Arthritis: Inflammatory & Degenerative

First split: mechanical vs inflammatory

Two mechanisms. Osteoarthritis is degenerative and mechanical: wear and loss of articular cartilage. Rheumatoid arthritis and the spondyloarthropathies are autoimmune inflammatory synovitis. The history usually separates them before any test is sent.

Inflammatory clues. Morning stiffness lasting over 1 hour that improves with use, warm swollen joints, and systemic features such as fatigue, raised ESR/CRP, and anemia of chronic disease.

Mechanical clues. Stiffness under 30 minutes that worsens with use, pain that builds toward the end of the day, and no systemic signs.

Osteoarthritis

Pathology. Progressive cartilage loss in weight-bearing and high-use joints: knees, hips, spine, DIP, PIP, and the first CMC at the base of the thumb. Chondrocytes respond to mechanical stress with matrix breakdown, so the cartilage fissures and thins. Exposed subchondral bone becomes sclerotic and polished (eburnation), subchondral cysts form, and reactive bony spurs (osteophytes) grow at the joint margins; fragments can break off as loose bodies. Age, obesity, and prior joint injury are the main risk factors.

Clinical picture. Pain worsens with use and at day's end, and morning stiffness lasts under 30 minutes. Marginal osteophytes on the fingers form bony nodes: Heberden nodes at the DIP and Bouchard nodes at the PIP, while the MCPs are spared. X-ray shows osteophytes, joint-space narrowing, and subchondral sclerosis and cysts. There is no systemic inflammation, and joint fluid is noninflammatory.

OA hits the DIP (Heberden nodes); RA spares the DIP. That single joint is a fast discriminator between the two.

Rheumatoid arthritis

Joint disease. A symmetric inflammatory synovitis of small joints (MCP, PIP, wrists) that spares the DIP, more common in women. The hyperplastic, inflamed synovium forms a pannus of granulation tissue rich in lymphocytes, plasma cells, and macrophages that erodes cartilage and bone. Chronic damage produces ulnar deviation at the MCPs, swan-neck and boutonniere deformities, and a Z-thumb. Morning stiffness lasts over 1 hour and eases with use.

Serology and genetics. Anti-CCP (anti-citrullinated peptide) antibody is about 95% specific for RA and predicts erosive disease. Rheumatoid factor, an IgM directed against the Fc portion of IgG, is sensitive but nonspecific: it is also positive in hepatitis C, Sjögren syndrome, and endocarditis. HLA-DR4 confers genetic risk, and smoking promotes the protein citrullination that anti-CCP targets.

RA reaches beyond the joints.

• Rheumatoid nodules: central fibrinoid necrosis ringed by palisading histiocytes, typically over pressure points.
• Lung: interstitial lung disease; Caplan syndrome (RA plus pneumoconiosis nodules).
• Felty syndrome: RA plus splenomegaly plus neutropenia.
• Secondary Sjögren syndrome, pericarditis, AA amyloidosis, and anemia of chronic disease.
• Atlantoaxial (C1–C2) subluxation, which risks cervical cord injury during neck extension for intubation.

Atlantoaxial subluxation is a pre-anesthesia red flag in long-standing RA; the cervical spine is the one part of the axial skeleton RA commonly attacks.

Treatment principle. Methotrexate is the first-line disease-modifying drug; biologics such as TNF-α inhibitors are added for refractory disease after screening for latent tuberculosis.

Seronegative spondyloarthropathies (PAIR)

Shared features. These arthritides are RF-negative (hence "seronegative"), associated with HLA-B27 (an MHC class I allele), and more common in men. They share axial disease (sacroiliitis), enthesitis (inflammation where tendons and ligaments insert into bone, such as the Achilles), dactylitis, and anterior uveitis. Mnemonic PAIR: Psoriatic arthritis, Ankylosing spondylitis, IBD-associated arthritis, Reactive arthritis.

Ankylosing spondylitis. Young men with inflammatory low-back pain and sacroiliitis: pain is worse in the morning and at rest and better with exercise. Progressive vertebral fusion produces a bamboo spine, and costovertebral involvement reduces chest expansion. Extra-articular disease includes anterior uveitis and aortic regurgitation. Labs show HLA-B27 and an elevated ESR.

Reactive arthritis (formerly Reiter syndrome). Follows, by weeks, a GI infection (Shigella, Salmonella, Campylobacter, Yersinia) or genitourinary Chlamydia. The joint itself is sterile; the arthritis is an immune reaction to a distant infection. Classic triad: conjunctivitis/uveitis, urethritis, and arthritis ("can't see, can't pee, can't climb a tree"), plus keratoderma blennorrhagicum and circinate balanitis.

Psoriatic and IBD-associated arthritis. Psoriatic arthritis affects up to a third of psoriasis patients: asymmetric, involving the DIP, with dactylitis (sausage digit), nail pitting and onycholysis, and a pencil-in-cup deformity on X-ray. IBD-associated arthritis (Crohn disease, ulcerative colitis) causes both peripheral and axial disease; peripheral flares tend to track bowel activity, whereas axial disease runs its own course.

Septic arthritis and synovial fluid

Septic arthritis is an emergency. An acutely red, hot, swollen, exquisitely painful monoarticular joint with fever, most often the knee. Staphylococcus aureus is the most common cause overall; it seeds the joint hematogenously and destroys cartilage within days. Prior joint damage (e.g., RA), prosthetic joints, and IV drug use raise risk. Arthrocentesis is mandatory before or together with empiric antibiotics.

Gonococcal arthritis. In sexually active young adults, disseminated Neisseria gonorrhoeae (a Gram-negative diplococcus) is a leading cause. It presents either as a purulent monoarthritis or as a triad of migratory polyarthralgia, tenosynovitis, and vesiculopustular dermatitis. Joint cultures are often negative, so culture joint, blood, and mucosal sites; treat with ceftriaxone.

Synovial fluid sorts the arthritis. Always tap a hot joint and send cell count, Gram stain, culture, and crystal analysis.