The slide's first pass divides inflammatory arthritis (RA, connective-tissue disease, SpA, crystal arthritis) from non-inflammatory causes of joint pain such as OA and fibromyalgia. ^[1]

Fibromyalgia is a non-inflammatory pain-processing syndrome, not a destructive arthropathy. OA also is not simply passive “wear”: whole-joint biology, including intermittent synovitis and subchondral remodelling, contributes even though the typical clinical pattern is mechanical rather than systemic inflammatory arthritis.

Why does the inflammatory vs. non-inflammatory distinction matter?

• Inflammatory arthritis causes pain, stiffness and objective synovitis; persistent RA synovitis can form pannus, erode cartilage/bone and produce irreversible deformity. Prompt specialist assessment and disease-modifying treatment prevent damage.
• OA produces load-related symptoms and whole-joint structural change. Management is not merely analgesia or surgery: education, exercise and weight management when relevant are core treatments. ^[10]

The lecture's clinical features comparison slide (slide 4) is a classic exam discriminator. ^[1]

Physical exam classifies arthritis by: (1) number — monoarthritis / oligoarthritis / polyarthritis; (2) symmetry — symmetrical vs. asymmetrical; (3) specific joints involved — DIP, MCP, MTP, knee, spine. ^[1]

Why this matters for diagnosis:

• Symmetrical polyarthritis involving MCP, PIP, wrists, MTP → RA
• Asymmetrical oligoarthritis with axial involvement → SpA
• DIP + weight-bearing joints in elderly → OA
• Monoarthritis (especially acute) → gout, septic arthritis, pseudogout, haemarthrosis

What the Examination Images Add

• Do not count “painful joints” from across the room. Confirm true synovitis by soft, boggy swelling, warmth, tenderness and restricted movement; distinguish it from hard bony enlargement.
• The montage contrasts symmetric RA-pattern polyarthritis with asymmetric SpA-pattern disease. Count the joints, then map which joints are involved.
• The DIP photograph includes nail dystrophy beside distal-joint disease, a visual clue to psoriatic arthritis. The MCP photograph shows established ulnar drift, the first-MTP image shows podagra, and the knee image shows a large effusion. These are pattern clues, not diagnoses in isolation.
• A new hot swollen monoarthritis is septic until adequately assessed. When septic arthritis is suspected, obtain urgent synovial fluid for cell count, Gram stain/culture and crystals, ideally before antibiotics unless the patient is septic and treatment cannot wait. ^[15]

The concept of arthritis is Inflammation → Joint damages (slide 5). ^[1]

This is the pathological principle: ongoing inflammation (synovitis) eventually causes structural damage (erosions, deformity, secondary OA). This is why "treat-to-target" strategies aim to suppress inflammation early.

OA is a common cause of non-inflammatory joint pain and its prevalence increases with age. The slide's “75% of women aged ≥65” figure is lecture-era and depends on whether radiographic or symptomatic OA and which joint are measured; do not use it as a universal current prevalence. ^[1]

Typical sites include knees, hips, spine, DIP/PIP joints and the thumb base (1st CMC/trapeziometacarpal joint). The deck uses “three or more joints” for generalised OA, but definitions vary by study and site set. ^[1]

Physical exam: crepitus. Primary OA vs secondary OA. ^[1]

Why these specific joints?

• OA targets joints under maximal mechanical load (knees, hips) or those with unique biomechanical stresses (1st CMC — pinch grip; DIP — terminal loading).
• Primary OA = idiopathic, related to genetics and aging.
• Secondary OA = due to prior injury (fracture, meniscal tear), prior inflammatory arthritis (RA → "burnt out" secondary OA), AVN, Paget's disease. ^[6]

Heberden's nodes (DIP) and Bouchard's nodes (PIP) are bony swellings of OA — these are osteophytes, NOT synovitis. ^[6]

The lecture shows a comparison of normal vs. OA femoral head cartilage. ^[1]

Normal femoral-head cartilage in the gross photograph is smooth and glistening. The OA specimen is irregular, pitted and focally denuded, exposing/remodelling the underlying bone. The paired knee diagram adds capsular thickening, low-grade synovial hypertrophy and these structural responses:

