Arthritis

Slide 1 · Arthritis

Pathogenesis, morphology, and clinicopathologic differentiation

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives: Interpret joint disease by mechanism

Explain how synovium and articular cartilage maintain normal joint function.

Separate degenerative, autoimmune, infectious, and crystal-induced pathways.

Recognize the distinctive joint lesions of OA, RA, infection, gout, and CPPD.

Use joint distribution and tissue pathology to frame the differential diagnosis.

Slide 3 · Joints: Stability and mobility require different anatomy

Solid (nonsynovial) joints

No joint cavity; Minimal movement.

Fibrous connections include sutures and tooth–jaw attachments.

Cartilaginous connections include pubic symphysis.

Synovial joints

A cavity permits a broad range of motion.

Synovial membrane encloses joint within a fibrous capsule.

Cartilage surfaces transmit load and limit friction.

Slide 4 · Synovial joint: Structures vulnerable to arthritis

Synovial cavity

(hyaluronic acid–rich fluid)

Fibrous capsule

Articular cartilage

Synovial membrane

Subchondral bone

Schematic—not a histologic section

Slide 5 · Two synoviocyte populations perform complementary tasks

Type A synoviocytes

Specialized macrophage-like cells.

Phagocytose debris within the synovial environment.

Type B synoviocytes

Fibroblast-like cells.

Synthesize hyaluronic acid and synovial proteins.

Slide 6 · Synovial fluid is a nutrient and lubricant medium

The synovial lining lacks a basement membrane.

Exchange of gases, nutrients, and waste occurs across synovium.

Synovial fluid is a hyaluronic acid–rich plasma filtrate.

It lubricates surfaces and supports avascular articular cartilage.

Slide 7 · Hyaline cartilage: Structure supports mechanical function

Water

70%

Resists compression with proteoglycans

Type II collagen

10%

Tensile integrity and load transmission

Proteoglycans

8%

Hydration and resistance to compression

Chondrocytes maintain this avascular, aneural, and alymphatic matrix.

Slide 8 · Articular cartilage: Maintained by regulated turnover

Chondrocytes

Produce cartilage matrix

Degradative enzymes

Remodel aged or damaged matrix

Endogenous inhibitors

Keep enzyme activity in check

Pathologic interpretation

Joint disease disturbs the balance between matrix synthesis and destruction.

Cytokines such as IL-1 and TNF may accelerate matrix degradation.

Slide 9 · Arthritis: Four major pathogenetic families

Degenerative

Osteoarthritis

Cartilage damage and failed repair

Autoimmune / immune-mediated

Rheumatoid arthritis; Spondyloarthritis

Synovitis or enthesitis

Infectious

Suppurative, tuberculous, viral, Lyme

Organisms or infection-associated inflammation

Crystal-mediated

Gout and calcium pyrophosphate deposition

Crystal-triggered innate inflammation

Slide 10 · The tissue compartment predicts the dominant lesion

Cartilage-centered degeneration

OA begins with chondrocyte and extracellular matrix dysfunction.

Cartilage fissures precede exposed subchondral bone.

Inflammation-centered disorders

RA produces cellular synovitis and invasive pannus.

Spondyloarthropathies often involve entheses.

Crystals activate leukocytes; Infection introduces organisms.

Slide 11 · Clinical pattern helps classify arthritis

Distribution: Monoarticular, oligoarticular, or polyarticular.

Tempo: Abrupt attack, persistent inflammation, or gradual progression.

Tissue response: Effusion, erosions, osteophytes, or ankylosis.

Associated findings: Infection, autoantibodies, enthesitis, or tophi.

Slide 12 · Osteoarthritis: Degenerative cartilage failure

Osteoarthritis (OA) is the commonest joint disease.

Its primary lesion is degeneration of articular cartilage.

Cartilage damage compromises whole-joint structure and function.

Low-grade inflammation contributes secondarily rather than defining the initial lesion.

Slide 13 · Primary and secondary OA differ in predisposing context

Primary (idiopathic) OA

Usually insidious onset with age.

Typically oligoarticular; May become generalized.

No specific precipitating abnormality recognized.

Secondary OA

Associated with previous trauma or joint deformity.

Systemic predispositions include obesity, diabetes, and ochronosis.

Consider underlying causes when OA presents in a younger patient.

