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4. • Osteoarthritis is non inflammatory degenerative condition of joints.
• Occurs due to
• uncoupling of balance between cartilage degeneration and regeneration,
• characterized by focal loss of cartilage with periarticular bone response,
• clinically presents as joint pain and crepitus,
• radiologically decreased joint space, osteophytes and a variety of deformities.
5. Epidemiology
• World wide:
• Prevalence in patients age 45 and older
• 5.9 and 13.5 percent in men
• 7.2 and 18.7 percent in women. (AAOS 2013)
• India :
• Prevalence of 22% to 39% in India.
• Prevalence of 28.7% (CP Pal et al. IJO 2016)
• Prevalence increases drastically with age(45% by the age of 65)
• 80% have limitations
6. CLASSIFICATION OF OSTEOARTHRITIS
PRIMARY OA
• More common than secondary OA
• Cause- Unknown
• Common in elderly population where there is no previous pathology.
• Its mainly due to wear and tear changes occurring in old ages mainly
in weight bearing joints.
7. SECONDARY OA
Due to factors such as :
• Trauma
• Malalignment.
• Post septic knee.
• Chondrocalcinosis.
• Synovial chondromatosis.
• Pigmented villonodular synovitis.
• Osteonecrosis.
8. Systemic risk factors
Multifactorial entity.
• Ethnicity: Knee osteoarthritis is more common in Asians.
• Age and sex: Prevalence increases significantly after age of 40 in women
and 50 in men.
• Hormonal status: Estrogen has a protective role.
• Postmenopausal women are at a higher risk.
• Bone density: A high bone mineral density is associated with increased
prevalence.
• osteoporosis may have a protective effect.
• Metabolic and nutritional factors:
• Hyperglycemia and high serum cholesterol are associated with increased frequency.
• Vitamin D deficiency impairs the reparative process of bone against the damage of
the disease process.
9. Local biomechanical factors
• Obesity: Overweight persons have higher risk of developing osteoarthritis
and increased risk of radiographic progression.
• A loss of 5 kg decreases risk of knee Osteoarthritis by 50%.
• Acute joint injury and joint deformity: Joint instability due to torn ligaments
and menisci, joint dysplasia and fractures are aggravating factors.
• Occupational factors: Jobs that involve repetitive overloading of joint or
heavy physical labour lead to an increased risk of osteoarthritis.
• Sports: Competitive sports participation (e.g. Football) that demand high
intensity, acute, direct joint impact increase the risk.
• Muscle weakness: Quadriceps weakness is a risk factor for structural joint
damage and osteoarthritis progression.
10. PATHOPHYSIOLOGY
OA is a degenerative condition affecting
• Articular cartilage
• Bone Synovial membrane
• Capsule
• Ligament
• Muscles
Articular cartilage.
• First structure to be affected
• Erosion occurs often central and frequently in weight bearing areas.
• Fibrillation - softening, splitting and fragmentation of cartilage occur
• Collagen fibres split and there is disorganization of the proteoglycan
collagen relationship.
11. Bone – eburnation
• Bone surface becomes hard and polished due to loss of protection of cartilage
• Cystic cavities form in subchondral bone as eburnated bone is brittle and microfractures occur
• Venous congestion occurs in subchondral bone
• Osteophytes form at the margins of articular surface.
• May get projected into capsule.
• Alteration in shape of bones-tibial condyles becomes flattened
12. Synovial membrane
• Undergoes hypertrophy and becomes edematous (cold effusions)
• Reduction of synovial fluid secretion results in loss of nutrition and
lubrication articular cartilage
• Capsule undergoes fibrous degeneration and there are low grade
inflammatory changes
13. Ligament,muscles and synovial fluid.
• Undergoes fibrous degeneration.
• Low grade chronic inflammation becomes contracted or elongated
Muscles :
• Undergoes atrophy due to restricted movements and function.
• Synovial fluid- viscosity becomes high, wbc-200-2000 per mm.
14.
15. CLINICAL FEATURES
• Pain: Steady or intermittent
• Stiffness: follows periods of inactivity, such as sleep or sitting.
• Swelling and tenderness.
