Orthopaedics
Trauma and orthopaedics for the Indian MBBS final-year exam — fractures, dislocations, bone and joint infection, tumours, the spine, arthritis, paediatric and regional orthopaedics. Full-length explanation-first answers with diagrams.
Definition & Importance
Bone tumours are neoplasms arising in bone; they may be primary (from bone-forming, cartilage-forming, fibrous or marrow cells) or secondary (metastatic), and benign or malignant. Primary bone tumours are relatively rare, but early recognition matters because a missed malignancy loses the window for limb-salvage and cure, whereas an unnecessary aggressive biopsy of a benign lesion causes harm. A logical, staged approach is therefore essential.
Tissue of origin Benign Malignant Bone-forming Osteoid osteoma, osteoblastoma Osteosarcoma Cartilage-forming Osteochondroma, enchondroma, chondroblastoma Chondrosarcoma Marrow (round cell) — Ewing’s sarcoma, myeloma, lymphoma Fibrous Fibrous dysplasia, non-ossifying fibroma Fibrosarcoma Uncertain/other Giant cell tumour, ABC, simple bone cyst Metastatic carcinoma (commonest) Assessing a Bone Lesion
Assessment integrates age (each tumour has a typical age range), the bone and the site within it (epiphysis vs metaphysis vs diaphysis), the clinical picture, and the radiographic character. Key radiographic questions define aggressiveness: the zone of transition (narrow/sclerotic = benign; wide/permeative = aggressive), the pattern of bone destruction (geographic vs moth-eaten vs permeative), the periosteal reaction (solid = benign; interrupted ‘sunburst’, ‘onion-skin’ or Codman’s triangle = aggressive), and any soft-tissue mass or matrix mineralisation.
💡Benign lesions tend to be well-defined with a narrow zone of transition and a sclerotic margin; malignant lesions show a wide zone of transition, cortical destruction, aggressive periosteal reaction and a soft-tissue mass. Age is one of the most useful single clues.Clinical Features Suggesting Malignancy
Warning features are progressive deep-seated pain (often worse at night and unrelated to activity), a enlarging mass, a pathological fracture through a lesion, and constitutional symptoms. Any persistent unexplained bone pain, particularly around the knee in a young person, warrants a radiograph.
Investigations & Staging
Plain radiographs in two planes are the essential first step. MRI defines intramedullary and soft-tissue extent and the relationship to neurovascular structures; CT chest detects pulmonary metastases; a bone scan / PET assesses skeletal spread. The definitive diagnosis rests on biopsy. Malignant tumours are staged by the Enneking (Musculoskeletal Tumour Society) system, which combines grade (low I / high II), compartment status (intra- A / extra-compartmental B) and the presence of metastases (III).
⚠️The biopsy must be planned by the treating surgical oncology team and placed so the tract can be excised at definitive surgery. A poorly placed or contaminated biopsy can convert a limb-salvageable tumour into an amputation — never biopsy a suspected sarcoma casually.Principles of Management
Benign lesions are observed or treated by curettage/excision as needed. Malignant tumours are managed by a multidisciplinary team with a combination of surgery (wide local excision with limb-salvage where possible, or amputation), chemotherapy (neoadjuvant and adjuvant for osteosarcoma and Ewing’s) and radiotherapy (central to Ewing’s, adjunctive in others), tailored to tumour type, grade and stage.
The Biopsy — Principles
Biopsy is the definitive diagnostic step but is fraught with pitfalls. Whether by needle (core) or open (incisional) technique, it must be performed or directed by the surgeon who will carry out the definitive resection. The tract is placed in line with the planned excision so it can be removed en bloc, avoids contaminating neurovascular structures or separate compartments, and takes representative tissue from the growing edge rather than a necrotic centre. A carelessly placed biopsy can seed tumour and compromise limb salvage.
Biopsy tract must be excisable at definitive surgery. 🔑KEY POINTS TO REMEMBER- Classify by tissue of origin and benign vs malignant; metastasis is the commonest bone malignancy.
