Osteoarthritis (OA) is a degenerative disease affecting synovial joints (arthropathy) that occurs due to loss of articulating cartilage. It is a multi-factorial disease (genetic, biological and environmental factors all play a role) but its aetiology is not entirely known.
ποΈ Epidemiology
It is the most common arthropathy worldwide affecting about 10% of men and 18% of women worldwide.
Prevalence varies on the affected joint:
- Knee - 18% of >45 year olds have sought treatment for OA of the knee.
- Hip - 8% of >45 year olds have sought treatment for OA of the hip.
- Hand and wrist - 6% of >45 year olds have sought treatment for OA of the hand. Most common in postmenopausal women.
β οΈ Risk factors
- Age - >45 years old
- Family history
- Female sex
- Obesity
- Hypermobility of joint
- Occupation - jobs requiring repetitive squatting, bending, kneeling and heavy lifting carries a greater risk.
- Joint trauma - this includes microtrauma caused by exercise and sports (for example in footballers).
- Articular congenital deformities
- High bone mineral density - therefore osteoporosis may be protective.
- Low bone density - in postmenopausal women for example, this increases risk of knee and hip OA specifically.
Pathophysiology
OA was previously considered a disease occurring due to wear and tear, however, this is no longer thought to be the case. Ultimately is a failure of of homeostasis in cartilage synthesis/degradation which ends up in increased cartilage degradation.
Letβs look at some of the factors involved in this failed homeostasis:
- Collagenases and matrix metalloproteinases (MMPs) break down collagen and proteoglycans. They are at higher concentrations in OA cartilage. Nitric oxide is believed to activate these MMPs and may potentiate degradation.
- Pro-inflammatory mediators drive joint destruction. Chondrocytes also respond to the inflammatory environment with abnormal metabolism (aerobic β anaerobic process) and ultimately senescence.
- IGF-1 and other anabolic cytokines decrease with OA.
These factors lead to cartilage degradation and bone remodelling. When the articular cartilage is broken down, there is exposure of the underlying bone which initiates bone remodelling and results in sclerotic bone, osteophytes and subchondral bone cysts. Joint space is also progressively lost over time
These changes can lead alteration of the anatomy by altering the joint load distribution, for example genu varum (bow legs) or genu valgum (knock-knees) in the knee.
π· Presentation
OA most commonly affects:
- Knee
- Hip
- SI joint
- Distal interphalangeal joint
- Carpometacarpal joint
- Wrist
- Cervical spine (cervical spondylosis)
Patients with osteoarthritis may feel no symptoms despite radiological evidence of osteoarthritis. Symptomatic osteoarthritis can vary in severity and also vary depending on the joints involved. The general presentation includes:
- Pain - slow onset, chronic and gradually worsening.
- Stiffness - activity-related. Morning stiffness may also present and lasts <30 minutes.
Other general signs include:
- Effusions around the joint - mostly seen in knee.
- Bony swelling and deformity
- Warmth or tenderness - indicative of synovitis, but more associated with RA.
- Crepitus - grating sound due to friction between bone and cartilage. More prevalent in knee and hip.
- Instability
- Referred pain - to the adjacent joints (e.g. hip OA and knee pain).
Letβs now take a look at specific signs and symptoms of the hand, knee and hip:
Generally, the carpometacarpal (CMC) and distal intephalangeal (DIP) joints are most affected as opposed to the proximal interphalangeal joints (PIP). That being said the specific signs in the hand are:
- Bouchardβs nodes of the PIP - bony nodules on the dorsum.
- Heberdenβs nodes of the DIP - bony nodules on the dorsum.
- Fixed flexion deformity for the CMC - with distal hyperextension (typically at the thumb).
- Squaring at the base of the thumb - due to subluxation (partial dislocation), and bony remodelling.
- Weak grip - pain may be exacerbated by pinching actions or a strong grip. Functional loss isnβt usually present though.
- Thenar wasting - disuse atrophy.
OA of the knee is generally bilateral and symmetrical, if unilateral it is usually secondary to truama/disease. It affects 3 compartments:
- Medial tibiofemoral compartment - causing anteromedial pain (on walking).
- Lateral tibiofemoral compartment - causing anterolateral pain (on walking).
- Patellofemoral compartment - cuases anterior knee pain that is worse with inclines/stairs, especially when going down. There may be progressive aching when sitting that is relieved by standing.
Other features may be:
- Knee locking - suggestive of a loose meniscus.
- Genu valgum - knock-knees.
- Genu varus - bow-legged.
- Crepitus
- Effusion
- Instability
This presents with:
- Deep anterior groin pain - when walking or climbing stairs. Pain is worse with exercise and relieved by rest.
- Referred pain - to lateral thigh, buttocks, anterior thigh, or knee.
- Restricted internal rotation
- Antalgic gait - less time spent weight-bearing on affected hip.
- Trendelenburg gait - due to atrophy and weakness of gluteal and anterior thigh muscles.
Severity can be measured using the Oxford Hip Score.
π Investigations
A good history should be taken, asking about risk factors, trauma history, hand dominance, functional impairment and treatments tried.
- π₯ Clinical diagnosis can be made based on typical features on examination and history.
- π X-ray can be used if there is uncertainty or to exclude alternative diagnosis, but not routinely needed
- L - Loss of joint space
- O - Osteophytes. These are bony spurs on otherwise smooth bone.
- S - Subchondral sclerosis. Increased density of the bone along the joint line.
- S - Subchondral cysts. Cysts that form within the bone itself.
π§° Management
NICE recommends patient education and self-care management for symptomatic relief. This includes:
- Weight loss
- Muscle strengthening - it is important to advise patients that initiating the exercise might be painful but consistent and regular exercise will be beneficial and will reduce pain for the joints.
- Orthotic footwear
- Simple analgesia
- For knee osteoarthritis - NICE recommends offering a topical NSAID.
- Topical NSAIDs can be considered with OA affecting other joints.
- If ineffective β oral NSAID can be considered along with PPI.
- Paracetamol and weak opioids should not be used unless for short-term pain relief. All other pharmacological treatments are considered ineffective.
Intra-articular steroid injections are often given in outpatient clinics. It has varying success. It is usually mixed with a local anaesthetic and this is what could be improving symptoms.
If self-care management is not sufficient, we can consider:
- Physiotherapy referral
- Occupational therapy referral
- Podiatry referral - as pain in one joint may lead to increased stress and pain at other sites due to biomechanical compensatory changes. Orthotics may also be recommended.
- Orthopaedic surgery referral - this is prior to severe functional limitation and pain if:
- There is substantial impact on quality of life.
- Atypical symptoms or uncertain diagnosis.
- Non-surgical management is ineffective or unsuitable.
- Sudden worsening of symptoms.
- Joint replacement (arthroplasty)
- Joint fusion (arthrodesis)
- Arthroscopic lavage and debridement - if there is a clear history of mechanical locking.