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OSTEOARTHRITIS
PRESENTED BY:
Dr. Aryan
(Anish Dhakal)
Components of
Synovial Joint
Articular cartilage
Subchondral bone
Synovial membrane
Synovial fluid
Joint capsule
Synovial Joint
Joint Stability
It is the most common joint disease
It is a chronic degenerative disorder of synovial joints in
which there is progressive softening and erosion/disintegration
of articular cartilage
a frequent, if not inevitable, part of aging
Osteoarthritis
Prevalence
More prevalent in high income countries comparatively
25% with osteoarthritis have multiple joints involvement
Prevalence
1% < 30 years of age
0ver 50%  >60 years of age
80% over 80 years of age have radiographic evidence
Risk Factors for Osteoarthritis
Age (strongest predictor)
Gender (females are more prone)
Genetics (no single gene implicated)
Joint injury (post traumatic OA)
Anatomic factors (joint shape and alignment)
Obesity (weight bearing joints)
Lifestyle (occupational, higher paced physical activity)
Smoking, muscle weakness, physical activity, bone density, etc.
Pathophysiology of Osteoarthritis
formerly considered to be simply a degenerative "wear and
tear" process and therefore often misnamed as degenerative
joint disease (an absolute misnomer)
Pathogenesis of OA is much more complex
"-itis" is indicative of an inflammatory process is actually
correct
Destruction and loss of the articular cartilage is a central
component of OA, all joint tissues are affected in some way
8
9
Pathophysiology
Morphology
At early OA, water content of matrix increases and
concentration of proteoglycans decreases
Proteoglycan content of the cartilage matrix
provides turgor and elasticity
Vertical and horizontal fibrillation and
cracking of the matrix
Eventually chondocyte die and
full thickness of cartilage are
sloughed.
Pathology
1. Eburnated articular surface
2. Subchondral cyst
3. Residual articular cartilage
Osteoarthritic Changes
17
Primary Osteoarthritis
 more common
 occurs in joint de novo
 occurs in old age
 mainly in weight bearing joints (knee, hip)
Secondary Osteoarthritis
 there is underlying primary disease of joint
 occurs in any age after adolescence
 occurs mainly in the hip
Classification
Localized OA (Monoarticular or Pauciarticular)
Classic form of OA
Pain & dysfunction of one or more large weight bearing joints
Nodal OA, Hip OA, Knee OA
Generalized OA (Polyarticular)
Most common form of OA
Erosive OA (Rapidly Destructive OA)
Rapid progression of bone destruction occurs
Occurs in elderly women
Associated with deposition of calcium pyrophosphate crystals
Clinical Variants of Osteoarthritis
21
Signs and Symptoms
Primary symptoms of osteoarthritis (OA) are joint pain,
stiffness, and locomotor restriction
On clinical grounds:
Persistent usage-related joint pain in one or few joints
Age ≥ 45 years
Morning stiffness ≤ 15 minutes
Imaging and laboratory investigations are reserved for patients
presenting with atypical symptoms and signs
Usually a middle aged women who
presents with pain, swelling &
stiffness of the finger joints
The following joints are affected at
almost same time:
1st carpometacarpal joint
Big toe
Meta-tarsophalangeal
Knee joints
Lumbar facet joints
Generalized Osteoarthritis
Progressive Vs Non-progressive
Heberden’s & Bouchard’s nodes
(Osteophytes)
Clinical Findings
29
Thumb-base OA: prominence and "squaring" of the thumb base: Osteophyte formation
and subluxation at the first CMC joint
30
Erosive hand OA: marked radial deviation and fixed flexion deformity in the left middle PIP joint, radial
deviation with restriction in the index PIP joint, and bony swelling
31
Unilateral knee OA: swollen left knee with varus and fixed flexion deformity history of knee trauma. On
palpation, there was marked crepitus, restricted flexion, bony swelling, and a small effusion.
32
Right hip OA with painful restriction with internal rotation in flexion. “Tight-pack" position for the hip (when
the capsule is at its tightest) and is the first movement to be affected.