- Integrate age, site, clinical picture and radiographic aggressiveness.
- Aggressive signs: wide zone of transition, cortical destruction, interrupted periosteal reaction, soft-tissue mass.
- Stage malignant tumours by Enneking (grade, compartment, metastasis); biopsy is definitive.
- Malignant tumours need MDT care: surgery ± chemotherapy ± radiotherapy; plan the biopsy carefully.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Epidemiology
Osteosarcoma (osteogenic sarcoma) is the commonest primary malignant bone tumour (excluding myeloma). It is a high-grade tumour whose malignant cells produce osteoid. It has a bimodal age distribution: chiefly adolescents/young adults (10–20 years) during the growth spurt, and a second peak in the elderly (often secondary to Paget’s disease or previous irradiation). It arises in the metaphysis of long bones, most commonly around the knee (distal femur, proximal tibia) and proximal humerus.
Osteosarcoma of the metaphysis around the knee, showing a ‘sunburst’ spiculated periosteal reaction and Codman’s triangle where the lifted periosteum lays down new bone. Clinical Features
A young patient with progressive pain (often worse at night) and a firm, tender, warm swelling near a large joint, sometimes with a history of trivial trauma that draws attention to the area. There may be limitation of movement and, occasionally, a pathological fracture. Systemic features are usually late.
Investigations
Radiographs show a metaphyseal lesion with bone destruction and new-bone formation, a sunburst/spiculated periosteal reaction and Codman’s triangle, with cortical breach and a soft-tissue mass. MRI of the whole bone defines intramedullary extent and skip lesions; CT chest and bone scan/PET stage for metastases (the lung is the commonest site). Alkaline phosphatase is often raised. Biopsy confirms the diagnosis (malignant osteoid-producing cells).
💡The radiographic triad to remember is a metaphyseal tumour around the knee with a sunburst spiculation and Codman’s triangle. Osteosarcoma metastasises early to the lungs — always stage the chest.Management
Modern treatment is neoadjuvant (pre-operative) chemotherapy → surgical wide excision (limb-salvage with endoprosthetic replacement or biological reconstruction wherever a safe margin is achievable, otherwise amputation) → adjuvant (post-operative) chemotherapy. The degree of tumour necrosis in the resected specimen after neoadjuvant chemotherapy is an important prognostic indicator. This multi-agent chemotherapy approach has transformed survival from <20% (surgery alone) to around 60–70% in non-metastatic disease.
⚠️Osteosarcoma is relatively radioresistant, so radiotherapy has only a limited, palliative role — the mainstay is chemotherapy plus surgery, unlike Ewing’s sarcoma which is radiosensitive.Prognosis
Prognosis depends on stage (especially the presence of metastases), tumour grade, resectability and the histological response to chemotherapy. Non-metastatic, chemo-responsive tumours that are widely excised do best; the lungs are the dominant site of relapse.
Feature Osteosarcoma Ewing sarcoma Age 10–20 years 5–15 years Site Metaphysis — around knee Diaphysis of long bones, pelvis Radiograph Sunray spicules, Codman triangle Onion-peel periosteal reaction Histology Malignant osteoid Small round blue cells Genetics RB1, p53 t(11;22) EWS-FLI1 Mimics — Osteomyelitis — fever, raised ESR 🔑KEY POINTS TO REMEMBER- Commonest primary malignant bone tumour; adolescents (+ elderly Paget/radiation).
- Metaphysis around the knee; osteoid-producing; sunburst + Codman’s triangle; ↑ ALP.
- Metastasises early to lungs — stage the chest.
- Treat with neoadjuvant chemo → wide excision (limb salvage) → adjuvant chemo.
- Relatively radioresistant; % necrosis after chemo is prognostic; survival ~60–70% if non-metastatic.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Epidemiology
Ewing’s sarcoma is a highly malignant small round-cell tumour of bone (and soft tissue), thought to arise from primitive neuroectodermal cells and characterised by the t(11;22) translocation (EWS-FLI1 fusion). It typically affects children and adolescents (5–15 years) — a slightly younger group than osteosarcoma — and arises in the diaphysis of long bones and in flat bones (pelvis, ribs, scapula).