• Sclerosis (increased bone density from attempted repair)
• Cyst formation (synovial fluid intrusion through microfractures)
• Osteophyte formation (new bone at joint margins — the body's attempt to stabilize the joint)

Imaging features of OA: preserved bone density, joint space narrowing (cartilage destruction), sclerosis of subchondral bone, subchondral cysts, marginal osteophytes, joint deformity. ^[1]

Reading the radiographs: the knee image demonstrates compartment-predominant joint-space loss with adjacent subchondral sclerosis; the hip image shows severe superior joint-space loss, osteophytes and femoral-head deformity. The lucent rounded area in subchondral bone is a geode/cyst. Unlike RA, OA narrowing is often non-uniform and load-distribution dependent.

RA is a common autoimmune inflammatory polyarthritis. The slides quote older ancestry-stratified prevalence estimates, a peak onset of 35–55 years and a female predominance. RA can occur in every population and at any adult age; the slide's phrase “rare in blacks” is inaccurate and should not be reproduced as a clinical rule. ^[1]

Recorded prevalence varies with genetics, smoking and other exposures, age structure, case definition and access to diagnosis. Do not infer an individual's likelihood or disease severity from race.

The lecture shows normal vs rheumatoid synovium. The arthroscopic RA image is red, villous and hypertrophic rather than smooth and pale; histology shows a thickened lining with dense inflammatory cellularity. This proliferative tissue (pannus) invades cartilage and marginal bone. ^[1]

A useful mechanistic model (not a mandatory linear sequence):

1. Genetic susceptibility plus environmental/mucosal exposures—especially smoking—promotes loss of tolerance to modified proteins such as citrullinated antigens.
2. ACPA and RF may appear before clinical arthritis, but neither antibody alone causes or proves RA.
3. Macrophage, T-cell, B-cell, fibroblast-like synoviocyte and cytokine networks sustain synovitis.
4. The synovial lining proliferates into pannus; matrix-degrading enzymes and osteoclast activation damage cartilage and marginal bone.
5. Persistent activity produces deformity, secondary OA and disability, which is why early treat-to-target care matters.

RA involves: hands and feet — MCP and PIP, earliest changes in 2nd & 3rd MCP and 3rd PIP; wrists, elbows, knees, ankles, shoulders, hips. Axial skeleton: apophyseal and atlantoaxial joints of cervical spine (C1/2). ^[1]

C1/2 (atlantoaxial) subluxation in RA is a potentially life-threatening complication — pannus erodes the transverse ligament of C1 → anterior subluxation of C1 on C2 → spinal cord compression. The lecture shows an image of the anterior arch of C1 and odontoid (slide 29). ^[1]

The lateral radiograph/MRI series is a safety image, not merely an exam sign: neck pain, occipital pain, limb weakness/numbness, gait disturbance or sphincter symptoms in longstanding RA require urgent assessment. Known/suspected cervical instability must be communicated before anaesthesia or procedures involving neck manipulation.

Disease activities: Pain, Swelling, Stiffness (morning), Functional limitation. Assessed by DAS score, CRP/ESR, ultrasound, MRI. ^[1]

Disease damages: Pain, Deformities (subluxation including C1/2, tendon rupture, dislocation), Secondary OA, Functional limitation. Assessed by X-rays, CT. ^[1]

This distinction is critical: activity = ongoing inflammation (reversible with treatment); damage = structural destruction (irreversible, needs surgery).

44-Joint Swollen Joint Count

The lecture shows a body diagram of the 44 joints assessed for swelling (slide 17). ^[1]

The 44-joint count is used to quantify synovitis in RA and is a component of composite disease activity scores (e.g., DAS28 uses a 28-joint subset). The 44 joints assessed bilaterally are: ^[1]

• Upper limb: sternoclavicular (2), acromioclavicular (2), shoulder (2), elbow (2), wrist (2), MCP 1–5 (10), PIP 1–5 (10)
• Lower limb: knee (2), ankle (2), MTP 1–5 (10)
• Total: 44 joints

Boutonnière deformity, Swan neck deformity, Mallet finger ^[1]

Past paper SAQ (2020) directly asked: "Name four possible deformities in the hands and wrists if the disease further progresses" → Answer: Swan neck, Boutonnière, Z-thumb/hitchhiker's thumb, ulnar deviation of MCP, subluxation of wrist, tendon rupture. ^[3]

