening, ulceration, and focal disintegration of the articular cartilage; synovial inflammation also can occur.” Harris: Kelley's Textbook of Rheumatology, 7th ed. “Despite its prevalence, the precise etiology, pathogenesis, and progression of OA remain beyond our understanding…”

Slide 9 :

What is Hyaline Cartilage? Functions as a low-friction, wear-resistant tissue designed to bear and distribute loads. Low metabolic activity; no blood supply, no lymphatic drainage, no nerve supply, poor regenerative capacity. Site primarily affected by degenerative osteoarthritis.

Slide 10 :

Hyaluronic Acid Core Protein-Aggrecan Chondroitin Sulfate Chain Link Glycoprotein What is Hyaline Cartilage composed of? Chondrocytes, water, proteoglycans, and type 2 collagen. Chondrocyte metabolism is responsible for the extra-cellular matrix.

Slide 11 :

What Causes the Pain? Cartilage is aneural, so the joint pain must arise from other structures: Subchondral bone: microfractures, meduallary hypertension with bone angina Osteophytes: stretching of nerve endings in the periosteum Ligaments: stretch Joint capsule: inflammation, distention Synovium: inflammation Periarticular muscle: spasm

Slide 12 :

What Causes the Destruction? Biomechanical Forces? OA is mechanically driven Biochemical Forces? Chemically mediated Cytokine activation

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Associated Risk Factors Risk Factors and Possible Causes: Age Female versus Male sex Obesity Lack of Osteoporosis Occupation Sports Activities Prior injury Muscle weakness Propioceptive deficits Acromegaly Calcium crystal deposition disease Up-To-Date 2005 Risk Factors for and Possible Causes of Osteoarthritis

Slide 14 :

Clinical Features Joints Affected: Hand interphalangeal joints, spine, knees, hips, and first MTP. Symptoms:joint pain worsens with use and is alleviated with rest, stiffness, crepitus, functional impairment. Signs: limp, deformity, alteration in joint shape, muscle atrophy, weakness, increased effusion, crepitus, restricted movement, joint line and peri-articular tenderness, bony swelling, soft tissue swelling.

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Clinical Features No primary extra-articular manifestations. Usually only one or a few joints are symptomatic at a given time. Slow evolution of symptoms and structural damage. Strong association with age – uncommon before middle age. Poor correlation between severity of symptoms, disability and structural damage. Symptoms and signs related primarily to joint damage, rather than to inflammation.

Slide 16 :

Radiographic Appearance Radiographic Criteria: Loss of joint space Subchondral sclerosis or cyst formation Presence of new bone formation or osteophytes Bone demineralization, osteopenia, extra-articular changes would suggest other diagnoses.

Slide 17 :

Synovial Fluid Analysis

Slide 18 :

1986 Criteria for Classification of Idiopathic Osteoarthritis (OA) of the Knee R. Altman, E. Asch, D. Bloch, G. Bole, D. Borenstein, K. Brandt, et al. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the knee. Arthritis Rheum 1986;29:1039--1049. Clinical and Laboratory + at least 5 of 9 - age >50 - stiffness <30 minutes - crepitus - bony tenderness - bony enlargement - no palpable warmth - ESR <40 mm/hr - RF <1:40 - SF OA UpToDate 2005 Diagnosing Osteoarthritis

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Radiographic Classification Kellgren and Lawrence grading system of OA of the knee. Grades: 0 (none), 1 (doubtful) 2 (minimal) 3 (moderate) 4 (severe)

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Inflammatory vs. Non-Inflammatory Up-To-Date 2005 Non-inflammatory OA: pain and disability related complaints. Exam demonstrates tenderness, bony prominence and crepitus. Inflammatory OA: complain of articular swelling, morning stiffness lasting more than 30 minutes, and night pain. Effusion and warmth noted on examination, as well as synovitis on examination. Both can be polyarticular, pauciarticular, or monoarticular. No specific comment on SF analysis

Slide 21 :

Functional Classification System International Classification of Functioning, Disability and Health Category 1: Mild Osteoarthritis Modest discomfort, with little or no difficulty with quality of life Category 2: Moderate Osteoarthritis Significant pain and discomfort, with impairment in normal activities or participation in aspects of life important to that individual. Category 3: Moderate with other Health Problems Same as above, combined with significant medical co-morbidities. Category 4: Severe Osteoarthritis Pain with sleep and of such severity to prevent many activities of daily living.

Slide 22 :

Are there Guidelines available to assist with Diagnosis and Management?