Slide 14 · OA pathogenesis: Stress exceeds reparative capacity

Mechanical loading

Chronic articular stress

Chondrocyte injury

Genetic susceptibility can contribute

Matrix imbalance

Degradation outpaces repair

Structural damage

Cartilage and subchondral bone change

Pathologic interpretation

Mechanical stress is central; Inflammatory mediators amplify progression.

Susceptibility polymorphisms may involve matrix and signaling proteins.

Slide 15 · Early OA: Chondrocyte proliferation does not restore matrix

Chondrocytes form proliferative clusters as an attempted repair response.

Proteoglycan synthesis continues, but degradation exceeds replacement.

Cartilage matrix water content increases.

Surface integrity deteriorates despite compensatory cell activity.

Slide 16 · MMP-mediated collagen cleavage creates cartilage fissures

Activated chondrocytes

Release matrix metalloproteinases

Type II collagen injury

Network loses integrity

Surface clefts

Fibrillation and splitting

Progression

Cartilage fragmentation

Pathologic interpretation

Loss of the tensile collagen network permits clefts at the articular surface.

Slide 17 · OA inflammatory mediators aggravate structural damage

TGF-β, IL-1, IL-6, prostaglandins, and nitric oxide are implicated.

Chondrocytes and synovial cells participate in local signaling.

TGF-β can promote matrix metalloproteinase production.

Bone morphogenetic proteins and TGF-β contribute to osteophyte formation.

Slide 18 · Osteoarthritis: A progression of structural injury

Maintained cartilage

Intact articular matrix

And chondrocytes

Early degeneration

Fibrillation and fissures

With repair attempts

Advanced cartilage loss

Eburnation, osteophytes

And subchondral changes

Schematic—not a tissue specimen

Slide 19 · Advanced OA: Exposed bone and loose cartilage fragments

Full-thickness cartilage can detach to form loose bodies (“joint mice”).

Exposed subchondral bone becomes a friction-polished articular surface.

This ivory-like change is termed bone eburnation.

Subchondral bone damage contributes to pain and functional limitation.

Slide 20 · Osteophytes and subchondral cysts have distinct mechanisms

Peripheral bony outgrowths are capped by fibrocartilage and hyaline cartilage.

Chondral caps may later ossify: The mature lesion is an osteophyte.

Microfractures in subarticular bone permit joint fluid entry.

A ball-valve mechanism can expand fibrous-walled subchondral cysts.

Slide 21 · OA radiographic–pathologic correspondence

Imaging feature

Structural substrate

Joint-space narrowing

Loss of hyaline articular cartilage

Subchondral sclerosis

Reactive dense bone beneath damaged surface

Marginal osteophytes

Bony outgrowths at articular margins

Subchondral cysts

Fluid enters damaged subarticular bone

Slide 22 · OA symptom pattern reflects mechanical loading

Deep joint pain typically worsens with use.

Stiffness improves as the joint begins moving.

Crepitus and restricted range of motion are characteristic.

Spinal osteophytes can impinge nerve roots and cause radicular symptoms.

Slide 23 · OA favors selected weight-bearing and hand joints

Predominant location

Characteristic involvement

Axial or weight-bearing

Knees, hips, cervical and lumbar spine

Hand

Distal and proximal interphalangeal joints

Thumb base

First carpometacarpal articulation

Foot

First tarsometatarsal articulation

Slide 24 · OA: Structural severity and symptoms may diverge

Radiographic disease burden does not correlate closely with pain or disability.

Heberden nodes reflect osteophytes at distal interphalangeal joints.

Joint deformities occur, but OA does not characteristically cause ankylosis.

In typical advanced disease, radiography is diagnostically informative without tissue biopsy.

Slide 25 · RA: Systemic autoimmunity centered on destructive synovitis

Rheumatoid arthritis (RA) produces chronic nonsuppurative proliferative synovitis.

Inflammatory synovium can erode cartilage and adjacent bone.

Progression may lead to fibrous or bony ankylosis.

Extraarticular lesions may affect skin, lungs, vessels, heart, and eyes.

Slide 26 · RA initiation requires susceptibility and immune activation

Predisposition

HLA-DR4 association; Other genetic influences

Environmental triggers

Smoking and infection are proposed contributors

Modified antigens

Citrullination creates altered epitopes

Immune response

T- and B-cell activation

Pathologic interpretation

The initiating joint antigen is not definitively identified.