33
Patient with right hip OA, showing fixed flexion and external rotation deformity
Investigations
 Serum Uric acid and RF to rule out specific disorders.
 Radionuclide scanning with 99MTc-HDP: increased activity over subchondral regions: increased vascularity and new
bone formation
X-ray Findings
38
Complete loss of the articular cartilage at all four DIP joints, large osteophytes, and ankylosis of the DIP joint
of the middle finger
Differential Diagnosis
Rheumatoid arthritis (symmetric, atrophic rather than hypertrophic arthritis)
Psoriatic arthritis (may be in one finger as dactylitis, and characteristic nail changes are usually present)
Avascular necrosis (articular cartilage loss precedes bone destruction in OA)
Crystalline arthritis (urate or CPP crystals in synovial fluid, tophi on imaging in gout)
Hemochromatosis (targets the MCP joints and wrists, predominates in men, squared-off bone ends and
hook-like osteophytes in the MCP joints)
Infectious arthritis : RA, Ankylosing spondylitis, Reiter disease (inflammatory signs effusion, increased
warmth, erythema), culturing the pathogen from the synovial fluid or from the blood
Diffuse Idiopathic Skeletal Hyperostosis (bony spurs in pelvic apophyses and vertebral column, usually
asymptomatic)
Soft tissue abnormalities (bursitis, tendinitis, enthesitis, etc.)
Depends on:
Joint involved
Age of patient
Patient’s functional needs
Management of Osteoarthritis
Pain (5 items)
Stiffness (2 items)
Physical Function (17 items)
None (0), Mild (1), Moderate (2), Severe (3), and Extreme (4)
0-20 for Pain, 0-8 for Stiffness, and 0-68 for Physical Function
Activities of daily living, functional mobility, gait, general health, quality of life
 Symptoms characteristically wax and wane, and pain may
subside spontaneously for long periods
 Some forms of OA actually become less painful with the
passage of time and the patient may need no more than
reassurance and a prescription for pain killers
 At the other extreme, the recognition (from serial x-rays) that
the patient has a rapidly progressive type of OA may warrant
an early move to reconstructive surgery before bone loss
compromises the outcome of any operation
Management of Osteoarthritis
Symptomatic treatment
Tailored to the patient according to individual needs, goals,
and values and should be patient-centered, stall progress
Patient preferences for certain types of therapies should
also be assessed. Compliance must be assessed.
Principles:
maintain movement and muscle strength
protect the joint from ‘overload’
relieve pain
modify daily activities (quality of life)
Management of Osteoarthritis
Counseling (patient education)
Physical Therapy (massage, aerobic and muscle strengthening
exercises, local heat application)
Load Reduction
weight reduction in obese patients
wearing shock-absorbing shoes
avoiding activities like climbing stairs, standing and running or sitting
cross legged and squatting in knee osteoarthritis
braces and foot orthoses
Non Pharmacological Therapy
Pharmacological Therapy Most Recent Evidence
Topical NSAIDs Initial treatment one or few joints affected,
especially knee and/or hand OA
Topical capsaicin Use may be limited by common local side effects
Oral NSAIDs Inadequate symptom relief with topical NSAIDs,
patients with symptomatic OA in multiple joints,
and/or patients with hip OA (lowest dose, shortest
duration)
Duloxetine Contraindicated oral NSAIDs and for patients with
knee OA who have not responded satisfactorily to
other interventions
Intraarticular glucocorticoid Short duration of its effects (i.e. approximately four
weeks). Not recommended for regular use.
Opioids Strong analgesics. Potential side effects (e.g., nausea,
dizziness, drowsiness), especially for long-term use
and in the older adult population
46
Other Therapies (Uncertain Benefits)
Nutritional supplements such as glucosamine, chondroitin, vitamin D,
diacerein, avocado soybean unsaponifiables (ASU), and fish oil
Curcumin (active ingredient of turmeric) and/or Boswellia serrata
might be beneficial, but the data are limited
Insoles and footwear
Hyaluronans viscosupplementation weekly injection
Platelet-rich plasma (PRP)
Transcutaneous electrical nerve stimulation (TENS)
Acupuncture
Local heat
Progressive joint destruction, with increasing pain,
instability and deformity usually requires reconstructive
surgery
Realignment osteotomy (joint with deformities like high tibial
osteotomy for OA knee). Major part of articular cartilage is
still preserved. Dramatic pain relief.
