OSTEOARTHRITIS

Definition & Epidemiology Risk Factors Pathogenesis Clinical SymptomsIt is a joint failure

A disease all structures of the joint have undergone pathologic change, often in concert.

The pathologic sine qua non of disease:1. hyaline articular cartilage loss, present in a focal and, initially, nonuniform manner. 2. accompanied by increasing thickness and sclerosis of the subchondral bony plate, 3. by outgrowth of osteophytes at the joint margin, 4. by stretching of the articular capsule, 5. by mild synovitis in many affected joints, and 6. by weakness of muscles bridging the joint. 7. In knees, meniscal degeneration is part of the disease

Joint Vulnerability & Joint Loading

(Systemic Fxs)Old age: >60y/oFemale genderRace/ethnicityNutritional

(Local Envt Fxs)Previous injuryBridging muscle weaknessIncreasing bone densityMalalignmentProprioceptive deficiencies

Use (loading) factors acting on jointsObesityInjurious physical activities

Joint Protective Mechanisms and Their Failure

Joint protectors include:Joint capsuleLigamentsMuscle Sensory afferents Underlying bone

Cartilage and Its Role in Joint Failure

Two major macromolecules in cartilage

1.Type 2 collagenprovides cartilage its tensile strength.

2.Aggrecana proteoglycan macromolecule linked with hyaluronic acid, which consists of highly negatively charged glycosaminoglycans.

Pathologyinitially shows surface fibrillation and irregularity.focal erosions developextend down to the subjacent bonecartilage erosion down to bone expands to involve a larger proportion of the joint surface.Chondrocytes undergo mitosis and clustering.net effect of this activity is to promote proteoglycan depletion in the Matrix surrounding the chondrocytesCollagen matrix becomes damaged.Negative charges of proteoglycans get exposed.cartilage swells from ionic attraction to water moleculescartilage becomes vulnerable to further injury.

HistoryPattern of spread: Additive; however, only one joint may be involvedOnset: Usually insidiousProgression& Duration:Slowly progressive, with temporary exacerbations after periods of overuseAssociated Symptoms:1. Small effusions in the joints may be

present, especially in the knees; also bony enlargement

2. Possibly tender, seldom warm, and rarely red

3. Intermittent stiffness: Frequent but brief (usually 5–10 min), in the morning and after inactivity

4. Limitation of motion often developsGeneralized symptoms are usually absent

Physical ExaminationCommon locations: Knees, hips, hands (DIP,PIP), cervical and lumbar spine, wrists (first carpometacarpal joint), joints previously injured or diseased

Findings in osteoarthritis:1. Bony bumps on the finger joint closest to

the fingernail (Heberden's nodes )2. bony bumps on the middle joint of the

finger (Bouchard's nodes )3. bony bumps at the base of the thumb.4. Tenderness and/or swelling in weight-

bearing joints such as the hips and knees.

5. Pain, limited movement, and/or a creaking noise or feeling (crepitus) that occurs when the joints are moved. Pain on both active and passive movement

6. Joints that have been affected by injury or infection may also show signs of bone or tissue damage.

Diagnosis TreatmentClassification criteria by American College Supportive/Palliative

NONPHARMACOLOGICSURGICAL1. Arthroscopic debridement and lavage -

RheumatologyOA of HipHip pain plus femoral or acetabular osteophytes on radiographs or Hip pain plus joint space narrowing on radiographs and an ESR of less than 20 mm per hourOA of HandsHand pain, aching or stiffness +Hard tissue enlargement of two or more of 10 selected joints* +Fewer than three swollen metacarpophalangeal joints +Hard tissue enlargement of two or more distal interphalangeal joints or Deformity of two or more of 10 selected joints* * - 10 selected joints are the second and third distal interphalangeal joints, the second and third proximal interphalangeal joints and the first carpometacarpal joints (of both hands).OA of KneeKnee pain and osteophytes on radiographs or Knee pain plus patient age of 40 years or older, morning stiffness lasting 30 minutes or less and crepitus on motion

Synovial fluid analysisNoninflammatory syno-vial fluid is:1. clear, 2. viscous, and 3. amber-colored, 4. WBC count of <2000/μL and a predominance

of mononuclear cells.

RadiographyStructural abnormalities:1. cartilage loss (seen as joint space loss on

x-rays)2. osteophytes (a bony outgrowth)

Mainstay of treatment:1. altering loading across the painful joint2. improving the function of joint protectors

A. Alter loading across the painful joint1. Avoid activities that precipitate pain2. Lose weight 3. Splinting – minimize pain by limiting motion

of joints; for pts with first CMC , DIP or PIP joint involvement

4. Use cane in the hand opposite to the affected area for partial wt-bearing

5. Use crutches or walkers

B. Improve Function of Joint protectors1. Exercise

a. aerobic and/orb. resistance training - focuses on

strengthening muscles across the joint2. Correction of malalignment

a. fitted brace, which takes an often varus osteoarthritic knee and straightens it by putting valgus stress across the knee

b. use of orthotics in footwearc. Use a brace to realign patellar

malalignmentd. use of tape to pull the patella back into the

trochlear sulcus or reduce its tilte. neoprene sleeves pulled to cover the knee

lessen pain and are easy to use and popular among patients

3. acupuncture - produces modest pain relief compared to placebo needles and may be an adjunctive treatment

PHARMACOLOGIC- serves an important adjunctive role in OA treatment1. Acetaminophen- is the initial analgesic of

choice for patients with OA in knee, hip, or hands.

- Doses up to 1 g 4 times daily2. NSAIDs - administered topically or taken

orally on an "as needed" basisNaproxen – dose: 375-500mg BIDSalsalate – 1500mg BIDIbuprofen- 600-800mg 3-4 times a day3. COX-2 InhibitorsCelecoxib – low dose, 200mg a day

4. Glucocorticoid – used for acute flares of pain; given via intraarticular injection

5. Hyaluronic acid – given via intraarticular injection

Randomized trials evaluating this operation have showed that its efficacy is no greater than that of sham surgery or no treatment for relief of pain or disability

2. Arthroscopic meniscectomy - indicated for acute meniscal tears in which symptoms such as locking and acute pain are clearly related temporally to a knee injury that produced the tear.

3. For patients with knee OA isolated to the medial compartment, operations to realign the knee to lessen medial loading can relieve pain. These include:a. high tibial osteotomy - the tibia is

broken just below the tibial plateau and realigned so as to load the lateral, nondiseased compartment, or

b. a unicompartmental replacement with realignment.

4. total knee or hip arthroplasty – for patients with knee or hip OA in which medical treatment modalities have failed and remains in pain, with limitations of physical function that compromise the quality of life

Cartilage Regeneration1. Chondrocyte transplantation - has not

been found to be efficacious in OA, perhaps because OA includes pathology of joint mechanics, which is not corrected by chondrocyte transplants.

2. Abrasion arthroplasty (chondroplasty) has not been well studied for efficacy in OA, but it produces fibrocartilage in place of damaged hyaline cartilage. - Both of these surgical attempts to

regenerate and reconstitute articular cartilage may be more likely to be efficacious early in disease when joint malalignment and many of the other noncartilage abnormalities that characterize OA have not yet developed