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RGUHS Nat. J. Pub. Heal. Sci Vol: 14  Issue: 4 eISSN:  pISSN

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Review Article

Anita Basavaraj

Professor and Head, Department of Medicine, Government Medical College, Miraj, Maharashtra

Corresponding author

Dr. Anita Basavaraj

Professor and Head

Department of Medicine

Government Medical College,

Miraj, Maharashtra.

Received Date: 2020-09-05,
Accepted Date: 2020-10-16,
Published Date: 2020-10-31
Year: 2020, Volume: 10, Issue: 4, Page no. 183-186, DOI: 10.26463/rjms.10_4_10
Views: 650, Downloads: 18
Licensing Information:
CC BY NC 4.0 ICON
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0.
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INTRODUCTION

Osteoarthritis (OA) is the most common global chronic joint disease of the elderly. The disease may affect single or multiple joints and even be generalized.

This arthropathy affects the entire joint, involving the cartilage, joint lining, ligaments, and underlying bone and cartilage loss, osteophyte formation (bone spurs), and subchondral bone sclerosis leads to pain, disability, and a reduction in quality of life1 .

Structural changes, visible by radiography, include narrowing of the joint space, osteophyte formation, and bone remodelling around the joints. OA can arise in any synovial joint in the body but is most common in the large joints (knees and hips), hands, and spine.1

OA is believed to result from both biomechanical and molecular changes in the joint brought about by injury, joint malalignment, obesity, aging, and inflammation. Epidemiological studies have relied upon radiographic features to characterize the disease.2

Definition: OA is a non-inflammatory degenerative condition of joints characterized by degeneration of articular cartilage and formation of new bones i.e. Osteophytes

Clinical Features: The main presenting symptom of OA is pain and functional restriction. Pain may directly relate to the OA process through increased pressure in the subchondral bone (mainly causing night pain), trabecular microfractures, capsular distension, and low-grade synovitis, or may result from bursitis and enthesopathy secondary to the altered joint mechanics

Characteristics of Pain in OA:

• Insidious onset over months or years

• Variable or intermittent over time (‘good days, bad days”)

• Mainly related to movement and weightbearing, relieved by rest.

• Only brief (<15 minutes) morning stiffness and brief (<1 minute)” gelling” after rest

• Usually only one or few joints painful (not multiple regional pain)

Clinical Signs:

• Restricted movement (capsular thickening, blocking by osteophyte)

• Palpable, sometimes audible, coarse crepitus (rough articular surfaces)

• Bony swelling(osteophyte)around joint margins

• Deformity, usually without instability

• Joint line or periarticular tenderness

• Muscle weakness, wasting

• No or only mild synovitis (effusion, increased warmth)

Nodal Generalised OA: There are pain, stiffness, and swelling of one or a few finger interphalangeal joints (IPJs). Gradually, over many months, more finger IPJs(distal>proximal )get involved. Affected joints develop posterolateral swelling on each side of the extensor tendon which slowly enlarges and harden to become Heberden’s (distal IPJ) and Bouchard’s (proximal IPJ) nodes. Typically, each joint goes through a phase of episodic symptoms (1-5 years) while the node evolves and OA develops in the underline IPJ. Once fully established, however, symptoms usually subside and hand function often remains relatively unimpaired. Affected IPJs often show characteristic lateral deviation, reflecting the asymmetric focal cartilage loss of OA. Involvement of the first carpometacarpal joint is also common. At this site marked osteophyte and subluxation may result in ‘thumb-base squaring”

Characteristics of Nodal Generalised Osteoarthritis:1

• Polyarticular finger interphalangeal joint OA

• Heberden’s (+_Bouchards nodes)

• Marked female preponderance

• Peak onset in middle age

• Good functional outcomes for hands

• Predisposition to OA at other joints, especially Knees

• Strong genetic predisposition

Investigations

Radiology, X-rays of the affected joints are then the main way osteoarthritis is identified. The common X-ray findings of osteoarthritis include loss of joint cartilage, narrowing of the joint space between adjacent bones, and bone spur formation. Simple X-ray testing can be very helpful to exclude other causes of pain in a particular joint as well as assist the decision-making as to when surgical intervention should be considered. RI is done if Operative Intervention is planned.

Management: There are multiple components of the management of OA. They range from the approach to common OA-related conditions such as depression, sleeping disturbances, and social problems to joint-specific interventions including nonpharmacologic, pharmacologic, and surgical options. Ultimately, most are aimed at improving the pain and functional restriction that characterizes this prevalent disease

Non-Pharmacological treatment:

• Lifestyle modification e.g. exercise and weight reduction

• Avoid aggravating stress to the affected joint

• Implement corrective procedures if poor posture.

Physical activity

a) Avoid avoidance!!! Adherence is a must

b) Slowness of functional decline seen with:

1. Long term Walking

2. Resistance training program

c) Suggest low impact exercises e.g. Swimming

d) Stretching exercises increase range of motion.

Weight Reduction:

• Relieves stress on the affected knees or hips.

• Symptom relief and slowing in cartilage loss in weight-bearing joints (eg, knees).

• lowers levels of the inflammatory cytokines and adipokines that may play a role in cartilage degradation.