Vascular decompression of subchondral bone
Redistribution of load towards less damaged part of the joint
Operative Modalities
Debridement
synovectomy, excision of osteophytes, removal of loose bodies,
chondroplasty, and removal of damaged menisci
painful and often requires 6 months of postoperative rehabilitation
Arthroscopic treatments of osteoarthritis of the knee include simple
lavage, debridement, and abrasion chondroplasty (less postoperative pain
and shorter rehabilitation)
Success rate about 70%, placebo effect is also evident
Arthroscopic debridement procedures cannot alter the natural
progression of osteoarthritis
Arthroscopic view of the removal of cartilaginous loose body
54
Dervin et al.: 126 arthroscopic debridement procedures done for OA knee
44% of patients had significant pain relief at 2 years after surgery
Three variables were significantly associated with improvements in symptoms:
(1) medial joint line tenderness
(2) positive Steinmann test (forced external and internal rotation of a knee flexed to 90 degrees and pain
that is referable to either joint line)
(3) an unstable meniscal tear identified at arthroscopy
Operative Modalities
Arthrodesis, still a reasonable choice if the stiffness
is acceptable and neighboring joints are not
compromised (small joints that are prone to OA, e.g.
the carpal and tarsal joints and the large toe
metatarsophalangeal joint)
Operative Modalities
Total joint arthroplasty (replacement) is reserved for patients with
severe symptomatic OA who have failed to respond to non
pharmacologic and pharmacologic management (intolerable
symptoms, marked loss of function and severe restriction of daily
activities)
Alternatives to total knee arthroplasty for selected patients with knee
OA include unicompartmental knee arthroplasty and knee osteotomy
Alternatives to total hip arthroplasty for selected patients with hip OA
include hemiarthroplasty, hip osteotomy, and perhaps, for a very
specific group, hip resurfacing
57
58
59
Capsular Herniation (Baker’s cyst)
Loose bodies (cartilage and bone fragments: intermittent locking)
Rotator cuff dysfunction (OA of AC joint: impingement, tendinitis
and cuff tears)
Spinal stenosis (lumbar apophyseal joints OA)
Spondylolisthesis (degenerative spondylolisthesis at L4/L5)
Complications of Osteoarthritis
Natural History and Prognosis
Great variability among individuals and among different phenotypes
Courses of pain and physical functioning have been found to be
predominantly stable
No single biochemical or imaging markers to predict progressive course
Predominantly characterized by minimum/slow rather than marked
worsening over time
Certain poor prognostic factors have been identified which include
higher pain intensity at baseline, presence of depressive symptoms,
presence of bilateral knee symptoms
References
Solomon L, Warwick D, Nayagam S. Apley’s system of orthopedics and fractures, 9th edition
Leticia Alle Deveza et al., Overview of the management of osteoarthritis, https://www.uptodate.com/contents/overview-of-the-
management-of-osteoarthritis
Michael Doherty et al., Clinical manifestations and diagnosis of osteoarthritis, https://www.uptodate.com/contents/clinical-
manifestations-and-diagnosis-of-osteoarthritis
Leticia Alle Deveza et al., Management of knee osteoarthritis, https://www.uptodate.com/contents/management-of-knee-osteoarthritis
Lyn March, AM et al., Epidemiology and risk factors for osteoarthritis, https://www.uptodate.com/contents/epidemiology-and-risk-
factors-for-osteoarthritis
Lisa A Mandl et al., Overview of surgical therapy of knee and hip osteoarthritis, https://www.uptodate.com/contents/overview-of-
surgical-therapy-of-knee-and-hip-osteoarthritis
Karine Louati et al., Comorbidities that impact management of osteoarthritis, https://www.uptodate.com/contents/comorbidities-that-
impact-management-of-osteoarthritis
Campbells Operative Orthopedics, 14th edition
Maheshwari J, Essential Orthopedics, 6th Edition
Review of Orthopedics, Mark D. Miller, 8th Edition
Osteoarthritis 2021 Updated Guidelines

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Osteoarthritis 2021 Updated Guidelines

  • 2. Components of Synovial Joint Articular cartilage Subchondral bone Synovial membrane Synovial fluid Joint capsule Synovial Joint
  • 4. It is the most common joint disease It is a chronic degenerative disorder of synovial joints in which there is progressive softening and erosion/disintegration of articular cartilage a frequent, if not inevitable, part of aging Osteoarthritis
  • 5. Prevalence More prevalent in high income countries comparatively 25% with osteoarthritis have multiple joints involvement Prevalence 1% < 30 years of age 0ver 50%  >60 years of age 80% over 80 years of age have radiographic evidence
  • 6. Risk Factors for Osteoarthritis Age (strongest predictor) Gender (females are more prone) Genetics (no single gene implicated) Joint injury (post traumatic OA) Anatomic factors (joint shape and alignment) Obesity (weight bearing joints) Lifestyle (occupational, higher paced physical activity) Smoking, muscle weakness, physical activity, bone density, etc.