Environmental contribution is plausible but not fully defined in the source.

Slide 27 · Citrullination connects altered self-antigens to ACPA

Arginine modification

Citrullinated peptide epitopes

Antigen recognition

T- and B-cell responses

ACPA formation

Serum anti-citrullinated peptide antibodies

Persistent inflammation

Immune-cell recruitment into synovium

Pathologic interpretation

ACPA aids diagnosis but is not present in all patients.

Slide 28 · RA cytokines have different targets

Mediator

Major pathologic action

TNF, IL-1, IL-6

Recruit leukocytes; induce synovial proteases

IL-17

Recruit neutrophils and monocytes

RANKL

Stimulate osteoclast-mediated bone resorption

IFN-γ

Activate macrophages and synovial cells

Slide 29 · RANKL links immune activation to marginal bone erosion

Activated T cells

Express RANKL

Osteoclast activation

Bone-resorbing cells respond

Periarticular erosion

Synovium advances into bone

Pathologic interpretation

Bone erosion is a defining destructive element of RA.

TNF signaling sustains inflammation and joint damage.

Slide 30 · Rheumatoid pannus: Destructive proliferative synovitis

Inflamed synovium

Hyperplastic villi

Immune infiltrates

Angiogenesis

Pannus

Proliferating synovium

Fibroblasts

Inflammatory tissue

Articular injury

Cartilage invasion

Osteoclast erosions

Potential ankylosis

Pannus is tissue, not simply joint fluid: It invades cartilage and erodes bone.

Slide 31 · RA synovium: Hyperplasia, follicles, and vascular growth

Hyperplastic synoviocytes create villous synovial contours.

CD4+ T cells, B cells, plasma cells, macrophages, and dendritic cells infiltrate.

B cells may form lymphoid follicles; New vessels reflect angiogenesis.

Fibrin-rich surface exudates may contain neutrophils.

Slide 32 · Rheumatoid nodule: Palisading around fibrinoid necrosis

Central fibrinoid

Necrosis

Palisaded activated

Macrophages

Peripheral lymphocytes

And plasma cells

Schematic—not histology

Slide 33 · RA distribution: Small-joint symmetric inflammatory arthritis

Metacarpophalangeal and proximal interphalangeal joints are characteristic.

Hand and foot joints typically precede wrists and larger articulations.

Warm, swollen, painful joints are prominent.

Stiffness and pain are most pronounced after inactivity or in the morning.

Slide 34 · RA serology: Informative but not universally positive

ACPA

Targets citrullinated protein epitopes.

Supports diagnosis and can be associated with more persistent disease.

Negative ACPA does not exclude RA.

Rheumatoid factor

Often IgM or IgA binding the Fc portion of IgG.

Not specific to RA and not present in all patients.

Seronegative RA is a clinical–radiologic diagnosis.

Slide 35 · RA imaging captures inflammatory bone and cartilage injury

Periarticular osteopenia accompanies chronic inflammatory arthritis.

Marginal erosions reflect osteoclast-mediated bone resorption.

Joint-space loss reflects cartilage destruction.

Late disease can develop destructive deformities and ankylosis.

Slide 36 · Extraarticular RA arises beyond articular synovium

Subcutaneous rheumatoid nodules have fibrinoid necrosis and macrophage rims.

Vasculitic injury may involve arterial walls.

Pleural, pericardial, and pulmonary inflammatory lesions may occur.

Ocular complications include uveitis and keratoconjunctivitis.

Slide 37 · Osteoarthritis versus rheumatoid arthritis

Feature

Osteoarthritis

Rheumatoid arthritis

Primary injury

Mechanical cartilage degeneration

Autoimmune synovitis

Inflammation

Usually secondary and mild

Primary and often severe

Articular pathology

Fibrillation, osteophytes, cysts

Pannus, erosions, ankylosis

Serology

No characteristic autoantibodies

ACPA or rheumatoid factor may occur

Systemic lesions

Not typical

May occur in multiple organs

Slide 38 · Why OA and RA produce different late morphology

OA: Failed cartilage maintenance

Articular cartilage fragments.

Eburnation and sclerosis appear.

Osteophytes develop at joint margins.

Inflamed pannus is not the dominant lesion.

RA: Proliferative synovial destruction

Immune-rich villous synovium expands.