Although not explicitly listed on a single slide, the lecture mentions "extra-articular features" (slide 18). From the senior notes and supporting material: ^[1][4][5]

Slide 20 provides approximate frequencies of joint involvement in long-standing RA and a more comprehensive list of extra-articular/systemic manifestations. ^[1]

Approximate frequency of joint involvement in long-standing RA: ^[1]

Additional findings in the lecture's systemic schematic: ^[1]

• Lymph nodes — reactive lymphadenopathy
• Kidney & gut — secondary AA amyloidosis (now uncommon where inflammation is well controlled); renal disease may instead be drug-related or unrelated
• Bone marrow — anaemia, thrombocytosis
• Muscle — wasting
• Skin — ulceration can reflect vasculitis; skin thinning may be glucocorticoid-related rather than RA itself
• Nervous system — peripheral neuropathy

The lecture references the 2010 ACR/EULAR classification criteria (slide 21). ^[1]

A score ≥ 6/10 classifies a patient as definite RA for the criteria's intended setting if there is clinical synovitis in ≥1 joint not better explained by another disease:

Radiological features of RA: (1) Soft tissue swelling and widened joint space — synovial inflammation and effusion; (2) Juxta-articular osteoporosis — hyperaemia and disuse; (3) Joint space narrowing — destruction of cartilage by pannus; (4) Periarticular erosions — pannus destruction of unprotected bone at insertion of joint capsule. ^[1]

Past paper (2020 SAQ Q2c): "Name three expected radiological findings in the affected joints" → Periarticular erosions, juxta-articular osteoporosis, joint space narrowing (and/or soft tissue swelling). ^[3]

Reading the RA Image Sequence

• The early finger films show fusiform soft-tissue swelling and subtle marginal erosions before gross deformity.
• At the MCP heads, look at the bare areas just beyond the cartilage margin for small cortical breaks; these are marginal erosions.
• The advanced bilateral hand film shows uniform joint-space loss, carpal collapse/destruction, MCP subluxation and ulnar drift with relative DIP sparing.
• The wrist close-up shows severe pan-carpal narrowing and erosive destruction. Once this is present, suppressing inflammation can prevent further damage but cannot restore lost architecture—hence the activity-versus-damage distinction.

SpA is a family of overlapping disorders that can present predominantly axially or peripherally: psoriatic arthritis, IBD-associated SpA, reactive arthritis and axial SpA. ^[1]

The lecture diagram places older diagnostic labels on a time arrow toward radiographic sacroiliitis. Do not read it as inevitable linear progression: peripheral and axial manifestations can coexist, and many people with non-radiographic axial SpA never develop radiographic disease. Current terminology distinguishes non-radiographic axial SpA from radiographic axial SpA (traditionally ankylosing spondylitis) by plain-radiograph sacroiliitis—not by calling one an “end stage.”

Why "spondyloarthritis" as a unifying concept? All these conditions share:

• HLA-B27 association
• Enthesitis (inflammation at tendon/ligament insertions)
• Axial involvement (sacroiliitis, spondylitis)
• Peripheral asymmetric arthritis
• Common extra-articular features (uveitis, psoriasis, IBD)

The lecture shows clinical photographs of psoriasis (scaly patches and plaques on the hand), moderate-to-severe nail dystrophy (thickened, discoloured, ridged nail plates with subungual debris), mild nail changes (toenail ridging and discolouration), and dactylitis ("sausage digit" with diffuse fusiform finger swelling). ^[1]

Key clinical features of PsA to recognise from the photographs: ^[1]

• Skin: typical erythematous scaly patches and plaques (may be subtle — check scalp, natal cleft, umbilicus)
• Nail changes: pitting, onycholysis, oil-drop discoloration, subungual hyperkeratosis and crumbling. The severe image is not specific enough to exclude onychomycosis; test for fungal infection when clinically relevant.
• Dactylitis ("sausage digit"): diffuse fusiform swelling of an entire digit due to combined flexor tenosynovitis, synovitis, and soft-tissue oedema — highly characteristic of PsA and other SpA
• The dactylitis image shows whole-digit swelling rather than enlargement confined to one joint; nearby small plaques reinforce the psoriasis association.
• The knee photograph shows asymmetric acute synovitis/effusion, a common peripheral-SpA pattern, but a hot swollen knee still requires exclusion of infection and crystals.
• The Achilles photograph localises swelling/tenderness to the tendon insertion. The calcaneal radiograph shows posterior/plantar enthesophytes; these chronic spurs are not specific for active SpA and can occur with mechanical loading.