Ewing’s sarcoma of the diaphysis with a laminated ‘onion-skin’ periosteal reaction and a permeative destructive pattern. Clinical Features
Pain and a swelling, often with fever, malaise, weight loss and a raised ESR/WCC — a picture that can closely mimic osteomyelitis. The overlying tissues may be warm and tender. Presentation with metastatic disease is not uncommon.
⚠️Because Ewing’s can present with fever, local warmth, a raised white count and a permeative lesion, it is a classic mimic of acute osteomyelitis. Any doubt must be resolved by biopsy before treating as infection.Investigations
Radiographs show a permeative (‘moth-eaten’) destructive diaphyseal lesion with a laminated ‘onion-skin’ periosteal reaction and often a large soft-tissue mass. MRI defines the extent (often larger than the radiograph suggests); staging includes CT chest, bone scan/PET and bone-marrow assessment. Biopsy shows sheets of small round blue cells (PAS-positive glycogen; CD99 positive) and the characteristic translocation confirms the diagnosis.
Management
Ewing’s is treated by a multimodal regimen: multi-agent chemotherapy (neoadjuvant and adjuvant) combined with local control by surgery and/or radiotherapy. Unlike osteosarcoma, Ewing’s is highly radiosensitive, so radiotherapy has a major role in local control, particularly for surgically inaccessible sites (e.g. parts of the pelvis/spine); wide surgical excision is preferred where feasible.
💡Two contrasts with osteosarcoma: Ewing’s is diaphyseal (osteosarcoma metaphyseal), shows an onion-skin reaction (osteosarcoma sunburst/Codman), and is radiosensitive (osteosarcoma radioresistant).Prognosis
Prognosis depends chiefly on the presence of metastases at diagnosis, tumour size/site and response to chemotherapy. Localised disease has a reasonable cure rate with modern multimodal therapy, but metastatic disease (lungs, bone, marrow) carries a much poorer outlook.
Differential Diagnosis
The main differentials are acute osteomyelitis (shared fever, warmth and raised inflammatory markers), other small round-cell tumours (metastatic neuroblastoma in young children, lymphoma of bone), and eosinophilic granuloma. Histology with CD99 immunostaining and demonstration of the EWS gene rearrangement is decisive, which is why tissue diagnosis is mandatory before committing to treatment.
🔑KEY POINTS TO REMEMBER- Malignant small round-cell tumour; t(11;22)/EWS-FLI1; children/adolescents.
- Diaphysis of long bones and flat bones; onion-skin periosteal reaction; permeative destruction.
- Mimics osteomyelitis (fever, ↑WCC/ESR) — biopsy resolves doubt; CD99 positive.
- Multimodal chemo + local control; highly RADIOSENSITIVE (unlike osteosarcoma).
- Prognosis hinges on metastases at diagnosis and chemo response.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Epidemiology
Giant cell tumour (GCT, osteoclastoma) is a locally aggressive, usually benign tumour with a small but real potential for local recurrence and, rarely, pulmonary metastasis (‘benign metastasising GCT’) or malignant transformation. It characteristically occurs in young adults (20–40 years) after physeal closure and is located in the epiphysis/epi-metaphysis of long bones, most often the distal femur, proximal tibia (around the knee) and distal radius.
Feature Giant cell tumour Age 20–40 years (skeletally mature) Site Epiphyseal, extends to subchondral bone; around the knee, distal radius X-ray Eccentric, expansile, lytic ‘soap-bubble’; no sclerotic rim Behaviour Benign but locally aggressive; recurs; rare lung metastasis Clinical Features
Pain, swelling and reduced joint movement near a large joint in a young adult; a pathological fracture may be the presentation. Because the lesion reaches the subchondral bone, an effusion and joint symptoms are common. The clinical course is unpredictable: some lesions grow slowly over months while others enlarge rapidly and breach the cortex into the soft tissues.