Pannus invades articular cartilage.

Bone erosions accompany inflammation.

Ankylosis may follow progressive destruction.

Slide 39 · Juvenile idiopathic arthritis is a heterogeneous childhood group

Onset occurs before age 16 and arthritis persists at least six weeks.

Oligoarthritis and large-joint involvement are relatively common.

Systemic inflammatory manifestations occur in some subgroups.

ANA positivity is common; Rheumatoid nodules are usually absent.

Slide 40 · Seronegative spondyloarthropathies target entheses

Rheumatoid factor is typically absent.

Inflammation concentrates at ligament and tendon insertions.

Sacroiliac and vertebral joints are frequently involved.

HLA-B27 association and new bone formation with ankylosis are shared features.

Slide 41 · Enthesitis: Inflammation at tendon–bone attachment

Tendon / ligament

Bone

Inflammatory focus

At enthesis

Inflammation at insertion sites helps distinguish spondyloarthropathy from primary synovitis.

Schematic

Slide 42 · Ankylosing spondylitis: Axial inflammation and fusion

Sacroiliac and vertebral apophyseal joints are prominent targets.

Patients often present with inflammatory low back pain and reduced mobility.

Articular destruction and new bone formation may cause bony ankylosis.

HLA-B27 is associated, but its precise pathogenic role remains uncertain.

Slide 43 · Reactive arthritis follows an extraarticular infection

Antecedent infection

Genitourinary or gastrointestinal

Interval

Days to weeks

Peripheral arthritis

Often asymmetric oligoarthritis

Enthesitis

Heel or other insertions may inflame

Pathologic interpretation

Triggers mentioned include Chlamydia and enteric bacterial infections.

Joint symptoms are postinfectious; The classic triad need not be complete.

Slide 44 · Reactive arthritis: Recognize the peripheral–extraarticular cluster

Asymmetric lower-limb arthritis often affects the knee.

Achilles tendon or plantar fascial enthesitis may produce heel swelling.

Dactylitis produces diffuse “sausage-like” digit swelling in some patients.

Conjunctivitis, uveitis, urethritis, cervicitis, and mucosal lesions may coexist.

Slide 45 · Infectious arthritis: Three routes to the joint

Hematogenous

Organisms disseminate from a distant focus

Direct inoculation

Entry after joint penetration

Contiguous spread

Extension from soft tissue or bone

Pathologic interpretation

Articular cartilage regenerates poorly after rapid infectious destruction.

The affected joint may become permanently damaged.

Slide 46 · Suppurative bacterial arthritis is a destructive emergency

An acute bacterial joint infection often arises through bloodstream spread.

S. Aureus is the dominant cause in the United States.

Host factors and exposure settings influence other likely organisms.

Delay in recognition can permit rapid permanent cartilage damage.

Slide 47 · Suppurative arthritis: Clinical context suggests organisms

Setting

Source-associated consideration

Neonate

Group B Streptococcus; spread from osteomyelitis

Sickle cell disease

Salmonella susceptibility

Terminal complement C5–C9 deficiency

Disseminated gonococcal infection

Immunodeficiency or injected substance use

Increased risk of septic arthritis

Slide 48 · Acute suppurative arthritis: Aspirate the inflamed joint

Typically presents abruptly with intense pain and limited movement.

Warmth, swelling, fever, leukocytosis, and high CRP are common.

Most cases are monoarticular; Large joints are frequent sites.

Purulent aspirate with an identifiable organism supports diagnosis.

Slide 49 · Mycobacterial arthritis: Granulomatous chronic damage

M. Tuberculosis can reach a joint through blood or adjacent osteomyelitis.

The course is insidious, with progressively increasing pain.

Confluent caseating granulomas form in infected synovium.

Erosive pannus and eventual fibrous ankylosis may obliterate the joint space.

Slide 50 · Viral arthritis can be infectious or immune-mediated

Reported causes include alphaviruses, parvovirus B19, and rubella.

Epstein–Barr virus and hepatitis B or C also can be associated.

The course varies from acute to subacute.

Joint symptoms may reflect direct infection or immune responses triggered by infection.

Slide 51 · Lyme arthritis: A joint manifestation after dissemination

Tick-borne Borrelia

Inoculation during Ixodes bite

Dissemination

Spread beyond skin

Joint episodes

Often one or two large joints

Recurrence

New joints may be affected over time

Pathologic interpretation

The knee is a particularly common site.