Slide 23 :

Current Guidelines American College of Rheumatology www.rheumatology.org American Academy of Orthopedic Surgery www.aaos.org European League Against Rheumatism www.eular.org

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American College of Rheumatology American College of Rheumatology Subcommittee on Osteoarthritis Guidelines. Recommendations for the medical management of osteoarthritis of the hip and knee: 2000 update. Arthritis and Rheum 2000;43(9):1905-15.

Slide 25 :

American Academy of Orthopedic Surgery www.aaos.org chart_oakn.pdf Osteoarthritis of the Knee A Compendium of Evidence-based Information and Resources

Slide 26 :

European League Against Rheumatism Propositions

Slide 27 :

Questions to be Answered Clinical predictors of the response to pharmacologic and non-pharmacologic interventions need to be determined. What are the long term effects of COX inhibition on joint tissues, primarily joint cartilage and bone? There is an urgent need to examine the efficacy and utility of surgical procedures. EULAR Recommendations 2000

Slide 28 :

What’s constitutes a good Diagnostic Assessment?

Slide 29 :

The History and Physical of the Patient with Osteoarthritis Goals of Therapy Education of the Patient Alleviate Pain Optimize Function Modify Progression Objectives: Confirm the diagnosis Identify risk factors Assess function Assess comorbidities Assess patient goals

Slide 30 :

Confirm the Diagnosis History Family history Disability Mechanical symptoms Physical Distribution Alignment Effusion Range of Motion Quadriceps Strength Extra-articular manifestations Radiographs Weight bearing 45 degree Flexion Synovial Fluid Crystals Labs Rheumatoid panel Risk Stratify ICF Model

Slide 31 :

Diagnostic Pitfalls Diagnostic Pitfalls Referred pain Pes anserine bursitis Neuropathy Radiculopathy Other joint with osteoarthritis Some other form of arthritis Rheumatoid Septic Gouty Secondary soft tissue rheumatism Enthesopathy Ligamentous instability Bursitis Other Avascular necrosis Tumor

Slide 32 :

Assess the Individual Patient Functional Ability WOMAC Pain Subscale Medical Co-Morbidities GI intolerance Neuropathy Thyroid disease Obesity Individual Patient Goals Exercise choice Weight loss Dr. St. Pierre Rule Osteoarthritis + Runner = Cyclist

Slide 33 :

Does Weight loss Really make a Difference?

Slide 34 :

Absolutely! For a woman of normal height, weight loss of only 5kg reduces the risk of OA by more than 50%. Estimated that substantial weight loss e.g. obese to overweight, or overweight to normal weight, could prevent 33% of OA in women and 20% in men. Felson et al: Obesity and knee osteoarthritis. Annals of Internal Medicine 1998.

Slide 35 :

Isn’t Weight Bearing Exercise Recommended? Yes…but… Obesity is currently felt to be the single most important modifiable risk factor for the development of osteoarthritis. Strong association with numerous cohort studies. Women in the highest tertile of BMI c/w women in the lowest tertile had an odds ratio of 8.57 for radiographic and symptomatic OA of the knee. Hart et al: The relationship of obesity, fat distribution and osteoarthritis in women in the general population: The Chingford study. Journal of Rheumatology 1993.

Slide 36 :

Do Oral Medications (Tylenol, NSAIDs) help or hurt?

Slide 37 :

Tylenol Is acetaminophen effective for Osteoarthritis? Is acetaminophen the drug of choice? Is it safe? Acetaminophen has clearly been demonstrated to be effective in the treatment of the pain of OA when c/w placebo, with a NNT of 3.6 for 50% pain reduction when using 1000mg. Acetaminophen is the drug of choice in both the ACR and EULAR guidelines. Acetaminophen has been demonstrated to be safe in doses up to 4gm/day.

Slide 38 :

Traditional NSAIDs Are NSAIDs more effective than acetaminophen? Are some NSAIDs more efficacious than others? Do I need to elevate the dosage to an “anti-inflammatory” range? Do NSAIDs destroy cartilage in the long term? Cochrane Review 1997: no evidence to assess clinical differences among the various NSAIDs. Decisions should be made upon safety, acceptability and cost. No…as OA is principally non-inflammatory NSAIDs should clearly be titrated for clinical effect. Consensus expert opinion and clinical data appear to state that in the treatment of mild to moderate osteoarthritis acetaminophen and NSAIDs have comparable efficacy. There is no reliable evidence in human models by clinical trials that NSAIDs are either chondroprotective or chondrodestructive.

Slide 39 :

COX2 Inhibitors What are those COX enzymes again? COX breaks down arachadonic acid into prostaglandins. COX1: responsible for normal physiologic processes like GI protection and platelet aggregation. COX2: involved in the inflammatory response. These new drugs are either called COX2 inhibitors or COX1 sparing. COX3 and so on are coming!