Investigations
Radiographs show a characteristic eccentric, expansile, purely lytic lesion in the epiphysis extending to the subchondral bone, with a ‘soap-bubble’ appearance, thinned or breached cortex and no surrounding sclerotic rim or matrix mineralisation. MRI defines soft-tissue extent; CT chest is done because of the small risk of lung deposits. Biopsy shows a stroma of mononuclear cells with numerous evenly distributed multinucleated osteoclast-like giant cells.
💡Think of GCT in a skeletally mature young adult with an eccentric, expansile, lytic epiphyseal lesion (‘soap-bubble’) around the knee reaching the articular surface — the age and epiphyseal location are the giveaways.Management
Treatment is primarily surgical. Extended (aggressive) intralesional curettage — curettage with adjuvant measures such as a high-speed burr, and local adjuvants (phenol, hydrogen peroxide, or cryotherapy) — followed by filling of the cavity with bone cement (PMMA) or bone graft, is the usual approach, aiming to reduce the high recurrence rate while preserving the joint. Wide excision and reconstruction is reserved for extensively destructive or recurrent tumours. Denosumab (a RANK-ligand inhibitor) is used for inoperable, axial or advanced disease. Radiotherapy is generally avoided (risk of malignant transformation).
⚠️GCT has a high local recurrence rate after simple curettage, so ‘extended’ curettage with adjuvants and cavity filling is preferred. A small proportion behave malignantly or seed the lungs, so staging the chest and follow-up are important.Differential Diagnosis
An epiphyseal lytic lesion in a young adult should be distinguished from other subarticular lesions: chondroblastoma (typically before physeal closure, with matrix calcification), aneurysmal bone cyst (may coexist as a secondary change, fluid–fluid levels), a brown tumour of hyperparathyroidism (check calcium and PTH — an important mimic), and, when aggressive, a giant-cell-rich osteosarcoma. Correlation of age, site and biochemistry with histology resolves most cases.
Prognosis & Follow-up
Although histologically benign, GCT is locally aggressive and recurs in a significant proportion after intralesional treatment, usually within the first two to three years — hence the emphasis on extended curettage with adjuvants and on regular clinical and radiological follow-up, including chest imaging for the small risk of benign pulmonary ‘metastases’. Frank malignant transformation is rare and carries the prognosis of a sarcoma.
💡A useful summary: GCT is the classic benign-but-troublesome tumour — benign histology, epiphyseal location in a skeletally mature adult, but a genuine tendency to recur locally and, rarely, to seed the lungs, which is why treatment aims at both eradication and joint preservation.Benign but locally aggressive — can metastasise to lung rarely. 🔑KEY POINTS TO REMEMBER- Benign but locally aggressive; young adults after physeal closure; rare lung metastasis.
- Epiphyseal/subchondral around the knee & distal radius; eccentric expansile lytic ‘soap-bubble’.
- Numerous osteoclast-like multinucleated giant cells on histology.
- Extended curettage + adjuvants + cement/graft; wide excision if extensive/recurrent; denosumab for advanced.
- Avoid radiotherapy (malignant transformation); stage the chest.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Importance
Metastatic (secondary) bone disease is by far the commonest malignant tumour of bone in adults — far more frequent than all primary bone sarcomas combined. Any bone lesion in a patient over 40 should be considered metastatic until proven otherwise. The primary tumours that most often spread to bone are remembered as the ‘famous five’: breast, prostate, lung, kidney (renal) and thyroid.
Osteolytic Osteoblastic (sclerotic) Typical primaries Kidney, thyroid, lung, breast Prostate (breast can be mixed) X-ray Bone destruction/lucency Increased bone density Fracture risk High Lower Clinical Features
Bone pain (progressive, often worse at night), a pathological fracture (sometimes the presenting event), and features of hypercalcaemia (thirst, polyuria, confusion, constipation). Spinal deposits may cause cord or cauda equina compression. There may be symptoms of the primary tumour, or the primary may be occult.
