OA Module

What is the main reason why ppl w/ OA have co morbidities?

Due to walking limitations

Sedentary behaviour

High incidence of CVD

OA Myths

Natural + inevitable: ppl make it far w/o symptomatic OA

Wear & tear?: fear of movement

Just a disease of cartilage

What is OA?

Progressive disease of synovial joints

Failed repair of joint damage

From joint level/systemic stresses on joint tissues: synovium, subchondral bone, ligaments, menisci, cartilage

Break down cartilage + bone

Signs + symptoms of OA

• Atrophy

• Bone remodelling + sclerosis

• Cartilage breakdown

• Meniscal damage

• Synovial hypertrophy

• Osteophytes

• Ligament dysfxn

• Altered fat metabolism

• Inflammed synovium

• Capsule hypertrophy

• Osteophytes

• Thickening of subchondral bone

• Degradation of cartilage

Does OA involve whole joint?

Yes, all tissues

Unknown pathological change

What happens in early & late stages of OA?

Synovial inflammation (synovitis)

• Chronic low grade inflammation

What’s released that causes cartilage breakdown?

Inflammatory degradative substances

Cartilage breakdown is “by stander effect”

Is there a common OA pathway?

No common etiology

Share a final common pathway with similar clinical outcomes

OA Pathogenesis

Joint level factors [affects loading + biomech] + Systemic factors

= Cartilage matrix destruction, failed repair, mechanical failure of joint

→ joint destruction

Joint level risk factors that alter joint loading

1. Obesity/BMI: most significant factor. Lose weight, reduce risk of OA

2. Joint injury: ACL/Meniscal tears. Surgery not prevent OA

3. Limb mal-alignment/asymmetry= imbalanced loading. Makes joint more lax.

4. Bone shape: hip dysplasia, shallow acetabulum, abnormal femoral head shape

5. Neuromuscular abnormalities: mm weakness predicts pain + fxnl decline

MODIFIABLE

Valgus Knees

Lateral OA

Varus OA

Medial OA

What precedes knee OA?

Quad weakness

What is involved in dynamic movement?

MM + spinal reflex coordination

Intact proprioception

Systemic Risk Factors

Affect the whole body

1. Aging: ↑ bone turnover, less bone mass, sub chondral fx

2. Sex/gender

3. Genetics

4. BMI

NON-MODIFIABLE

Aging & OA

↑ Bone turnover, less bone mass, subchondral fx

↓ chondrocyte maintain + repair cartilage

• soften articular surface, lose matrix tensile strength + stiffness

Sarcopenia

Mm weakness

Sex/gender @ risk for OA

Females

• Hormones, body shape, genetics, social determinants of health

• Live alone

Genetics & OA

No specifc gene found

Hip + hand OA runs in families (NOT KNEE)

Genes determine shape + quality of bone

BMI

Systemic inflammation

↑ Stress on WB joints

Fat tissue makes inflammatory mediators that affect bones, cartilage → degradation of joint

Systemic inflammation is due to….

Metabolic syndrome

Do you need an xxray to diagnose OA?

NO

Symptoms ≠ structural changes

Can just be made based of clinical exam

Signs of OA on Imaging

Joint space narrowing

Osteophytes

• Indicates late stage of disease

Early symptoms of OA? Is it visible on an X-ray

NO!

Synovitis

Subjective symptoms of OA

• Fluctuates w/ ↑ pain over time

• Gradual, insidious onset

• Stiff in morning + after inactivity < 30 mins

• Pain w/ WB activities (Knee + hip): stairs, kneel, squat, high impact

• Intermittent → constant

• Pain w/ pinch grip (thumb OA), gripping objects (hand OA)

Trajectory of OA Pain

1. Mild/mod, intermittent pain after trigger. Predictable sharp pain. Limits high-impact or excessive activities. Not much impact on ADL

2. Mild constant pain ± intermittent pain. Predictable → unpredictable locking/buckling. Affects ADL (stairs, walking)

3. Moderate-to-severe constant pain ± intense intermittent pain. Dull/achy pain. Unpredictable/intense hip/knee pain. Significant avoidance of ADL (social + rec)

• Change in pain processing mechanisms - central sensitization

Objective symptoms of OA

• Less ROM- capsular restriction [later stages]