  • 7. Pathophysiology of Osteoarthritis formerly considered to be simply a degenerative "wear and tear" process and therefore often misnamed as degenerative joint disease (an absolute misnomer) Pathogenesis of OA is much more complex "-itis" is indicative of an inflammatory process is actually correct Destruction and loss of the articular cartilage is a central component of OA, all joint tissues are affected in some way
  • 8. 8
  • 9. 9
  • 11. Morphology At early OA, water content of matrix increases and concentration of proteoglycans decreases Proteoglycan content of the cartilage matrix provides turgor and elasticity Vertical and horizontal fibrillation and cracking of the matrix Eventually chondocyte die and full thickness of cartilage are sloughed.
  • 12.
  • 14. 1. Eburnated articular surface 2. Subchondral cyst 3. Residual articular cartilage
  • 16.
  • 17. 17
  • 18. Primary Osteoarthritis  more common  occurs in joint de novo  occurs in old age  mainly in weight bearing joints (knee, hip) Secondary Osteoarthritis  there is underlying primary disease of joint  occurs in any age after adolescence  occurs mainly in the hip Classification
  • 19.
  • 20. Localized OA (Monoarticular or Pauciarticular) Classic form of OA Pain & dysfunction of one or more large weight bearing joints Nodal OA, Hip OA, Knee OA Generalized OA (Polyarticular) Most common form of OA Erosive OA (Rapidly Destructive OA) Rapid progression of bone destruction occurs Occurs in elderly women Associated with deposition of calcium pyrophosphate crystals Clinical Variants of Osteoarthritis
  • 21. 21
  • 22. Signs and Symptoms Primary symptoms of osteoarthritis (OA) are joint pain, stiffness, and locomotor restriction On clinical grounds: Persistent usage-related joint pain in one or few joints Age ≥ 45 years Morning stiffness ≤ 15 minutes Imaging and laboratory investigations are reserved for patients presenting with atypical symptoms and signs
  • 23.
  • 24. Usually a middle aged women who presents with pain, swelling & stiffness of the finger joints The following joints are affected at almost same time: 1st carpometacarpal joint Big toe Meta-tarsophalangeal Knee joints Lumbar facet joints Generalized Osteoarthritis
  • 26.
  • 27. Heberden’s & Bouchard’s nodes (Osteophytes)
  • 29. 29 Thumb-base OA: prominence and "squaring" of the thumb base: Osteophyte formation and subluxation at the first CMC joint
  • 30. 30 Erosive hand OA: marked radial deviation and fixed flexion deformity in the left middle PIP joint, radial deviation with restriction in the index PIP joint, and bony swelling
  • 31. 31 Unilateral knee OA: swollen left knee with varus and fixed flexion deformity history of knee trauma. On palpation, there was marked crepitus, restricted flexion, bony swelling, and a small effusion.
  • 32. 32 Right hip OA with painful restriction with internal rotation in flexion. “Tight-pack" position for the hip (when the capsule is at its tightest) and is the first movement to be affected.