⚠️A pathological fracture or spinal metastasis with neurological signs is an oncological emergency. New back pain with neurology in a cancer patient is metastatic spinal cord compression until proven otherwise — arrange urgent MRI and treatment (steroids, radiotherapy or surgery).Investigations
Radiographs of the symptomatic site (lytic or sclerotic deposits); a bone scan surveys the skeleton (though purely lytic myeloma may be missed). Blood tests: calcium, alkaline phosphatase, renal and liver function, PSA (prostate), and a myeloma screen where relevant. The primary is sought with CT chest/abdomen/pelvis, mammography, PSA, thyroid imaging, etc.; biopsy confirms metastasis and identifies the tissue of origin when the primary is unknown.
Management
Treatment is usually palliative and multidisciplinary, aimed at pain relief, preserving function and preventing/treating fractures. Modalities include analgesia, radiotherapy (excellent for localised bone pain and after fixation), bisphosphonates or denosumab (to reduce skeletal events and treat hypercalcaemia), and systemic therapy for the primary (hormonal, chemotherapy, targeted agents). Surgical stabilisation (internal fixation or prosthetic replacement) is indicated for an actual or impending pathological fracture (predicted by the Mirels score) and for spinal instability/cord compression.
💡For a suspected impending fracture of a long-bone metastasis, the Mirels score (site, pain, lytic vs blastic, and size of the lesion) guides prophylactic fixation — fixing before the bone breaks is far better than after.Prognosis
Prognosis depends on the primary tumour and the overall disease burden. Breast, prostate and thyroid bone metastases may be compatible with prolonged survival with modern systemic therapy, whereas lung primaries generally carry a poorer outlook; the goal throughout is quality of life and function.
Routes of Spread & Distribution
Bone metastases usually spread haematogenously, favouring the red-marrow-rich axial skeleton — the spine, pelvis, ribs, skull and proximal femur/humerus — whereas deposits distal to the elbow and knee are uncommon (and, when present, are classically from a bronchial or renal primary). The vertebral venous plexus of Batson is an important valveless route that helps explain the predilection of prostate and other pelvic tumours for the spine.
⚠️Because a solitary bony metastasis can occasionally be the first sign of an unknown primary, and because a solitary destructive lesion in an older adult could still be a primary sarcoma or myeloma, biopsy is advisable before fixing a presumed metastasis when the diagnosis is not already secure — confirming the tissue of origin also guides systemic treatment.Commonest bone malignancy overall — far exceeds primary tumours. 🔑KEY POINTS TO REMEMBER- Commonest bone malignancy in adults; any bony lesion >40 y is metastatic until proven otherwise.
- Primaries: breast, prostate, lung, kidney, thyroid. Prostate is classically osteoblastic; kidney/thyroid lytic.
- Bone pain, pathological fracture, hypercalcaemia, cord compression.
- Bone scan surveys skeleton (myeloma may be missed); seek the primary; biopsy if unknown.
- Palliative MDT care: analgesia, radiotherapy, bisphosphonates/denosumab; fix actual/impending fractures (Mirels).
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Osteochondroma (exostosis) is the commonest benign bone tumour. It is a cartilage-capped bony outgrowth on the external surface of a bone, arising from the metaphysis of a long bone (typically around the knee or proximal humerus) and pointing away from the adjacent joint. Its medullary cavity is continuous with that of the parent bone.
Clinical Features
Usually a painless, hard, fixed swelling noticed in a child or adolescent, which stops growing at skeletal maturity. Symptoms arise from mechanical effects: pressure on tendons, nerves or vessels, an overlying bursitis, or a cosmetic lump. Multiple lesions occur in the hereditary condition multiple hereditary exostoses (diaphyseal aclasis).
⚠️A previously stable osteochondroma that starts to grow or become painful after skeletal maturity, or whose cartilage cap thickens (> ~1.5–2 cm on MRI), raises concern for malignant transformation to chondrosarcoma — uncommon in solitary lesions but higher in multiple hereditary exostoses.Management
Asymptomatic lesions are simply observed. Excision is indicated for pain, mechanical symptoms (nerve/vessel/tendon impingement), cosmetic concern, or suspicion of malignant change; the whole cartilage cap and its perichondrium are removed to prevent recurrence.
