Osteoarthritis is a chronic disease characterized by the deterioration of cartilage in joints, resulting in bones rubbing together and causing stiffness, pain, and impaired movement. It is common in individuals over 60 years of age, and prevalence is higher in women than men. Risk factors include age, obesity, injury, family history, and certain occupations. Symptoms include joint pain, tenderness, and limited range of motion. Treatment involves exercise, weight loss, medications like acetaminophen, NSAIDs, and corticosteroid injections, and may require surgery like joint replacement for severe cases.

1. OSTEOARTHRITIS
Dr. V. S. Swathi
Assistant Professor

2. DEFINITION
Osteoarthritis is a long term chronic disease
characterised by the deterioration of cartilage in
joints which results in bones rubbing together and
creating stiffness, pain and impaired movement

3. EPIDEMIOLOGY
 In the world 9.6% of men and 18% of women of age
greater than 60 years have symptomatic
Osteoarthritis
 In India, prevalence of Osteoarthritis is 22%-39%

4. TYPES
Primary Osteoarthritis
 Also called as idiopathic OA
 Cause of this type is unknown
Secondary Osteoarthritis
It is occurs due to specific cause like:
 Rheumatoid Arthritis
 Other type of arthritis
 Trauma
 Metabolic and endocrine disorders
 Congenital factors

6. RISK FACTORS
 Age- Increasing the age increases risk of Osteoarthritis
 Gender-Women are greater risk of getting Osteoarthritis
than men
 Obesity
 Traumatic injury
 Persons with family history of OA
 Persons working in:
 Construction sites
 Health care settings
 Factories
 Carpentry works
 Farming
 Sports persons like:
 Wrestlers
 Boxers
 Cyclers
 Football and base ball players

7. ETIOLOGY
Abnormal expression of genes like:
 Col11A1 (extracellular matrix)
 Chrom 19 (cartilage morphogenesis)
 MCFL (pain perception)
 CHST11 (cartilage morphogenesis)
 GDF5 (TGF-beta signaling)
 Chrom7Q22

8. PATHOGENESIS

10. CLINICAL PRESENTATION
 Pain
 Tenderness
 Crepitus
In joints of hands, knee, hip, spine and feet
 Limited motion with passive or active movement
 Deformities like:
 Herberden’s nodes (at distal interphalangeal joints)
 Bouchard’s nodes ( at proximal interphalangeal joints)
 Bow legs
 Loss of reflexes if spine is affected
 Parasthesia

12. COMPLICATIONS
 Chondrolysis
 Osteonecrosis
 Stress fractures
 Bleeding inside the joint
 Infection in the joint
 Deterioration of tendons and ligaments
 Pinched nerve

14. DIAGNOSIS
 Medical history of other arthritic problems
 Physical examination
 Radiograph findings
 Lab tests

16. DIAGNOSIS CRITERIA
For hip OA
 Pain in the hip
 Any 2 of the following:
 ESR<20mm/hour/
 Femoral / Acetabular Osteophytes on
radiography/
 Joint space narrowing

17. DIAGNOSIS CRITERIA
For Knee OA
 Pain in the knee
 Osteophytes on radiography
 Any 1 of the following:
 Age greater than 50 years
 Morning stiffness not more than 30 minutes
 Crepitus on motion
 Bony enlargement
 Bony tenderness
 Palpable warmth

18. NON PHARMACOLOGICAL TREATMENT
 Exercise
 Weight loss
 Patient education
 Use of assistive devices
 Use of shoe insoles
 Application of heat
 Use of fitted knee braces
 Lateral patellar taping
 Surgeries like:
 Arthroplasty
 Osteotomy
 Arthrodesis
 Joint replacement

19. TOTAL KNEE ARTHROPLASTY

20. TREATMENT ALGORITHM
Knee and hip osteoarthritis
First line agents include:
 Acetamiophen
 Topical NSAIDs
 Oral NSAIDs
 Tramadol
 Intraarticular corticosteroids
IF ABOVE DRUG FAILS
Second line agents (if above treatment fails or contraindicated) include:
 Opiod analgesics
 Surgery
 Duloxetine
 Intraarticular hyaluronates

21. Hand Osteoarthritis
 Topical NSAIDs
 Oral NSAIDs
 Topical Capsaicin
 Tramadol
If above single drug treatment fails, use
combination if above drugs

22. DRUGS USED IN TREATMENT OF
OSTEOARTHRITIS
Drug Category Mode of action Dose Adverse effects
Paracetamol NSAID Inhibit
prostaglandin
synthesis
325-650mg/day  Angioedema
 Stevon johnson’s
Syndrome
 Tissue necrotic
syndrome
 Hepatotoxicity
 Nephrotoxicity
Aspirin NSAID Inhibit
prostaglandin
synthesis
325-650mg/day  Angioedema
 Bronchospasm
 GI disturbances
 Hepatotoxicity
 Nephrotoxicity
Diclofenac NSAID Inhibit
prostaglandin
synthesis
100-200mg/day  Abdominal distension
 Constipation
 Dyspepsia
 Edema
 Nephrotoxicity

23. Ibuprofen NSAID Inhibit
prostaglandin
synthesis
1.2-3.2g/day  Dizziness
 Epigastric pain
 Heart burn
 Rash
 Tinnitus
Indomethacin NSAID Inhibit
prostaglandin
synthesis
50mg/day  Nephrotoxicity
 Hepatotoxicity
 Dyspepsia
 GI ulcers
 Indigestion
Naproxen NSAID Inhibit
prostaglandin
synthesis
375-750mg/day  Abdominal pain
 constipation
 Dizziness
 Drowsiness
 Heartburn

24. Tramadol NSAID Inhibit ascending
pain pathways by
acting on mu
receptors
50-100mg/day  Nausea
 Vomiting
 Constipation
 Somnolence
 Vertigo
Capsaicin Topical analgesic Initially stimulate
transient receptor
potential vanillod -
1 agonist and
causes pain and
finally cause pain
relief by reduction
in TRPV-1
expressing
nociceptive nerve
endings
0.025%-0.075%  Pain at Application site
 Erythema
 Pruritis
 Papules
 Edema
Traimcinolone Intraarticular
corticosteroids
Supress migration
of PMN leucocytes
and fibroblasts
and reversing
capillary
permeability
10-40mg in large joints  Joint swelling
 Contusions
 Sinusitis
 Hypertension
 Diabetes
Methyl
Prednisolone
Intraarticular
corticosteroids
Supress migration
of PMN leucocytes
and fibroblasts
and reversing
capillary
permeability
10-40mg in large joints  Acne
 Amenorrhea
 Poor wound healing
 Hypertension
 Diabetes

25. RESOURCES
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456
984/
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5830
849/
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3792
285/
 https://www.ncbi.nlm.nih.gov/pubmed/24114251
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6302
694/