  • 33. 33 Patient with right hip OA, showing fixed flexion and external rotation deformity
  • 34. Investigations  Serum Uric acid and RF to rule out specific disorders.  Radionuclide scanning with 99MTc-HDP: increased activity over subchondral regions: increased vascularity and new bone formation
  • 36.
  • 37.
  • 38. 38 Complete loss of the articular cartilage at all four DIP joints, large osteophytes, and ankylosis of the DIP joint of the middle finger
  • 39. Differential Diagnosis Rheumatoid arthritis (symmetric, atrophic rather than hypertrophic arthritis) Psoriatic arthritis (may be in one finger as dactylitis, and characteristic nail changes are usually present) Avascular necrosis (articular cartilage loss precedes bone destruction in OA) Crystalline arthritis (urate or CPP crystals in synovial fluid, tophi on imaging in gout) Hemochromatosis (targets the MCP joints and wrists, predominates in men, squared-off bone ends and hook-like osteophytes in the MCP joints) Infectious arthritis : RA, Ankylosing spondylitis, Reiter disease (inflammatory signs effusion, increased warmth, erythema), culturing the pathogen from the synovial fluid or from the blood Diffuse Idiopathic Skeletal Hyperostosis (bony spurs in pelvic apophyses and vertebral column, usually asymptomatic) Soft tissue abnormalities (bursitis, tendinitis, enthesitis, etc.)
  • 40.
  • 41. Depends on: Joint involved Age of patient Patient’s functional needs Management of Osteoarthritis
  • 42. Pain (5 items) Stiffness (2 items) Physical Function (17 items) None (0), Mild (1), Moderate (2), Severe (3), and Extreme (4) 0-20 for Pain, 0-8 for Stiffness, and 0-68 for Physical Function Activities of daily living, functional mobility, gait, general health, quality of life
  • 43.  Symptoms characteristically wax and wane, and pain may subside spontaneously for long periods  Some forms of OA actually become less painful with the passage of time and the patient may need no more than reassurance and a prescription for pain killers  At the other extreme, the recognition (from serial x-rays) that the patient has a rapidly progressive type of OA may warrant an early move to reconstructive surgery before bone loss compromises the outcome of any operation Management of Osteoarthritis
  • 44. Symptomatic treatment Tailored to the patient according to individual needs, goals, and values and should be patient-centered, stall progress Patient preferences for certain types of therapies should also be assessed. Compliance must be assessed. Principles: maintain movement and muscle strength protect the joint from ‘overload’ relieve pain modify daily activities (quality of life) Management of Osteoarthritis
  • 45. Counseling (patient education) Physical Therapy (massage, aerobic and muscle strengthening exercises, local heat application) Load Reduction weight reduction in obese patients wearing shock-absorbing shoes avoiding activities like climbing stairs, standing and running or sitting cross legged and squatting in knee osteoarthritis braces and foot orthoses Non Pharmacological Therapy
  • 46. Pharmacological Therapy Most Recent Evidence Topical NSAIDs Initial treatment one or few joints affected, especially knee and/or hand OA Topical capsaicin Use may be limited by common local side effects Oral NSAIDs Inadequate symptom relief with topical NSAIDs, patients with symptomatic OA in multiple joints, and/or patients with hip OA (lowest dose, shortest duration) Duloxetine Contraindicated oral NSAIDs and for patients with knee OA who have not responded satisfactorily to other interventions Intraarticular glucocorticoid Short duration of its effects (i.e. approximately four weeks). Not recommended for regular use. Opioids Strong analgesics. Potential side effects (e.g., nausea, dizziness, drowsiness), especially for long-term use and in the older adult population 46
  • 47. Other Therapies (Uncertain Benefits) Nutritional supplements such as glucosamine, chondroitin, vitamin D, diacerein, avocado soybean unsaponifiables (ASU), and fish oil Curcumin (active ingredient of turmeric) and/or Boswellia serrata might be beneficial, but the data are limited Insoles and footwear Hyaluronans viscosupplementation weekly injection Platelet-rich plasma (PRP) Transcutaneous electrical nerve stimulation (TENS) Acupuncture Local heat
  • 48.
