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'Arthritis', osteoarthritis, etiology, pathophysiology, sign & symptoms, diagnosis, treatment

Arthritis| what is osteoarthritis|

Etiology of osteoarthritis | 

Pathophysiology of osteoarthritis | 

Sign& symptoms of osteoarthritis | 

Diagnostic test of osteoarthritis | 

Treatment of osteoarthritis|

Non pharmacological treatment |

pharmacological treatment|

 Treatment of Hip and knee OA|

Treatment of Hand OA|

Arthritis

Arthritis means ; any disorders of bones that affect joints of bones. Symptoms generally include joint pain, stiffness of jojnts, redness, warmth and swelling of joints.There are several forms of Arthritis mainly; osteoarthritis, rheumatoid arthritis, gout, SLE, and ankylosing spondylitis. 
  Here I'm going to explain about osteoarthritis, etiology of osteoarthritis, pathophysiology of osteoarthritis, sign & symptoms of osteoarthritis and treatment of osteoarthritis.

Osteoarthritis 

• Osteoarthritis (OA) is a common, progressive disorder affecting primarily weight bearing diarthrodial joints, characterized by progressive deterioration and loss of articular cartilage, osteophyte formation, pain, limitation of motion, deformity, and disability. Osteoarthritis is one of the leading causes of disability in the United States.

Etiology of osteoarthritis

The etiology of OA is multifactorial and complex, with development of OA depending on interplay between factors such as genetic predisposition and joint injury. Many patients have more than one risk factor for the development of OA. The most common risk factors for the development of OA include age, obesity, sex, occupation, participation in certain sports, history of joint injury or surgery, and genetic predisposition.

Obesity

Obesity is the most important preventable risk factor for OA. This linkage is strongest for knee OA, although hip OA and even hand and wrist OA may be linked with obesity. Men who are obese at baseline had a 2.8-fold increase in developing knee OA compared with the non-obese men, whereas women who were obese at baseline had a 4.4-fold increased risk in developing knee OA compared with non-obese women. Also, there was an increased risk for severe knee OA in obese subjects. 

Occupation, Sports, and Trauma

OA risk is increased for people in occupations involving excessive mechanical stress. Work that involves prolonged standing, kneeling, squatting, lifting, or moving of heavy objects increases risk of OA. Such occupations include construction, mining, healthcare assistance, factory work, carpentry, and farming. Repetitive motion also contributes to hand OA, with the dominant hand usually affected.
Traumatic injury to articular cartilage during sports and other activities or in accidents greatly increases OA risk.

Genetic Factors

Genetic influences on OA have been appreciated for many years. Heberden nodes are 10 times more prevalent in women than in men, for example, with a two fold higher risk if the woman’s mother had them. Genetic links have been shown with OA of the first metatarsophalangeal joint and with generalized OA. Twin studies indicate that OA can be attributed substantially to genetic factors. The  genes include Col11A1 (extracellular matrix), Chrom 19 (cartilage morphogenesis), MCFL (pain perception), CHST11 (cartilage morphogenesis), GDF5 (TGF beta signaling), and Chrom7Q22.

Pathophysiology of osteoarthritis

• Primary (idiopathic) OA, the most common type, has no known cause.

• Secondary OA is associated with a known cause, such as trauma, metabolic or endocrine disorders, and congenital factors.

• OA usually begins with damage to articular cartilage through injury, excessive joint loading from obesity or other reasons, or joint instability or injury. Damage to cartilage increases activity of chondrocytesin attempt to repair damage, leading to increased synthesis of matrix constituents with cartilage swelling. Normal balance between ­cartilage breakdown and resynthesis is lost, with increasing destruction and cartilage loss.

• Subchondral bone adjacent to articular cartilage undergoes pathologic changes and releases vasoactivepeptides and matrixmetalloproteinases (MMPs). Neovascularization and increased permeability of adjacent cartilage occur, which contribute to cartilage loss and chondrocyte apoptosis.

• Cartilage loss causes joint space narrowing and painful, deformed joints. Remaining cartilage softens and develops fibrillations, followed by further cartilage loss and exposure of underlying bone. New bone formations (osteophytes) at joint margins distant from cartilage destruction are thought to help stabilize affected joints.

• Inflammatory changes can occur in the joint capsule and synovium. Crystals or cartilage shards in synovial fluid may contribute to inflammation. Interleukin-1, prostaglandin E2, tumor necrosis factor-α (TNF-α), and nitric oxide in synovial fluid may also play a role. Inflammatory changes result in synovial effusions and thickening.

• Pain may result from distention of the synovial capsule by increased joint fluid; micro fracture; periosteal irritation; or damage to ligaments, synovium, or the meniscus.

Sign & symptoms of Osteoarthritis

• Predominant symptom is deep, aching pain in affected joints. Pain accompanies joint activity and decreases with rest.

