Osteoarthritis is a chronic degenerative disorder of synovial joints in which there is progressive softening and erosion/disintegration of the articular cartilage. In the presentation, I will deal in detail about the condition in every dimension with the most recent evidence.
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
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.
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
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
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.
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
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.)
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
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
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
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.
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.
The prognosis of any hip preservation surgery is improved
when it is done in patients with lower Tönnis grades.
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.
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
Thumb-base OA: prominence and "squaring" of the thumb base, due to osteophyte formation and subluxation at the first CMC joint.
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.
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.
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.
Patient with right hip OA, showing fixed flexion and external rotation deformity.
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.
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.
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.
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),
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.