Slide 40 :

New FDA Recommendations April 6, 2005 The three COX2 agents are associated with an increased risk of serious adverse CV events c/w placebo. Data from large clinical trials do not demonstrate a significant increased CV risk of the COX2 agents over the non-selective NSAIDs. The COX2 agents reduce the incidence of GI ulcers visualized at endoscopy. Box warning label for all prescription NSAIDs including increased risk of CV events.

Slide 41 :

COX2 Inhibitors Celebrex is currently the only COX2 inhibitor on the market. Pfizer Recommendations: COX2 Candidates: High Risk for GI Complications Failure with Conventional NSAIDS Concomitant use of Cardioprotective ASA Of note…a COX2 and ASA has similar risk of GI complication, therefore a high risk individual requires anti-ulcer prophylaxis. (UpToDate 2005).

Slide 42 :

Issues With NSAIDs and COX2 Inhibitors: Gastrointestinal and Cardiovascular Risk, Concurrent Aspirin Use How should these medications be used with patients at risk for GI complications? How does concurrent ASA use effect need for GI prophylaxis? How does an NSAID affect the cardioprotective effect of ASA?

Slide 43 :

NSAIDs and Gastric Protection High risk identification: Age >65 years Anti-coagulant use Prior GI bleeding Use of oral steroids H. Pylori If history of GI bleed, test and treat If asymptomatic, consider “test and treat” Treatment options: NSAID and PPI NSAID and misoprostol Celecoxib UpToDate 2006

Slide 44 :

Issues With Aspirin Use Evidence (from CLASS) suggests that aspirin use, even in low doses, is a more important risk factor for the occurrence of upper GI events than was anticipated Patients taking low-dose aspirin for CV prophylaxis and who are at risk for upper GI ulcer complications should also receive GI mucosal protective therapy, irrespective of whether they are receiving COX-2 selective inhibitors Simon LS et al. (2002), J Rheumatol 29(7):1501-1510

Slide 45 :

FDA’s Conclusion Regarding Ibuprofen and ASA Cardioprotective effect of ASA, when used for secondary prevention of MI, could be minimized or negated A negative clinical impact on ASA’s cardioprotection is unlikely from an occasional dose of ibuprofen because the effect of ASA taken daily is long-lasting Ibuprofen given at least 30 minutes after immediate-release ASA or at least 8 hours before taking immediate-release ASA does not appear to interfere with ASA’s anti-platelet effect Available at: www.fda.gov/cder/drug/Infopage/ibuprofen/science_paper.htm. Accessed Oct. 29, 2006

Slide 46 :

Opioids Is there a role for opioid analgesia in osteoarhtritis? Is there a role for chronic therapy with opioid analgesics? Yes…all the guidelines and UpToDate recommend considering narcotic analgesia for acute exacerbations unresponsive to conventional therapy. Tramadol is specifically identified by the ACR as well as UpToDate as the initial agent of choice. Yes…some patients may require chronic therapy with opioids. ACR guidelines support opioid therapy when other treatments have failed or are not appropriate. American Pain Society guidelines for nonmalignant pain should be followed.

Slide 47 :

Making Sense of Oral Medications Up-to-Date 2005 Recommendations Continuous versus As Needed Preferable on a periodic basis in patients with non-inflammatory OA; continuous only if this regimen is inadequate. Medications normally take 2 to 4 weeks to assess; if inadequate, the dose should be increased. If not effective after 2 to 4 weeks, then another agent should be tried. If there is a history of GI disease, a selective COX2 inhibitor or a nonselective agent with anti-ulcer prophylaxis may be used. Opioids may be used for severe breakthrough pain, patients who have failed other therapies, and where surgery is not an option.

Slide 48 :

Use of Nonsteroidal Antiinflammatory Drugs An Update for Clinicians: A Scientific Statement From the American Heart Association Elliott M. Antman, MD; Joel S. Bennett, MD; Alan Daugherty, et al: Circulation. 2007;115:1634-1642.

Slide 49 :

Slide 50 :

What about the Role of Steroid Injections?

Slide 51 :

Steroid Injections -How they Might Work Mechanism of action is unknown, however: Inhibit accumulation of inflammatory cell lines Reduction of prostaglandin synthesis Inhibit leukocyte secretion from synovial cells Decrease interleukin secretion by the synovium Increase viscosity of synovial fluid

Slide 52 :

Steroid Injections Systemic corticosteroid therapy has no place in the treatment of osteoarthritis. Generally employed no more than 3 to 4 times per year secondary to risks of direct articular cartilage damage; however, some argue the steroid may prevent the biochemical degradation. Variable duration of activity modification after injection. Not clear who will benefit from a steroid injection; some authors recommend the patient with an effusion or acute synovitis.