• Pain w/ overpressure

• Crepitus

• Tenderness

• Mild effusion

• Bony enlargement

• Deformities @ DIP/PIP

Red flags of OA

Recent injury

Frequent locking

Prolonged morning stiffness

Rapid onset of symptoms

Hot, swollen

Fever, chills, sweats, feeling unwell

• Gout, inflammatory arthritis, septic arthritis, malignancy

Goals of OA Management

Pain

Improve fxn/prevent disability → improve QoL

Prevent symptom progression

Treatment pyramid

1. Core therapies: Exercise, weight management, self-management program > EVERYONE

2. Injections/creams: topical NSAID, corticosteroid injections + brace, orthotics, walking aids

3. Systemic therapies: acetaminophen, oral NSAIDS, duloxetine

4. Joint replacement

Higher risk of adverse effects

Inconclusive evidence for…

Glucosamine

Chondroitin

Rosehip

Mineral baths

Hyaluronic acid injections for knee + thumb OA

Self management

Problem-based approach to gain confidence in the ability to develop skills to manage their OA

• Active role in OA care

• Involve family

• Individual programs or groups

Patient: Identify challenges, set goals, action plan, problem solve, monitor progress

Provider: Support in developing plan, review plan continuously, info on access to services!

Patient Education

• 1-1

• Group edu

• Community-based edu programs

Include

• Causes, consequences, prognosis

• Chronic pain, pain science, limits of rx

• Address myths/maladaptive beliefs

• Goal setting

• Activity pacing

• Self regulate (meditation)

• Problem solving

• Importance of active lifestyle, weight management

• Protect joints (pace/rest)

• train w/ walking aides + braces

Weight loss

Decreases pain + disability

Improves systemic inflammation.

Dose-response relationship btwn weight loss + pain/fxn

Diet + exercise > diet

Exercise and OA

Most effective non-surgical treatment for Hip + knee OA

Prescribe exercise management regardless of OA severity

No 1 exercise best. Supervised > non

Therapeutic Exercise

Plan of PA designed + prescribed for specific therapeutic goals

Goal to restore normal MSK fxn or reduce pain caused by disease or injury

PA Guidelines for OA

150 min/wk of mod-vig in >10 min bouts

Not necessarily an increased level of PA

Not necessarily meet PA guidelines to see benefit. No min threshold for activity

• Small amounts of PA improve pain + disability

Pain cycle of OA

Joint pain → activity avoidance → sedentary behaviour → increases pain and contd

Walking programs for OA

Effective in relieving pain and promoting remodelling

Improves stability, biomechanics, neuro fxn, aerobic capacity + activity tolerance

Start w/ 70 min/wk of brisk walking

How to progress walking program

Use time or step count goals

• Time: 25 min 3x/wk, ↑ 5 min/mo until 45 min 3x/wk

• STEP: ↑ step count by 10%/mo until 30% above baseline count

Intensity: difficulty talking/100 steps/min = mod-vig PA

Components of Therapeutic exercise

1. Strengthening exercises

2. ROM/Flexibility

3. Neuromuscular training

Benefits: ↑ mm strength, joint stability, rom, fxn, less pain, better cartilage quality

Strengthening + flexibility Exercises

No conclusive dosage

Min 3x/wk

Individualized approach

Ex. Bridge, knee flex stretch, butterfly stretch, Quad ext, hamstring curl, sit-stand, step ups, step down

Neuromuscular training

Sensorimotor dysfxn contributes to fxnl instability → abnormal joint loading

Goal: restore fxnl stability by improving sensorimotor control

Fxnl (dynamic) stability

Stay stable in PA

Sensorimotor control

Produce controlled movement thru coordinated mm activity

Neuromm Training Principles

CKC exercises

Multiple joints + mm groups in fxnl WB positions

Quality + efficiency of movement + Alignment

Target: postural control, proprioception, mm activation, mm strength, coordination

Pain management during exercise

Pain is ok during exercise

Pain ≠ harm/damage

• Stay btwn 2-3/10

Pain should subside within 24 hrs

What to do during flare ups

Stop aggravating activity until back to baseline

Restart w/ lower dosage

Encourage to continue exercise after flare. This is normal.

• Gentle ROM, core

• fewer mins, lower reps, weight

OA exercises + Co morbidies

Hypertension: no HITT

Coronary heart disease: use max/symptom limited ex test to determine aerobic capacity, prolong warm up + cool down, monitor HR + BP

T2DM: Monitor glucose, foot ulcers, sensory deficits, autonomic neuropathy

Other non-surgical interventions

Biomechanical aids: walkers, braces, orthotics, splints, shock-absorbing insoles

Splints for thumb OA

THERMAL THERAPY: paraffin wax for hand OA, heat pad-self management

Unloader braces for knee OA

Uni-compartmental knee OA

Lowers load on part of joint most damaged

Alter abnormal force made by valgus or varus malalignment

Can pain be a facilitator?