• Crepitus: Crunching feeling or sound of bone rubbing on bone
• Locking: Limitation of movements
• Deformity: valgus or varus
18. Diagnosis of Knee OA
Classic Clinical Criteria
• established by ACR, 1981
• sensitivity 95%, specificity 69%
Knee pain plus at least 3 of 6 characteristics:
• > 50 years
• Morning stiffness < 30 min
• Crepitus
• Bony tenderness
• Bony enlargement
• No palpable warmth
20. KELLGREN AND LAWRENCE
Radiological grading of Osteoarthrosis of knee joint
• Grade 0: No radiographic features of OA are present
• Grade 1: Doubtful joint space narrowing (JSN) and possible osteophytic lipping
• Grade 2: Definite osteophytes and possible JSN on anteroposterior weight bearing radiograph
• Grade 3: Multiple osteophytes, definite JSN, sclerosis, possible bony deformity
• Grade 4: Large osteophytes, marked JSN, severe sclerosis and definite bony deformity
25. Management: Medical
• Glucosamine/Chondroitin
• 1500 mg/1200 mg daily
• Glucosamine: building block for glycosaminoglycans
• Chondroitin: glycosaminoglycan in articular cartilage
• GAIT study, NEJM, Feb 23, 2006
• Multicenter, double blind, placebo-controlled, 24 wks, N=1583
• Symptomatic mild or moderate-severe knee OA
• Infrequent mild side effects e.g. bloating
• For mild OA, not better than placebo
• For moderate-severe OA, combination showed benefit
• Patient satisfaction
26. Management: Medical
• Acetaminophen
• Indication: mild-moderate pain
• 1000 mg Q6h Pro re nata
• Better than placebo but less efficacious than NSAIDs
• Caution in advanced hepatic disease
• NSAIDs
• Indication: moderate-severe pain, failed acetaminophen
• GI/renal/hepatic toxicity, fluid retention
• If risk of GIB, use anti-ulcer agents concurrently
• Agents have highly variable efficacy and toxicity
27. Management: Medical
• Cox-2 inhibitors
• Indication: mod-severe pain, failed NSAID, risk of GIB
• OA pain relief similar to NSAIDs
• Fewer GI events e.g. symptomatic ulcers, GIB
• Celecoxib 200 mg daily
• GI/renal toxicity, fluid retention
• Increased risk of CV events.
28. Management: Medical
• Opioid Analgesics
• Indication:
• Moderate-severe pain
• Acute exacerbations
• NSAIDs/Cox-2 inhibitors failed or contraindicated
• Oxycodone synergistic with NSAIDs
• Tramadol/acetaminophen vs codeine/acetaminophen
• Similar pain relief
• Avoid long-term use
• Caution in elderly
• Confusion, sedation, constipation
29. Injections for Knee Osteoarthritis
• Intra-articular steroid therapy as adjunctive therapy to a conventional
management program.
INDICATIONS FOR INTRASYNOVIAL CORTICOSTEROIDS
• To provide pain relief and suppress the inflammation of synovitis.
• To provide adjunctive therapy for one or two joints not responsive to other
systemic therapy.
• To facilitate a rehabilitative and physical therapy program or orthopedic
corrective procedures
• To prevent capsular and ligamentous laxity (large knee effusion).
• To treat patients unresponsive to or intolerant of oral systemic therapy.
• To treat acute effusions occurring with associated crystal deposition
disease
30. Intraarticular Injections
• Glucocorticoids
• Indication: pain persists despite oral analgesics
• 40 mg/mL triamcinolone (kenalog-40)
• Solution: 5 mL (lidocaine 4 mL + kenalog 1 mL)
• Limit to Q3months, up to 2 yrs
• Effective for short-term pain relief < 12 wks
• Acute flare w/in 48 hrs post-injection
31. Intraarticular Injections
• Technique
• 22 gauge 1.5 inch needle
• Approach accuracy:
• Lateral mid-patellar 93%
• Patient supine
• Leg straight
• Manipulate patella
• Angle needle slightly posteriorly
• Inject after drop in resistance or fluid aspirated
32. RELATIVE CONTRA-INDICATIONS TO INTRA-ARTICULAR THERAPY
• Infection (local or systemic)
• Anticoagulant therapy
• Hemorrhagic effusions
• Uncontrolled diabetes mellitus
• Severe joint destruction and/or deformity
COMPLICATIONS OF INTRA-ARTICULAR THERAPY.