Earlier treatment of infection reduces subsequent arthritis risk.

Slide 52 · Lyme arthritis: Serology and persistent inflammation

Serologic anti-Borrelia antibody testing is central to diagnosis.

Borrelia DNA may also be detected in synovial fluid using PCR.

Most cases respond to appropriate antimicrobial treatment.

Persistent arthritis after treatment may reflect a postinfectious immune process.

Slide 53 · Crystal-induced arthritis is an innate inflammatory response

Monosodium urate crystals cause gout.

Calcium pyrophosphate crystals produce CPP deposition disease (CPPD).

Basic calcium phosphate and prosthetic wear debris are additional triggers.

Crystal deposits provoke joint inflammation that can damage cartilage.

Slide 54 · Gout requires urate excess plus joint crystallization

Hyperuricemia

Elevated urate in fluids

Crystal precipitation

Monosodium urate in joints

Acute synovitis

Innate leukocyte response

Recurrent episodes

Tophi and erosive damage may follow

Pathologic interpretation

Urate elevation is necessary but insufficient for clinical gout.

Not every person with hyperuricemia develops symptomatic disease.

Slide 55 · Urate can increase through production or impaired excretion

Overproduction

Uric acid is the terminal product of purine catabolism.

High cell turnover and purine salvage defects increase urate synthesis.

HGPRT defects illustrate disturbed purine salvage.

Underexcretion

Reduced renal clearance is common in primary gout.

Transport genes contribute to urate homeostasis.

Chronic renal disease and some medications reduce excretion.

Slide 56 · Factors influencing symptomatic gout

Prolonged elevation of serum urate increases the opportunity for crystallization.

Genetic variants can influence transport, ion handling, and inflammation.

Obesity and alcohol exposure are associated with risk.

Diuretic use may reduce renal urate excretion.

Slide 57 · Urate crystals amplify acute innate inflammation

Crystals

Precipitate into joint

Macrophages

Phagocytose urate

Inflammasome

Caspase-1 activation → IL-1

Neutrophils

Recruited into synovial fluid

Injury

Proteases and inflammatory mediators

Recurring neutrophil recruitment sustains the acute flare.

Slide 58 · Acute gout becomes self-amplifying after neutrophil influx

Urate ingestion

Phagocytes ingest crystals

Mediator release

IL-1 and enzyme pathways

Cell recruitment

More neutrophils accumulate

Tissue injury

Proteases and radicals amplify synovitis

Pathologic interpretation

Phagolysosome damage and complement contribute to inflammation.

Slide 59 · Acute gout pathology is neutrophil-rich crystal synovitis

Synovial fluid and membrane contain dense neutrophilic infiltrates.

Slender urate needles may be found within aspirated neutrophils.

Crystals display negative birefringence with compensated polarized microscopy.

Inflammation subsides as crystallization episodes resolve.

Slide 60 · Tophaceous gout represents persistent crystal burden

Tophi are aggregates of urate surrounded by foreign-body giant cells.

Deposits may involve synovium, cartilage, tendons, bursae, and soft tissue.

Tophaceous synovitis causes juxtaarticular erosions and cartilage loss.

Extraarticular deposits can be associated with renal complications.

Slide 61 · Gout: Four clinical phases

Stage

Clinical–pathologic phenotype

Asymptomatic hyperuricemia

Excess serum urate without acute synovitis

Acute gouty arthritis

Abrupt, severe, often monoarticular inflammation

Intercritical gout

Symptom-free interval between attacks

Chronic tophaceous gout

Persistent tophi with structural erosive damage

Slide 62 · Crystal morphology: Urate versus calcium pyrophosphate

Monosodium urate (gout)

Calcium pyrophosphate (CPPD)

Slender needle-shaped crystals

Negative birefringence

Rhomboid crystals

Positive birefringence

Schematic—crystals not depicted from a specimen

Slide 63 · CPPD: Crystallization within cartilage precedes synovitis

CPP crystals accumulate in hyaline cartilage and fibrocartilage.

Proteoglycan loss is thought to favor mineral deposition around chondrocytes.

Deposits can disrupt the matrix even without overt inflammation.

Crystals entering the joint activate the inflammasome and IL-1 pathways.

