1. Osteoarthritis (OA)
Małgorzata Węgierska

2. Introduction
OA is the most common joint disorder worldwide. In western countries, radiographic evidence of this disease is present in the majority of people after 65 years of age and in about 80% of people over 75 years of age.
Pain and other symptoms of OA may have a strong effect on quality of life, affecting both physical and psychological functions.

3. Introduction
OA is a complex, active degradative and repair process of cartilage and subchondral bone with a synovial inflammation.
Several factors are involved in this process such as mechanical stress, biochemical and genetic factors.
Chondrocytes respond to injuries by producing degradative enzymes and by developing inappropriate repair responses. A lot of pro- degradative agents such as proteinases and proinflammatory cytokines have been extensively studied and may compromise macromolecular synthesis, resulting in the development of cartilage breakdown.

4. Introduction
OA is defined by focal lesions of the articular cartilage, combined with a hypertrophic reaction ( sclerosis) in the subchondral bone and new bone formation ( osteophytes) at the joint margins.
OA is diagnosed where there is joint pain, together with characteristic radiographic changes, in the absence of an alternative cause.

5. Symptoms of OA
Pain is the first predominant symptom of OA. It occurs after joint use and is relieved at rest. With disease progression, pain occurs with minimal motion or even at rest and finally, even during sleep.
Because cartilage has no nerve supply and is insensitive to pain, the pain in OA must arise from non-cartilaginous structures such as periost, intra-articular ligaments, pressure on subchondral bone with venous engorgement, intramedullary engorgement, capsular distension, alterations of synovium or tendons and fascia.

6. Symptoms of OA
Stiffness may also occur in the morning or after periods of inactivity during the day.
Morning stiffness generally resolves after <15 min.

7. Symptoms of OA
Limitations of motion and function develop as OA progresses and are related to joint surface incongruity with reduced joint space, muscle spasm or diminished strength, leading to instability and mechanical block from osteophytes and loose bodies.

8. Some risk factors that might lead to it include:
Being overweight
Female sex
Oestrogen deficiency
Getting older
Family history
Joint injury
Joints that are not properly formed
A genetic defect in joint cartilage
Stresses on the joints from certain jobs and playing sports

9. Physical examination
Joint enlargement results from joint effusion and/or osteophytes and/or synovitis.
Joints are usually tender during active motion testing and under pressure.
Joint deformities and subluxation reflect advanced disease resulting from cartilage loss, collapse of subchondral bone, formation of bone cysts and bony overgrowth.

10. Investigations
No single test can diagnose osteoarthritis. Most doctors use several methods, including medical history, a physical exam, x-rays, or lab tests.
Plain radiographs are the ‘gold standard ‘ for diagnosis. Characteristic changes on plain radiographs: include osteophytes, joint space narrowing and subchondral changes: sclerosis and cysts.
OA is typically not associated with high acute phase response.

11. Several forms of OA Primary Nodal (hand) Erosive (hand)
Generalized ( hand + knee/hip)
Diffuse idiopathic skeletal hyperostosis

12. Several forms of OA Secondary
Metabolic ( acromegaly, ochronosis, haemachromatosis)
Traumatic (major joint trauma, joint surgery, chronic injury)
Inflammatory ( any inflammatory arthropathy, septic arthritis)
Neuropathic ( diabetes mellitus)

13. Hand
The hand is one of the most common sites of OA. Bony enlargements of the proximal interphalangeal joints are called Bouchard’s nodes, whereas those of the distal interphalangeal joints are called Heberden’s nodes.
Erosions of the interphalangeal distal joints on x-ray examinations are prominent features in a subset of patients with OA called ‘erosive OA’.

14. Differential diagnosis
Psoriatic arthritis
Gout
Rheumatoid arthritis

15. Non-pharmacological therapy
Education about the disease and effective treatments.
Exercise therapy should include both aerobic conditioning and strengthening exercise.
Weight loss advice for all who are overweight or obese.
Hot and cold packs can be helpful for acute exacerbations of joint pain.
Transcutaneous electrical nerve stimulatin ( TENS) may give safe and effective pain relief in some patients with OA, and is recommended as a safe adjunctive modality in the majority of guidelines.

16. Pharmacological therapy
Paracetamol is preferred as first line analgesia, because of its favourable safety profile.
Non-steroidal anti-inflammatories ( NSAIDs) provide additional symptomatic benefit in some patients.
Gastrointestinal and cardiovascular risks must be considered befor use NSAIDs. They should be avoided in patients with established ischaemic heart disease or cerebrovascular disease, and used with caution in those with risk factors for these conditions.

17. Pharmacological therapy
Current European recommendations for prescribing NSAIDs in patients at increased risk of gastrointestinal toxicity are to use a COX-2 selective agent or a non-selective NSAID plus a proton pump inhibitor (PPI) for gastroprotection.
Opioids, such as codeine or higher strength opioids may be needed.

18. Topical treatments Certain topical NSAID preparations are effective.
Topical capsaicin – this is a lipophilic alkaloid derived from chilli peppers. Topical capsaicin applied three times daily can reduce pain associated with hand or knee OA. Capsaicin has a high rate of skin reactions.

19. Intra- articular injection
Intra-articular injection of corticosteroid is helpful for quick control of pronounced pain from knee osteoarthritis, thumb base and other joints. Corticosteroid injections can give short-term relief ( 2-3 weeks) in knee and as long as 3-4 months in hip.
There is little compelling evidence for the efficacy of intra-articular Hyaluronan.

20. SYSADOA ( symptomatic slow acting drugs in ostheoarthritis )
However, the main goal of OA therapy should be to delay cartilage degeneration and even help to regenerate the cartilage structure.
Medications having these properties are generally called ‘chondroprotectives’.
They are diffrrentiated as symptomatic slow acting drugs in OA ( SYSADOA) and disease-modifying OA drugs ( DMOAD).
Currently, glucosamine and chondroitin are the two most commonly used SYSADOA to modify the clinical and radiological course of OA.
Glucosamine and chondroitin are also the most frequently used nutraceuticals in humans as well as in animals to alleviate pain associated with arthritis.

21. Disease modifying OA drugs ( DMOADs)
There are currently no universally accepted disease-modifying OA drugs. Single studies have suggested efficacy for a number agents and toxicity has prevented development of others. Potential DMOADs include:
Diacerein
Doxycycline
Licofelone
Strontium ranelate
Bisphosphonates

22. Surgery
Surgery, including total joint replacement, should be considered for patients who have persistent pain, stiffness, and reduced function that are refractory to non-surgical treatments and which impact significantly on their quality of life.
Patient specific factors such as age, obesity or other comorbidity should not be barriers to surgery, and referral should be made early before there is prolonged and established functional limitation and serere pain.