• Infection
• Post injection flare
• Crystal-induced synovitis
• Cutaneous atrophy (local)
• Steroid arthropathy (rare)
33. VISCO SUPPLEMENTATION
• Adjunct to lubricate the joint
• Different molecular weights provide different levels of lubrication
• Restores elastic properties of pathologically altered synovial fluid
• Direct analgesic activity by reducing bradykinin and substance P
• Forms a barrier around the pain receptors (nociceptive receptors) and
reduces pain
• Provide pain reduction for up to 24 weeks in early OA
• Cost effectiveness is a concern
34. INTRA-ARTICULAR HYALURONATE (HYALURONIC
ACID)
• Synovial fluid is an ultrafiltrate of plasma composed of water and LMW
solutes transuded from blood.
• Hyaluronate is secreted by the synovial cells as a long chain polymer of
about 5000 repeating disaccharide units of N-acetyl-D-glucosamine and
beta-glucuronic acid.
• The HAs are administered intra-articularly in 1,3,4, or 5 injection series,
depending on the agent.
35. ROLE OF PRP IN OA
• AIM- is to restore the anabolic and catabolic imbalance seen in OA by
increasing the growth factors derived from activated platelets
• The various growth factors include: TGF beta, PDGF, VEGF, Insulin like
GF, EGF.
• PRP is safe and gives symptomatic relief in early OA knee
• Improvement noted by 2 to 3 weeks which gradually improves over 3
months
• Early OA shows better results than late OA
36. Complementory and Alternative Medicine
GLUCOSAMINE
• Amino-monosaccharide and constituent of the articular cartilage GAGs.
• Glucosamine is reduced in osteoarthritic cartilage
• Replenishing glucosamine by taking dietary supplements is appealing.
• Potential beneficial mechanism of action in OA.
• include countering enzymatic or inflammatory processes leading to degradation
of cartilage.
37. CHONDROITIN SULPHATE
• Important constituent of normal joint tissue.
• CS levels are altered in OA cartilage, plasma, and synovial fluid,
• Contributes to structural integrity.
TOPICAL ANALGESICS
• Topical agents with significant local effects tried as home remedies,
• including menthol rubs, alcohol rubs, and substances such as camphor.
38. SURGICAL METHODS
Arthroscopic Debridement
• Degenerating articular cartilage and synovium release
proinflammatory cytokines
• induce chondrocytes to release lytic enzymes leading to type II collagen and
proteoglycan degradation.
• Arthroscopic lavage and debridement may wash out or dilute these.
• Those who appear to benefit most present with a history of
mechanical symptoms, symptoms of short duration (i.e., <6 months),
normal alignment, and only mild to moderate radiographic evidence
of OA.
39. Osteochondral or chondrocyte transplantation
• Autologous chondrocyte implantation
• Biologically resurfaces the knee in the presence of focal cartilage damage.
• Cartilage defect in the knee joints repaired with the patient's own healthy
cartilage cells
• originally harvested through an arthroscopic procedure from separate, minor
load-bearing area in the knee.
40. High Tibial Osteotomy
• Indication:
• Unicompartmental arthritis
• Genu varus or valgus
• Realign mechanical axis
• Age < 60 years
• < 15 degrees deformity
42. Total Knee Arthroplasty
• Indication:
• Diffuse arthritis
• Severe pain
• Failure of conservative measures
• Limited motion
• Functional impairment
• Pain relief > functional gain
• ACL sacrificed
• PCL also may be sacrificed
• Prosthesis 10-yr survival: 90%
43. CONTRAINDICATIONS
• Severe osteoporosis
• Neuropathic joint
• Quadriceps insufficiency
• Prior infection
• Flexion deformity of more than 60 degree combined with valgus or
varus
• Hyperextension of more than 20 to 30 degrees