💡Osteochondroma grows away from the joint and has a cortex and medulla continuous with the parent bone — a useful diagnostic feature. Growth after maturity is the warning sign of transformation.Pathology
Histologically the lesion is a bony stalk capped by hyaline cartilage that behaves like an aberrant growth plate; it enlarges by endochondral ossification during skeletal growth and normally ceases growing at maturity. In multiple hereditary exostoses, an autosomal-dominant disorder (EXT gene mutations), numerous lesions cause bony deformity, limb-length discrepancy and a higher lifetime risk of malignant transformation than a solitary lesion, and often warrant surveillance into adult life.
💡Continuity of the cortex and medulla with the parent bone on imaging confirms an osteochondroma and distinguishes it from a surface lesion such as a periosteal chondroma or, worryingly, a surface osteosarcoma.Commonest benign bone tumour. 🔑KEY POINTS TO REMEMBER- Commonest benign bone tumour; cartilage-capped metaphyseal outgrowth pointing away from the joint.
- Medulla continuous with parent bone; usually painless; stops growing at maturity.
- Multiple lesions = hereditary multiple exostoses (higher malignant risk).
- Observe if asymptomatic; excise for symptoms or suspected chondrosarcoma (growth after maturity).
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Osteoid osteoma is a small, benign, bone-forming tumour consisting of a central vascular nidus (< 1.5 cm) of osteoid surrounded by dense reactive sclerosis. It typically affects adolescents and young adults and commonly arises in the diaphysis/metaphysis of long bones (femur, tibia) and the spine.
Clinical Features
The hallmark is persistent boring pain, characteristically worse at night, that is dramatically relieved by aspirin/NSAIDs — a very useful clinical clue explained by prostaglandin production within the nidus. A spinal lesion may cause painful scoliosis, and a periarticular one a joint effusion.
💡The classic story is night pain relieved by aspirin/NSAIDs in a young patient, with a radiograph showing a small lucent nidus surrounded by dense reactive sclerosis.Investigations & Management
Radiographs show a small radiolucent nidus with surrounding sclerosis; CT best demonstrates the nidus, and a bone scan is intensely hot. Many lesions burn out spontaneously over years and can be managed with NSAIDs. Definitive treatment for persistent pain is removal/ablation of the nidus, now usually by CT-guided percutaneous radiofrequency ablation (or surgical excision).
Pathology
The lesion consists of a small central nidus of vascular osteoid and woven bone with active osteoblasts, surrounded by a zone of dense reactive sclerosis. The nidus produces prostaglandins, which are responsible for both the characteristic pain and its relief by prostaglandin-inhibiting NSAIDs. By definition the nidus is less than about 1.5 cm; a larger, otherwise similar lesion is termed an osteoblastoma, which is more expansile, commoner in the spine, and less reliably relieved by aspirin.
Differential Diagnosis
The main differentials are a Brodie’s abscess (subacute osteomyelitis, which can also cause night pain and reactive sclerosis) and a stress fracture. CT demonstration of the nidus, together with the classic aspirin-sensitive night pain, usually clinches the diagnosis and separates it from these mimics.
Aspirin relief of night pain is the classic clue. 🔑KEY POINTS TO REMEMBER- Small benign bone-forming tumour: vascular nidus (<1.5 cm) + reactive sclerosis.
- Night pain relieved by aspirin/NSAIDs; young patients; long bones and spine.
- CT shows the nidus; bone scan intensely hot.
- NSAIDs (may burn out) or radiofrequency ablation/excision of the nidus.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Enchondroma is a common benign tumour of mature hyaline cartilage arising within the medullary cavity of a bone. It most often affects the small tubular bones of the hands and feet and the long bones, and is usually solitary.