Occupational Adjustments:

• Retraining of ADL

• Emphasis on joint protection and energy conservative techniques

Assistive Devices:

• Canes in contralateral hand for Hip OA or Knee OA

• Slip-on knee brace for Knee OA

Patient Education and self-management programs.

PT/OT (Physio Therapy/Occupational Therapy

• ROM Exercises

• Muscle strengthening

• Patellar taping

• Appropriate footwear

• Lateral wedge insoles

• Bracing

• Joint protection and energy conservation

• Heat and cold

• Tai Chi

• Electromagnetic field stimulation and TENS

Pharmacological Treatment:

Goals of pharmacologic treatment are pain relief and improved function, not a reversal of the disease

Acetaminophen: First line choice in the elderly due to safety and efficacy. Works centrally by decreasing prostaglandin activity and peripherally by decreasing pain transmission. Regularly scheduled dosing beneficial

NSAIDs (Non-Steroidal anti-inflammatory): Acetylsalicylic acid, ibuprofen, naproxen, diclofenac, indomethacin, celecoxib. Use Minimal dose for the shortest time possible and with food

Narcotics: Codeine, morphine, oxycodone, hydro morphine, fentanyl, tramadol, meperidine. Given with caution as renal dysfunction and dehydration increases the risk of toxicity. Start low and taper.

Injectables: Corticosteroids (methylprednisolone, triamcinolone) Given as intraarticular and effect last for days to months,

Hyaluronate: Replaces synovial fluid components in joints usually in knee OA. Benefit last for 6 months

Topicals: 1. Diclofenac: Minimal systemic absorption. The message effect of application also beneficial.2. Capsaicin: Depletes substance P, thus decreasing pain

Others:

• Duloxetine: selective serotonin-norepinephrine reuptake inhibitor, significant additional pain reduction, and functional improvement.

• Glucosamine: demonstrates slowing of OA

• Diacerein: Anthraquinone and works by inhibiting interleukin-1

• Prolotherapy: Small volumes of an irritant solution are injected at ligament and tendon insertions and in adjacent joint spaces over several treatment sessions offer significantly greater improvement in pain, function, and stiffness.

• Muscle relaxants: may benefit patients with evidence of muscle spasm.

• Judicious use of narcotics: (e.g., oxycodone and acetaminophen with codeine)

• Chondroprotective drugs: (i.e., matrix metalloproteinase [MMP] inhibitors and growth factors)as disease-modifying drugs;

• monoclonal antibodies: that inhibit nerve growth factor (NGF), such as tanezumab

Surgical Modalities:

Arthroscopy: Indicated for the removal of meniscal tears and loose bodies; Debridement of loose articular cartilage with a microfracture Technique and cartilaginous implants.

Osteotomy: Indicated in cases with misaligned hip or knee joint It shifts weight from the damaged cartilage on the medial aspect of the knee to the healthy lateral aspect of the knee.

Arthroplasty:Performed if all other modalities are ineffective and patient It cannot perform ADLs despite maximal therapy.

Fusion consists of the union of bones on either side of the joint.

• This relieves pain but prevents motion and puts more stress on surrounding joints.

• Used after knee replacements fail or as a primary procedure for ankle or foot arthritis.

Total Knee Replacement: Major Surgical procedure with many benefits

Complications4 :

• The rapid, complete breakdown of cartilage resulting in loose tissue material in the joint (chondrolysis).

• Bone death (osteonecrosis).

• Stress fractures (hairline crack in the bone that develops gradually in response to repeated injury or stress).

• Bleeding inside the joint.

• Infection in the joint.

• Deterioration or rupture of the tendons and ligaments around the joints, leading to loss of stability.

• A pinched nerve (in osteoarthritis of the spine).

Prevention:

1. Maintaining a healthy weight.

2. Exercise

3. Avoid Injuries or Get Them Treated

4. Eat Right including Omega-3 fatty acids.( fish oil and certain plant/nut oils, including walnut, canola, soybean, flaxseed/linseed, and olive) and vitamin D supplements . the body makes most of the vitamin D it needs in response to sunlight (salmon, mackerel, tuna, sardines, and herring; vitamin D-fortified milk, cereal; eggs)

5. Reducing Osteoarthritis Pain

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References

1. Davidson’s principles and Practice of Medicine,22nd edition.

2. Osteoarthritis and Ageing,valdes,Ana M,University of Nottingham-Research Repository.

3. Menkes C J Radiographic criteria for classification of osteoarthritis J Rheumatol suppl 27:13-5 PMID 2027113

4. Osteoarthritis,David T Felson,Chapter 394,harrisons principles of Internal Medicine,19th Edition.

1 References:

1. GPR Clunie,S H Ralston,Chapter 24, Rheumatology and bone disease, Osteoarthritis, Page 1007-1012, Davidson’s principles and Practice of Medicine,23nd edition.

2. Ana M Valdes, Genetic epidemiology of Hip and Knee osteoarthritis, Nature reviews Rheumatology, 7(1) 23-32, November 2010.

3. Menkes C J ,Radiographic crieteria for classification of osteoarthritis.,The Journal of Rheumatology , supplement, 01 February 1991, 27:13-15, PMID 2027113 1364, Harrisons Principles of Internal Medicine, Volume-2, 20th Edition

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