Slide 64 · CPPD is not synonymous with a symptomatic attack

CPPD may be silent despite cartilage crystal deposits.

Acute or subacute attacks commonly affect the knee or wrist.

Chronic joint pain may resemble OA or RA.

Chondrocalcinosis on imaging identifies calcification, not necessarily clinical arthritis.

Slide 65 · Gout versus CPPD: Microscopy and joint pattern

Characteristic

Gout (urate)

CPPD

Crystal morphology

Needle-shaped

Rhomboid

Compensated polarization

Negative birefringence

Positive birefringence

Primary deposition

Synovial / periarticular urate

Cartilage / fibrocartilage CPP

Typical acute site

First MTP joint common

Knee and wrist common

Distinctive chronic finding

Tophi and erosions

Chondrocalcinosis ± joint damage

Slide 66 · CPPD associations may point to an underlying condition

Many cases are age-associated and sporadic.

Secondary CPPD can be associated with prior joint damage.

Reported systemic associations include hyperparathyroidism and hemochromatosis.

Hypomagnesemia, hypothyroidism, ochronosis, and diabetes are also listed.

Slide 67 · An acutely swollen joint: Mechanism-based triage

Acute painful joint with swelling

Infection

Abrupt monoarthritis

Identify organism in aspirate

Crystal disease

Identify urate or CPP crystals

By polarization

Immune-mediated

Pattern of chronic synovitis

And other-organ findings

Suspected suppurative arthritis requires prompt aspiration and evaluation.

Slide 68 · Mechanism-based differential: Identify the decisive lesion

Pattern

Leading pathology clue

Slow mechanical pain

Cartilage fibrillation, osteophytes, eburnation

Symmetric small-joint inflammation

Hyperplastic immune-rich synovium and pannus

Axial pain with enthesitis

Insertion-site inflammation and possible ankylosis

Explosive hot monoarthritis

Exclude bacterial seeding; evaluate joint aspirate

Episodic crystal arthritis

Synovial crystals with neutrophilic inflammation

Slide 69 · Illustrative case: Mechanical versus immune-mediated symptoms

A 69-year-old develops knee pain with walking and gradually worsening crepitus.

Finger radiographs show prominent distal interphalangeal osteophytes.

There is no sustained inflammatory small-joint swelling.

Question: Which cartilage and bone lesions should be expected?

Slide 70 · Case interpretation: Degenerative architecture is expected

The presentation favors osteoarthritis over rheumatoid arthritis.

Expected pathology: Fissured cartilage, chondrocyte clusters, and eventual eburnation.

Peripheral osteophytes and subchondral cysts may develop.

ACPA or rheumatoid factor are not central to this degenerative diagnosis.

Slide 71 · Illustrative case: An acutely painful swollen knee

A patient develops sudden severe monoarticular knee pain with fever.

The joint is warm and movement is markedly restricted.

The history also includes previous gout attacks.

Question: What competing mechanisms must be considered immediately?

Slide 72 · Case interpretation: Do not overlook suppurative arthritis

Bacterial infection may rapidly destroy articular cartilage.

Joint aspiration can identify an organism in purulent fluid.

Crystal-associated synovitis also causes abrupt neutrophilic inflammation.

Urgent exclusion of infection takes precedence over assuming a gout flare.

Slide 73 · Arthritis: Anchor the diagnosis to the mechanism

Category

Primary lesion

Highest-value clue

Osteoarthritis

Cartilage breakdown

Osteophytes and eburnation

Rheumatoid arthritis

Immune proliferative synovitis

Pannus with marginal erosion

Spondyloarthritis

Enthesis / axial inflammation

Enthesitis and ankylosis

Infectious arthritis

Microbial joint injury

Organism in inflammatory aspirate

Crystal disease

Crystal-driven innate inflammation

Urate or CPP crystals

Slide 74 · Source reference and further reading

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th ed. Elsevier; 2026. Chapter 26, “Bones, Joints, and Soft Tissue Tumors,” pp. 1088–1097.

Sections: Joints; Arthritis; Osteoarthritis; Rheumatoid Arthritis; Spondyloarthropathies; Infectious Arthritis; Crystal-Induced Arthritis.

Chapter 26, Table 26.5: Comparative Features of Osteoarthritis and Rheumatoid Arthritis.

Chapter 26, Figs. 26.30–26.39: mechanisms and morphology of arthritis.