  • 49.
  • 50. Progressive joint destruction, with increasing pain, instability and deformity usually requires reconstructive surgery Realignment osteotomy (joint with deformities like high tibial osteotomy for OA knee). Major part of articular cartilage is still preserved. Dramatic pain relief. Vascular decompression of subchondral bone Redistribution of load towards less damaged part of the joint Operative Modalities
  • 51.
  • 52. Debridement synovectomy, excision of osteophytes, removal of loose bodies, chondroplasty, and removal of damaged menisci painful and often requires 6 months of postoperative rehabilitation Arthroscopic treatments of osteoarthritis of the knee include simple lavage, debridement, and abrasion chondroplasty (less postoperative pain and shorter rehabilitation) Success rate about 70%, placebo effect is also evident Arthroscopic debridement procedures cannot alter the natural progression of osteoarthritis
  • 53. Arthroscopic view of the removal of cartilaginous loose body
  • 54. 54 Dervin et al.: 126 arthroscopic debridement procedures done for OA knee 44% of patients had significant pain relief at 2 years after surgery Three variables were significantly associated with improvements in symptoms: (1) medial joint line tenderness (2) positive Steinmann test (forced external and internal rotation of a knee flexed to 90 degrees and pain that is referable to either joint line) (3) an unstable meniscal tear identified at arthroscopy
  • 55. Operative Modalities Arthrodesis, still a reasonable choice if the stiffness is acceptable and neighboring joints are not compromised (small joints that are prone to OA, e.g. the carpal and tarsal joints and the large toe metatarsophalangeal joint)
  • 56. Operative Modalities Total joint arthroplasty (replacement) is reserved for patients with severe symptomatic OA who have failed to respond to non pharmacologic and pharmacologic management (intolerable symptoms, marked loss of function and severe restriction of daily activities) Alternatives to total knee arthroplasty for selected patients with knee OA include unicompartmental knee arthroplasty and knee osteotomy Alternatives to total hip arthroplasty for selected patients with hip OA include hemiarthroplasty, hip osteotomy, and perhaps, for a very specific group, hip resurfacing
  • 57. 57
  • 58. 58
  • 59. 59
  • 60. Capsular Herniation (Baker’s cyst) Loose bodies (cartilage and bone fragments: intermittent locking) Rotator cuff dysfunction (OA of AC joint: impingement, tendinitis and cuff tears) Spinal stenosis (lumbar apophyseal joints OA) Spondylolisthesis (degenerative spondylolisthesis at L4/L5) Complications of Osteoarthritis
  • 61. Natural History and Prognosis Great variability among individuals and among different phenotypes Courses of pain and physical functioning have been found to be predominantly stable No single biochemical or imaging markers to predict progressive course Predominantly characterized by minimum/slow rather than marked worsening over time Certain poor prognostic factors have been identified which include higher pain intensity at baseline, presence of depressive symptoms, presence of bilateral knee symptoms
  • 62. References Solomon L, Warwick D, Nayagam S. Apley’s system of orthopedics and fractures, 9th edition Leticia Alle Deveza et al., Overview of the management of osteoarthritis, https://www.uptodate.com/contents/overview-of-the- management-of-osteoarthritis Michael Doherty et al., Clinical manifestations and diagnosis of osteoarthritis, https://www.uptodate.com/contents/clinical- manifestations-and-diagnosis-of-osteoarthritis Leticia Alle Deveza et al., Management of knee osteoarthritis, https://www.uptodate.com/contents/management-of-knee-osteoarthritis Lyn March, AM et al., Epidemiology and risk factors for osteoarthritis, https://www.uptodate.com/contents/epidemiology-and-risk- factors-for-osteoarthritis Lisa A Mandl et al., Overview of surgical therapy of knee and hip osteoarthritis, https://www.uptodate.com/contents/overview-of- surgical-therapy-of-knee-and-hip-osteoarthritis Karine Louati et al., Comorbidities that impact management of osteoarthritis, https://www.uptodate.com/contents/comorbidities-that- impact-management-of-osteoarthritis Campbells Operative Orthopedics, 14th edition Maheshwari J, Essential Orthopedics, 6th Edition Review of Orthopedics, Mark D. Miller, 8th Edition

Notas do Editor

  1. Articular cartilage has an important role in distributing and dissipating the forces associated with joint loading. When it loses its integrity these forces are increasingly concentrated in the subchondral bone. The result: focal trabecular degeneration and cyst formation, as well as increased vascularity and reactive sclerosis in the zone of maximal loading.