Yes

Facilitators for exercise adherence in OA

Pain

Specific advice

Individualized program

• FITT-P

• Pain management

BCTs

Strategies to overcome barriers

Offer reassurance, pain guidelines

Written ex handouts

Pics + videos

Motivational Interviewing

Collaboration w/ patient

OA is what type of pain

Nociceptive [mechanical or inflammatory] or nociplastic

Mechanical normal nociceptive pain

• Noxious stimulus

• In early OA

• Relieved by rest

• Aggravating factors

• Distinct location of pain

• Intensity related to strength of stimulus

• Sharp, pinch, catching

Tissue inflammation

Inflammatory Nociceptive Pain - Tissue pathology

Release of inflammatory mediators

Evoked pain

Hyperalgesia: tenderness around a localized area

Spontaneous pain: larger area w/ less distinct boundary

• Fluctuates in intensity follows edema

Peripheral neuropathic pain

spontaenous + evoked

no clear stimulus

area of pain = nerve root innervation

radiating, stabbing, burning, sharp, sudden, electric

NOT IN OA

Nociplastic Pain

Change in fxn of NS

General pain/location

Injury/pathology not account for degrees of self-reported pain + disability

Intensity not related to stimulus

RANGE of aggravating/easing factors

Location not related to stimulus [widespread]

OA Pain causes

Tissue-related nociceptive mechanical/inflammatory

NS sensitization → nociplastic

What causes acute → chronic pain

NS sensitization

Guidelines for clinical decision

1. Pain intensity and pattern: can injury, pathology, and dysfxn account for self reported pain + disability?

2. Distribution of symptoms: local to nerve innervation pattern?

BPS Model of Pain

Bio: tissue, comorbidities, pain mechanisms

Psych: emotions, thoughts, feelings, knowledge, previous rx response

Social factors: social support, culture, home, job factors

ABCDEFW Pain processing BPS Factors

Attitudes/beliefs: what do you believe is causing pain

Behaviour: what do you do in pain?

Compensation: financial issues

Diagnosis

Emotional: mood

Family: react to your pain

Work: managing @ work

Exercise for Nociplastic pain

Less on pain level

Time-contingent to grade exercise

Reassurance that discomfort normal

Pain education to understand flare ups (not tissue damage)

General exercise/PA program focus on strength/mobility/endurance

• Restore movement confidence

Adapting exercise thru pain changes

Short term: endogenous pain control

Long term effects:

• CNS: retrain brain, normalize central pain processing

• Immune: systemic inflammation, CNS: neuroimmune signalling prevents central sensitization

• Mood/cognition: general mood effects

Criteria for Total replacement

Symptoms significantly impacting QoL

Tried non surgical therapy and failed

Benefits of TJA > risks

Which replacement is better? THA or TKA?

THA > TKA

THA

Remove femoral head

New articular surface for acetabulum + femoral head

Surgical approaches

THA Precautions post-surgical

Follow surgeon protocol

No hip flex > 90

No adduction > neutral - no crossed legs, no trunk flexion, no sit in low soft chairs

No IR beyond neutral- pivot on non-operated leg

TKA

Replace both articular surfaces of tibiofemoral joint

Restore proper alignment

• Anterio-medial approach vs minimally invasive

General principles for TJA Management

• Assess: vitals, complaints, neuro assess

• Treat: deep breathe, circulation, bed mobility, transfer, walk, stairs, rom, education

• Discharge plan

• 1-3 days home

• Depends on surgical techniques, complications

Apply knowledge to stages of healing

Acute inflammatory: max protection

Sub-acute proliferation: controlled motion or moderate protection phase

Chronic maturation + remodel: return to fxn of minimal protection

General management of TJA

ROM (assisted - active)

Strengthening (iso - active assisted - active)

Gait training/stairs

Balance proprioception

Fxnl activities

ROM Progression post TKA

Flexion goal: 120 deg

• 110 arom for fxnl rom (stairs, sit to stand, gait)

• 120 arom for kneel

Extension goal: 0 deg

• Flexion deformity > 10 deg, fxnl leg length issue

TKA No-nos

No OKC resisted

High patellofemoral compression

Greater anterior tibial displacement bc NO ACL

Less fxnl

• Do CKC neuro training

Return to PA

Need PA plan to reverse sedentary behaviour