Systemic Lupus Erythematosus - Musculoskeletal

Musculoskeletal complaints are the most common reason a patient with SLE first presents to a clinician, and they remain the leading cause of morbidity through the disease course. The orthopaedic surgeon encounters SLE in three principal scenarios: a hand deformity that mimics rheumatoid arthritis (Jaccoud arthropathy), avascular necrosis of the femoral head in a young patient on steroids, and the perioperative management of an SLE patient listed for arthroplasty or fracture fixation. Each scenario has a defined evidence base and a checklist that examiners love to test.

SLE is one of the classic causes of multifocal AVN. A young patient on steroids with one painful joint should trigger MRI of at least both hips and both knees; some centres add shoulders and ankles. The detection of pre-collapse disease changes management from arthroplasty to joint-preserving core decompression. Missing the contralateral lesion is a recurring exam pitfall.

The one-pager lists "tendon rupture" but it deserves its own answer because it is a classic SLE viva trap: a steroid-treated lupus patient who ruptures a major tendon after trivial or no trauma.

• Mechanism: chronic steroid use plus a lupus enthesopathy degrades the tendon-bone junction; ruptures are typically at the insertion and the tendon quality is poor.
• Sites: the extensor mechanism is classic - patellar tendon, quadriceps tendon, Achilles tendon, and finger extensors; bilateral and multiple ruptures are characteristic and a strong clue to the diagnosis.
• Recognition: a sudden extensor lag, palpable gap and inability to straight-leg-raise after a minor stumble; always examine and image the contralateral side because simultaneous/sequential bilateral rupture is described.
• Management: surgical repair is harder than in normal tendon (friable tissue, high re-rupture), so use augmentation/reinforcement, protect with longer immobilisation, and optimise steroid dose first; a missed or late repair retracts and becomes a reconstruction.

Exam point: an atraumatic patellar or quadriceps tendon rupture in a young person on steroids is SLE (or chronic kidney disease/RA) until proven otherwise - and check the other leg.

AVN gets the attention, but the same steroids cause glucocorticoid-induced osteoporosis (GIOP) - the commonest cause of secondary osteoporosis and a distinct, examinable MSK complication in SLE that the surgeon must not conflate with AVN.

• Mechanism: glucocorticoids suppress osteoblasts and prolong osteoclast survival, causing rapid bone loss in the first 3-6 months of therapy that disproportionately affects trabecular bone (vertebrae, femoral neck) - so fractures occur at a higher bone-density level than in postmenopausal osteoporosis.
• Consequence: vertebral fragility (often atraumatic/asymptomatic) fractures and hip/wrist fractures; lupus adds inflammation, renal impairment, low vitamin D and reduced mobility on top of the steroid effect.
• Prevention/treatment: lowest effective steroid dose; calcium and vitamin D; assess fracture risk with FRAX (with the glucocorticoid adjustment) and DXA; start a bisphosphonate (or denosumab) for patients on significant ongoing steroids or with a prior fragility fracture, per glucocorticoid-osteoporosis guidance.
• Distinction from AVN: GIOP = generalised low bone mass / fragility fracture (DXA, vertebral imaging); AVN = focal subchondral bone death (MRI double-line sign). Both are steroid-driven and can coexist - a steroid-treated lupus patient needs both a bone-protection plan and AVN vigilance.

Good prognostic markers: early hydroxychloroquine, low cumulative steroid dose, quiescent disease at time of surgery, normal renal function, no APS antibodies.

Adverse prognostic markers: cumulative prednisolone greater than 5 g, lupus nephritis, positive lupus anticoagulant, multifocal AVN, recurrent infection, active serositis at the time of surgery.

Key message for the exam: the dominant modifiable driver of MSK morbidity in SLE is cumulative steroid exposure - protect the bone by using steroid-sparing agents early.

There is no dedicated arthroplasty registry for SLE AVN, but national joint registries (NJR, AJRR, AOANJRR) capture patients with secondary OA due to AVN, including SLE subgroups. Reported outcomes show higher PJI, VTE, and revision rates than matched primary OA, reinforcing the need for enhanced perioperative protocols. The evidence base for medical management is dominated by RCTs of biologics and DMARDs; surgical evidence is largely case series and cohort studies.