Clinical Features
Most enchondromas are asymptomatic and found incidentally, or they present as a pathological fracture through a weakened phalanx. Multiple enchondromas occur in Ollier’s disease, and multiple enchondromas with soft-tissue haemangiomas in Maffucci’s syndrome — both carry an increased risk of malignant change to chondrosarcoma.
Investigations & Management
Radiographs show a well-defined lucent medullary lesion, often with stippled or ‘popcorn’ calcification of the cartilage matrix and endosteal scalloping. Asymptomatic lesions are observed; a symptomatic lesion or pathological fracture is treated by curettage and bone grafting. Features suggesting malignant transformation (pain without fracture, cortical destruction, a soft-tissue mass, growth in an adult) warrant biopsy.
⚠️In an adult, a cartilage lesion that becomes painful (without fracture), enlarges or destroys cortex may be a chondrosarcoma rather than a benign enchondroma — the distinction can be difficult and needs specialist assessment.Pathology & Syndromes
The lesion is composed of lobules of mature hyaline cartilage within the medulla, separated by normal marrow. It is usually solitary, but two non-hereditary syndromes are important: Ollier’s disease (multiple enchondromatosis, often asymmetrical, with deformity and shortening) and Maffucci’s syndrome (multiple enchondromas plus soft-tissue haemangiomas). Both carry a substantially increased risk of malignant transformation to chondrosarcoma, so patients need long-term surveillance.
💡A phalangeal lucent lesion with popcorn calcification that presents as a pathological fracture in a young adult is very likely a benign enchondroma; multiple lesions should prompt thought of Ollier’s or Maffucci’s and their malignant potential.Multiple enchondromas — Ollier disease, Maffucci syndrome. 🔑KEY POINTS TO REMEMBER- Benign hyaline-cartilage tumour within the medulla; hands/feet and long bones.
- Often asymptomatic or presents as a pathological fracture of a phalanx.
- X-ray: lucent lesion with popcorn calcification & endosteal scalloping.
- Observe if asymptomatic; curette + graft if symptomatic; Ollier/Maffucci carry malignant risk.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Periosteal Reaction
A periosteal reaction is new bone laid down by the periosteum in response to an underlying process. Its pattern reflects the aggressiveness of the lesion: a solid, continuous reaction suggests a slow, benign process, whereas an interrupted (discontinuous) reaction suggests a rapidly growing, aggressive or malignant lesion that outpaces the periosteum.
Aggressive periosteal reactions: sunburst spiculation, laminated onion-skin, and Codman’s triangle. Key Patterns
Sunburst (‘sunray’) spiculation — spicules of new bone radiating perpendicular to the cortex, classic of osteosarcoma. Onion-skin (lamellated) — concentric layers, characteristic of Ewing’s sarcoma. Codman’s triangle — a cuff of new bone formed where an aggressive tumour lifts the periosteum off the cortex; the periosteum ossifies only at the margin, leaving a triangular spur. It indicates an aggressive lesion (osteosarcoma, Ewing’s, sometimes infection).
💡Codman’s triangle is not specific to one tumour — it simply signifies that a lesion (malignant tumour or aggressive infection) is expanding fast enough to lift and interrupt the periosteum.🔑KEY POINTS TO REMEMBER- Periosteal reaction pattern reflects lesion aggressiveness.
- Solid/continuous = benign; interrupted = aggressive/malignant.
- Sunburst → osteosarcoma; onion-skin → Ewing’s.
- Codman’s triangle = periosteum lifted by an aggressive lesion (not tumour-specific).
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Multiple myeloma is a malignant proliferation of plasma cells in the bone marrow producing a monoclonal immunoglobulin (paraprotein). Although a haematological malignancy, it is the commonest primary malignant tumour of bone and a key differential for destructive bone lesions in the older adult (typically > 60 years).
Clinical Features
Remembered by ‘CRAB’: hyperCalcaemia, Renal impairment, Anaemia and Bone lesions/Back pain. Patients present with bone pain (especially the spine), pathological fractures, fatigue from anaemia, recurrent infections and features of hypercalcaemia or renal failure.