Slide 53 :

Steroid Injections – The Evidence Cochrane review of intra-articular injections in the knee in osteoarthritis. The short-term benefit of IA corticosteroids in treatment of knee OA is well established, and few side effects have been reported. Longer term benefits have not been confirmed… “There is no clear objective evidence for intra-articular corticosteroid injections on the treatment of osteoarthritic or sports related injuries of the knee…” Snibbe, JC, Gambardella RA: Use of Injections for Osteoarthritis in Joints and Sports Activity. Clinics in Sports Medicine 24(2005); 83-91.

Slide 54 :

Who Deserves an Injection? AAOS Inflamed knees respond best to injections. Localized knee pain felt only with weight-bearing is less likely to respond. ACR Intraarticular glucocorticoid injections are of value in the treatment of acute knee pain in patients with, and may be particularly beneficial in patients who have signs of local inflammation with a joint effusion. EULAR Intra-articular injection of long acting steroid is indicated for acute exacerbation of knee pain, especially if accompanied by effusion

Slide 55 :

What about Braces, and Heel Wedges?

Slide 56 :

Braces and Heel Wedges Principal purpose of braces and wedges is to reduce pain, assist function, and possibly prevent disease progression. These goals are thought to principally be accomplished through changes or alterations of biomechanical force loads.

Slide 57 :

Heel Wedges Wedges are thought to assist patients with medial compartment osteoarthritis by mechanically decreasing the varus torque. Cochrane Review 2004: Limited evidence to support that a lateral heel wedge decreases concurrent NSAID utilization.

Slide 58 :

Braces Valgus or unloader braces are thought to assist patients with medial compartment osteoarthritis with a significant varus deformity. Cochrane Review 2004: Based on one brace study we conclude there is limited evidence that: a brace has additional beneficial effect (WOMAC, MACTAR, function tests) for knee osteoarthritis compared with medical treatment alone.

Slide 59 :

When are Chondroprotective Agents, like Glucosamine and Intra-Articular Hyaluronic Acid indicated, if at all?

Slide 60 :

Glucosamine Glucosamine sulfate and chondroitin sulfate are particularly popular treatments for osteoarthritis. Several early studies demonstrated that glucosamine was superior to placebo and comparable to NSAIDs for knee OA. (manufacturer supported) Other studies measuring changes in joint space narrowing suggested a “chondroprotective” effect against articular cartilage loss.

Slide 61 :

Glucosamine Sulfate How does it work? Studies of radiolabeled glucoasmine do demonstrate uptake in the joint articular cartilage. Thought to stimulate chondrocytes to make proteoglycans. Thought to possibly inhibit cartilage catabolic enzymatic activity. Some hypothesize the sulfate may be key to the effect. Real mechanism of action is largely unknown.

Slide 62 :

Glucosamine Cochrane Review 2005: WOMAC outcomes of pain, stiffness and function did not show a superiority of glucosamine over placebo for both Rotta and non-Rotta preparations of glucosamine. Glucosamine was as safe as placebo NIH multi-centered trial: Glucosamine and chondroitin alone or in combination did not reduce pain effectively in the overall group of patients Exploratory analyses suggest that the combination of glucosamine and chondroitin may be effective in the subgroup of patients with moderate-to-severe knee pain European trials that showed a benefit with glucosamine used as glucosamine sulfate; most of the American trials—including GAIT—used glucosamine hydrochloride Clegg DO et al. (2006), N Engl J Med 354(8):795-808

Slide 63 :

Glucosamine Using Glucosamine: Safe, however, questions exist as to adverse effects, purity and efficacy. Not recommended in patients with seafood allergy; chondroitin may have anticoagulant effect. No studies demonstrating consistent benefit of adding chondroitin. Trial of 1500 mg/d for 6 to 8 weeks is not unreasonable in an informed patient.

Slide 64 :

Hyalgan Synovial fluid is an ultrafiltrate of plasma modified by the addition of hyaluronic acid (HA), which is produced by the synovium. In osteoarthritis, the HA is decreased and compromised. Exogenous supplementation of intraarticular HA is thought to support changes in the character of synovial fluid.

Slide 65 :

Hyalgan What’s the Evidence? Cochrane Review 2005 Viscosupplementation is an effective treatment for OA of the knee with beneficial effects: on pain, function and patient global assessment; and at different post injection periods but especially at the 5 to 13 week post injection period. Questions? Is HA superior to corticosteroid injections or saline injections? Do HA injections result in lower utilization of NSAIDs?