• Joints most commonly affected are the distal interphalangeal(DIP) and proximal interphalangeal
(PIP) joints of the hand, first carpometacarpal joint, knees, hips,cervical and lumbar spine, and first metatarsophalangeal (MTP) joint of the toe.

• Limitation of motion, stiffness, crepitus, and deformities may occur. Patients with lower extremity involvement may report weakness or instability.

• Upon arising, joint stiffness typically lasts less than 30 minutes and resolves with motion.

• Presence of warm, red, and tender joints suggests inflammatory synovitis.

• Physical examination of affected joints reveals tenderness, crepitus, and possibly
enlargement. Heberden and Bouchard nodes are bony enlargements (osteophytes).

Diagnosis

• Diagnosis is made through patient history, physician examination, radiologic findings, and laboratory testing.

• American College of Rheumatology (ACR) criteria for classification of OA of the hips, knees, and hands include presence of pain, bony changes on examination, normal erythrocyte sedimentation rate (ESR), and radiographs showing osteophytes or joint space narrowing.

• For hip OA, patient must have hip pain and two of the following: (1)ESR less than 20 mm/h, (2) radiographic femoral or acetabular osteophytes, and/or (3)radiographic joint space narrowing.

• For knee OA, patient must have knee pain and radiographic osteophytes in addition
to one or more of the following: (1) age more than 50 years, (2) morning stiffness lasting 30 minutes or less, (3) crepitus on motion, (4) bony enlargement, (6) bony tenderness, and/or (7) palpable joint warmth.

• ESR may be slightly elevated if inflammation is present. Rheumatoid factor is negative.
Analysis of synovial fluid reveals high viscosity and mild leukocytosis (<2000 white blood cells/mm3 [<2 × 109/L]) with predominantly mononuclear cells.

Treatment of Osteoarthritis

NONPHARMACOLOGIC THERAPY:

• Educate patient about disease process and extent, prognosis, and treatment. Promotedietary counseling, exercise, and weight loss program for overweight patients.

• Physical therapy—with heat/cold treatment and an exercise program—helps maintain range of motion and reduce pain and need for analgesics.

• Assistive and orthotic devices (canes, walkers, braces, heel cups, insoles) can be used during exercise or daily activities.

• Surgical procedures (eg, osteotomy, arthroplasty, joint fusion) are indicated for functional disability and/or severe pain unresponsive to conservative therapy.

PHARMACOLOGIC THERAPY:

Knee and Hip OA : 

• Acetaminophen is a preferred first-line treatment; it may be less effective than oral nonsteroidal anti-inflammatory drugs(NSAIDs) but has less risk of serious gastrointestinal (GI) and cardiovascular events.
• If a patient fails acetaminophen, nonselective NSAIDs or cyclooxygenase-2 (COX-2) selective inhibitors (eg, celecoxib) are recommended.
• For knee OA, topical NSAIDs are recommended if acetaminophen fails and are preferred over oral NSAIDs in patients older than 75 years. Topical NSAIDs provide similar pain relief with fewer adverse GI events than oral NSAIDs.

Intra-articular (IA) corticosteroid injections are recommended for both hip and knee OA when analgesia with acetaminophen or NSAIDs is suboptimal. Injections can be given with concomitant oral analgesics for additional pain control. Do not administer injections more frequently than once every 3 months to minimize systemic adverse effects.

 Tramadol is recommended for hip and knee OA in patients who have failed scheduled full-dose acetaminophen and topical NSAIDs, who are not appropriate candidates for oral NSAIDs, and who are not able to receive IA corticosteroids.

Duloxetine can be used as adjunctive treatment in patients with partial response to first-line analgesics (acetaminophen, oral NSAIDs). It may be a preferred second-line medication in patients with both neuropathic and musculoskeletal OA pain.

IA hyaluronic acid is not routinely recommended for knee OA pain. Injections do not provide clinically meaningful improvement and may be associated with serious adverse events (eg, increased pain, joint swelling, and stiffness).

Glucosamine and/or chondroitin and topical rubefacients (eg, methyl salicylate, trolamine salicylate) lack uniform efficacy for hip and knee pain and are not preferred treatment options.

Hand OA: 

• Topical NSAIDs are a first-line option for hand OA. Diclofenac has efficacy similar to oral ibuprofen and oral diclofenac with fewer adverse GI events, albeit with some local application site events.

Oral NSAIDs are an alternative first-line treatment for patients who cannot tolerate the local skin reactions or who received inadequate relief from topical NSAIDs.

Capsaicin cream is an alternative first-line treatment and demonstrates modest improvement in pain scores. It is a reasonable option for patients unable to take oral NSAIDs. Adverse effects are primarily skin irritation and burning.

 Tramadol is an alternative first-line treatment and is a reasonable choice for patients who do not respond to topical therapy and are not candidates for oral NSAIDs because of high GI adverse effects ,cardiovascular, or renal risks. Tramadol may also be used in combination with partially effective acetaminophen, topical therapy, or oral NSAIDs.