Clinical features of SpA: Spondylitis, Peripheral arthritis, Enthesitis (Achilles tendinitis, plantar fasciitis), Anterior uveitis, Aortitis. Associated with HLA-B27. Other associated features: psoriasis, inflammatory bowel disease, dysentery, sexually transmitted disease. ^[1]

HLA-B27: first reported in 1973. ~8–9% of Caucasians carry HLA-B27. Positive in 90–95% of AS patients. Positive in 46–75% of axial SpA patients. HLA-B27 is NOT sensitive or specific in SpA diagnosis. It has a prognostic value. ^[1]

Three theories for HLA-B27 pathogenesis (slides 41–42): ^[1] 1. Arthritogenic peptide hypothesis — B27 trimolecular complex presents an "arthritogenic" or "enthesitogenic" peptide to CD8⁺ T cells. 2. Misfolding / UPR hypothesis — B27 heavy chain misfolding during synthesis in ER → unfolded protein response (UPR) → upregulated IL-23 → Th17 cell activation → IL-17 → IL-17-responsive cells release IL-6, IL-1, TNF-α → inflammation. 3. Free heavy-chain homodimer hypothesis — B27 expressed on cell surface as free heavy-chain homodimers → engage KIR and LILR receptors on NK cells, T cells, and B cells → aberrant immune activation. ^[1]

Modified New York Criteria for AS: ^[1] Clinical criteria: (a) Low back pain and stiffness for > 3 months, improves with exercise, NOT relieved by rest; (b) Limitation of motion of lumbar spine in sagittal AND frontal planes; (c) Limitation of chest expansion relative to age/sex normals. Radiological criteria: sacroiliitis grade ≥2 bilaterally OR grade 3–4 unilaterally. Definite AS = radiological criteria PLUS at least one clinical criterion. ^[1]

Grading of radiological sacroiliitis: ^[1]

The slide's historical “6–11 years” delay illustrates the limitation of waiting for plain-film change. MRI can show inflammation before definite radiographic sacroiliitis, but neither the modified New York nor ASAS criteria are stand-alone diagnostic rules. ^[11][12]

MRI SI joints with fluid-sensitive sequences can detect subchondral bone-marrow oedema before X-ray changes appear; T1-weighted imaging assesses structural lesions. ^[1]

Spine MRI findings in SpA — Inflammation: anterior/posterior spondylitis (corner inflammatory lesion [CIL]), spondylodiscitis, costovertebral joint arthritis, zygoapophyseal joint arthritis, enthesitis of spinal ligaments. Structural changes: fatty deposition (fatty corner lesion [FCL]), erosions, syndesmophytes, ankylosis. ^[1]

The lecture links inflammation → erosion/osteodestruction → repair/new-bone formation. This is a disease model, not a pathognomonic three-image test. ^[1]

The images show vertebral-corner marrow oedema on fluid-sensitive MRI, structural corner change/erosion, then syndesmophyte formation on radiograph. These lesions are supportive only after considering age, mechanical stress, infection, degeneration and the overall SpA phenotype.

Enthesitis is clinically localised pain/swelling at an insertion (for example Achilles). A calcaneal spur is an enthesophyte indicating chronic traction/remodelling and is not specific for SpA or proof of current inflammation.