  2. Osteoarthritis involves all of the joint tissues including the menisci in the knee, ligaments, synovium, articular cartilage, and bone. Damage to the menisci and ligament tears not only alter joint mechanics but, along with the inflamed synovium (synovitis), produce proinflammatory factors (cytokines and chemokines) and matrix-degrading enzymes (eg, matrix metalloproteinases [MMPs]). These factors are also produced by chondrocytes and serve to promote joint tissue destruction.
  3. The prognosis of any hip preservation surgery is improved when it is done in patients with lower Tönnis grades.
  4. Altman R et al. reported crepitus had a sensitivity of 89%, specificity of 58%, positive likelihood ratio of 3.0 and negative likelihood ratio of 0.2 for predicting osteoarthritis of the knee.
  5. Heberden's nodes (thumb, middle, ring, and little finger DIP joints), Bouchard's nodes (index finger PIP joint), and lateral radial/ulnar deviation (index PIP joint, ring DIP joint) in the left hand of a person with nodal OA. A number of studies have implicated bony osteophyte growth as the principal cause of Heberden’s and Bouchard’s nodes.11 Other contributing factors or theories include: • genetic predisposition • endochrondral ossification of hypertrophied cartilage as a result of chronic osteoarthritic changes12 • traction spurs growing in tendons in response to excessive tension and repetitive strain
  6. Thumb-base OA: prominence and "squaring" of the thumb base, due to osteophyte formation and subluxation at the first CMC joint.
  7. Erosive hand OA with marked radial deviation and fixed flexion deformity in the left middle PIP joint, radial deviation with restriction in the index PIP joint, and bony swelling of both fingers. Note the absence of Heberden's nodes.
  8. Unilateral knee OA: swollen left knee with varus and fixed flexion deformity in a 63-year-old man with a prior history of knee trauma. On palpation, there was marked crepitus, restricted flexion, bony swelling, and a small effusion. The cruciates were intact, but there was minor varus/valgus instability on stress testing.
  9. Patient with right hip OA, showing painful restriction with internal rotation in flexion. This is the "tight-pack" position for the hip (when the capsule is at its tightest) and is the first movement to be affected.
  10. Patient with right hip OA, showing fixed flexion and external rotation deformity.
  11. This plain film demonstrates complete loss of the articular cartilage at all four DIP joints, large osteophytes, and ankylosis of the DIP joint of the middle finger.
  12. For patients already on oral NSAIDs, topical therapies are generally not recommended because they are unlikely to provide additional pain relief. Gel measurements from tubes are approximate. ¶ Pain relief usually begins within the first week of treatment, and full effect is seen with regular application over approximately four weeks. Topical capsaicin should not come in contact with mucous membranes, abraded skin, eyes, or genital areas.
  13. Fairbank's changes describe the radiological changes observed on an AP radiograph of the knee after meniscectomy. Fairbank identified significant changes including squaring of the femoral condyles, peak eminences, ridging, and joint space narrowing.
  14. positive Steinmann test (forced external and internal rotation of a knee that is flexed to 90 degrees and recording pain that is referable to either joint line),
  15.  Patients with moderate to severe knee OA have persistent pain, which significantly impairs functionality, activity participation, and quality of life. ¶ If the patient has OA limited to the knees and hands, a trial of topical NSAIDs is reasonable before advancing to oral NSAIDs (if not otherwise contraindicated). Δ Assess the need for a proton pump inhibitor if increased risk for gastrointestinal side effects. ◊ Intraarticular glucocorticoid injections are not routinely recommended because the pain relief is mild to moderate and is short-lived.