Slide 66 :

Hyalgan Using Hyalgan: Indications: indicated for the treatment of osteoarthritis not responsive to non-pharmacologic measures and to simple analgesics. Requires sterile technique, remove joint effusion if present prior to injection. Three to five weekly injections recommended. Is it safe? No concern of inhibition of prostaglandins. Post-injection synovitis is described, and can last up to three weeks.

Slide 67 :

What’s the Role of Exercise as a Treatment? and as a Cause?

Slide 68 :

Does Exercise Cause Osteoarthritis? Multiple cross sectional studies have evaluated the prevalence of OA in groups engaged in regular exercise and demonstrated an increased risk: Wrestling (cervical spine, knee, elbows) Cycling (patellofemoral) Football (knees, feet, ankles) Boxing (metacarpals) Increased risk, however, studies with lack of suitable control groups. Longitudinal studies in runners have not demonstrated a consistent risk of arthritis. Studies do, however, consistently demonstrate that prior ligamentous or meniscal injury result in an increased risk for osteoarthritis.

Slide 69 :

Does Exercise Cause Osteoarthritis? Up-To-Date 2005 Neuroanatomically normal joints are at increased risk of developing osteoarthritis in the absence of exercise. Neuroanatomically normal joints are not at increased risk of developing osteoarthritis upon exposure to repetitive, low impact, recreational exercise. Neuroanatomically abnormal joints are at increased risk of developing osteoarthritis upon exposure to repetitive, low impact, recreational exercise. Neuroanatomically normal joints are at increased risk of developing osteoarthritis upon exposure to repetitive, high impact.

Slide 70 :

Am I going to make my Osteoarthritis Worse? Arthritis is the major reason that elderly individuals are not active or limit their activity. Several RCTs have shown that aerobic exercise can be effective in relieving symptoms of knee OA. Inactivity dramatically increases risk of cardiovacular morbidity and mortality. “It’s better to wear out than rust out.” Robert P. Nirschl, MD

Slide 71 :

Which Exercises help Manage Osteoarthritis? Cochrane Data Base 2005: Both high intensity and low intensity aerobic exercise appear to be equally effective in improving a patient's functional status, gait, pain and aerobic capacity for people with OA of the knee Land-based therapeutic exercise was shown to reduce pain and improve physical function for people with OA of the knee. There were insufficient data to provide useful guidelines on optimal exercise type or dosage. Supervised exercise classes appeared to be as beneficial as treatments provided on a one-to-one basis. Multiple studies have demonstrated that quadriceps strengthening exercises can increase strength and; Decrease dependency Improve function with ADLs Decrease pain.

Slide 72 :

Who needs to see an Orthopedic Surgeon, and When?

Slide 73 :

What about just cleaning up my knee, Doc? Classic Study: Mosely JB et al: A controlled trial of arthroscopic surgery for osteoarthritis of the knee. New England Journal of Medicine 2002. 180 pts randomly assigned to: Arthroscopic debridement Arthroscopic lavage Placebo surgery No significant benefit vs. placebo during 24 months of follow-up Most if not all of the effects of tidal irrigation can be attributed to the placebo effect

Slide 74 :

Indications for Arthroscopy Severe symptomatic OA that has failed to respond to non-surgical management. Evidence on clinical assessment of either: Loose bodies Mechanical symptoms: locking, giving way, or catching.

Slide 75 :

Indications for High Tibial Osteotomy Indications for osteotomy Age less than 60 years Unicompartmental arthritis 10 to 15 degrees of varus deformity on weightbearing radiographs Preoperative motion arc of at least 90 degrees Flexion contracture less than 15 degrees Ability and motivation to effectively and safely perform rehabilitation

Slide 76 :

Indications for Total Joint Replacement The main indication for total knee arthroplasty is for relief of pain associated with arthritis of the knee in patients who have failed non-operative treatments. American Academy of Orthopedics Up-To-Date 2005

Slide 77 :

So What’s a Primary Care Physician to Do? Do a good History and Physical Examination. Individualize the Patient. Non-pharmacologic therapy is the hallmark of treatment for Osteoarthritis. Exercise is always good…it’s the type that needs to be carefully determined. Pharmacologic therapy is adjunctive. Surgery is when all else has failed.

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Age; Female versus Male sex; Obesity; Lack of Osteoporosis; Occupation; Sports Activities; Prior in more Age; Female versus Male sex; Obesity; Lack of Osteoporosis; Occupation; Sports Activities; Prior injury; Muscle weakness; Propioceptive deficits; Acromegaly ... less

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