BASDAI is the patient-reported six-question instrument pictured in the lecture. It covers fatigue, axial pain, peripheral pain/swelling, enthesitis and the severity/duration of morning stiffness. ^[1]

BASDAI is scored 0–10, but a threshold such as ≥4 is a treatment-eligibility convention rather than a diagnosis. Current ASAS–EULAR recommendations prefer ASDAS, which incorporates an acute-phase marker, for disease-activity assessment and treat-to-target decisions. ^[13]

The lecture dedicates several slides (32–36) to standardised spinal mobility measurements from the ASAS handbook. ^[1]

These are used to assess and monitor spinal restriction in axial SpA:

In advanced AS, severe thoracic and cervical kyphosis develops — the patient is "unable to look ahead while walking" (slide 43). ^[1]

What the serial examination photographs teach:

• Standardisation matters more than a single cut-off: keep the heels/back positioned as instructed, prevent knee flexion or trunk rotation, take two attempts and record the best/mean exactly as the protocol specifies.
• Modified Schober assesses lumbar flexion; lateral-flexion fingertip excursion assesses coronal mobility; occiput/tragus-to-wall captures fixed kyphosis; cervical rotation uses a goniometer; intermalleolar distance reflects hip abduction.
• These measures monitor mobility and function; none diagnoses axial SpA by itself. Severe fixed kyphosis also creates horizontal-gaze difficulty and a rigid osteoporotic spine that can fracture after minor trauma—new spinal pain after injury warrants urgent imaging.

The lecture presents the ASAS classification criteria (slide 48), which are distinct from the Modified New York Criteria and allow earlier classification. ^[1]

Axial SpA (back pain ≥ 3 months, onset age < 45 years): ^[1]

Either:
  Sacroiliitis on imaging + ≥1 SpA feature
OR:
  HLA-B27 positive + ≥2 other SpA features

Peripheral SpA (peripheral symptoms only): ^[1]

Arthritis OR enthesitis OR dactylitis
  PLUS either:
    ≥1 of: uveitis, psoriasis, Crohn's/colitis, preceding infection, HLA-B27, sacroiliitis on imaging
  OR:
    ≥2 of: arthritis, enthesitis, dactylitis, IBP ever, family history of SpA

SpA features list: inflammatory back pain, arthritis, enthesitis (heel), uveitis, dactylitis, psoriasis, Crohn's/colitis, good response to NSAIDs, family history of SpA, HLA-B27, elevated CRP. ^[1]

Reported performance: sensitivity 79.5%, specificity 83.3% (n = 975). ^[1]

Goals: Suppress disease activity, prevent joint damage, preserve normal function, and pain relief. ^[1]

Treatment: Education, Physical therapy (physio/OT), Medical therapy, Surgery. ^[1]

Medications for arthritis: ^[1] 1. Symptom-modifying anti-rheumatic drug: NSAIDs (e.g., Diclofenac) 2. Disease-modifying anti-rheumatic drug (DMARD): (a) csDMARD: Methotrexate, Sulfasalazine, Leflunomide (b) bDMARD: anti-TNF, anti-IL6, anti-IL17, anti-CD20 (c) tsDMARD: JAK inhibitors (e.g., Tofacitinib) 3. Steroid ^[1]

Past paper (2020 EMQ): ^[2]

• Q1: Ulnar deviation of MCP joints → Hand splint (C)
• Q2: Improve aerobic exercise tolerance → Physiotherapy (G)
• Q3: Not responsive to DMARDs → TNF inhibitors (J)
• Q4: Glucocorticoid-induced osteoporosis → Alendronate (A)
• Q5: Methotrexate-induced oral ulcers → Folic acid (B)

Orthopedic surgery considerations — Patient factors: location of damaged joint, expectation of patient, age. Surgeon factors: availability of expertise, previous experience. ^[1]

From supporting notes: ^[5]

• Urgent problems: suspected septic arthritis needs immediate specialist management; neurological signs with possible C1/2 instability need urgent spinal assessment.
• Options: synovectomy, tendon reconstruction, decompression, osteotomy, arthrodesis or arthroplasty may be selected according to anatomy, damage and goals.
• Do not use a fixed “lower limb before upper limb” sequence or implant-lifespan promise. Prioritise pain, function, neurological risk, infection, frailty and shared goals.

The lecture shows pre- and post-operative AP knee radiographs (slide 64) demonstrating total knee arthroplasty with alignment reference lines, illustrating surgical correction of a narrowed/irregular medial compartment. ^[1]

Slide 65 shows a clinical before-and-after comparison of a patient with marked bilateral genu varum (bowed legs) corrected to substantially straighter limb alignment after surgery. ^[1]