Investigations
Blood/urine: monoclonal paraprotein on serum electrophoresis, Bence-Jones protein in urine, raised ESR, anaemia, hypercalcaemia, renal impairment and rouleaux on the film. Imaging classically shows multiple ‘punched-out’ lytic lesions (and diffuse osteopenia); note that the radionuclide bone scan is often negative because the lesions are purely lytic with little osteoblastic activity — a whole-body MRI/low-dose CT or skeletal survey is preferred. Bone-marrow biopsy confirms the plasma-cell infiltrate.
⚠️Do not rely on a bone scan to detect myeloma — the purely lytic deposits frequently do not light up. Use a skeletal survey, low-dose whole-body CT or MRI instead.Management
Management is by haemato-oncology with systemic chemotherapy/novel agents (proteasome inhibitors, immunomodulators ± autologous stem-cell transplant), bisphosphonates for skeletal protection and hypercalcaemia, and supportive care. The orthopaedic role is stabilisation of pathological or impending fractures and radiotherapy/decompression for spinal cord compression.
Solitary Plasmacytoma
A single focus of malignant plasma cells in bone is a solitary plasmacytoma; it often presents with a destructive lytic lesion or a pathological (frequently vertebral) fracture and is treated with radiotherapy, but a large proportion progress to multiple myeloma over subsequent years, so continued haematological follow-up is required.
Bone scan is falsely negative — use skeletal survey. 🔑KEY POINTS TO REMEMBER- Malignant plasma-cell proliferation; commonest primary bone malignancy; older adults.
- CRAB: hyperCalcaemia, Renal impairment, Anaemia, Bone lesions/back pain.
- Paraprotein + Bence-Jones protein; ‘punched-out’ lytic lesions; bone scan often NEGATIVE.
- Haemato-oncology treatment + bisphosphonates; orthopaedics stabilises fractures / treats cord compression.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Two Cystic Lesions
Two common benign cystic lesions of bone in the young must be distinguished: the simple (unicameral) bone cyst and the aneurysmal bone cyst (ABC).
Feature Simple bone cyst Aneurysmal bone cyst Age Children (5–15 y) Children/young adults Site Metaphysis (proximal humerus/femur) Metaphysis; eccentric; any bone incl. spine Contents Clear/straw-coloured fluid Blood-filled cavities X-ray Central, lucent, mild expansion Eccentric, markedly expansile, ‘blown-out’ Classic sign ‘Fallen fragment’ after fracture Fluid–fluid levels on MRI Clinical Features & Management
A simple bone cyst is often symptomless until it presents with a pathological fracture (the ‘fallen fragment’ sign — a piece of cortex lying dependently in the fluid — is diagnostic). Many heal after fracture or respond to steroid/marrow injection or curettage and grafting. An ABC is a rapidly expansile, locally destructive blood-filled lesion causing pain and swelling; it is treated by curettage (with adjuvants) and grafting, sometimes with embolisation, and can recur. Secondary ABC change can overlie another tumour, so histology is important.
💡The ‘fallen fragment’ sign points to a simple bone cyst; fluid–fluid levels on MRI point to an aneurysmal bone cyst.Behaviour & Pitfalls
The simple bone cyst is a self-limiting lesion that tends to migrate away from the physis and often heals with growth, so an incidental asymptomatic cyst may simply be observed; treatment (steroid or marrow injection, or curettage and grafting) is directed at painful or fracture-prone lesions, and recurrence is not unusual in young children. The aneurysmal bone cyst is more aggressive and expansile and can arise secondarily within another lesion (e.g. GCT, chondroblastoma, osteosarcoma), so representative tissue must be examined to avoid missing an underlying tumour.
⚠️Any expansile blood-filled lesion should be examined histologically, because an aneurysmal bone cyst can be a secondary reactive change masking a more serious underlying tumour that determines prognosis and treatment.Fallen leaf sign indicates pathological fracture of a simple cyst. 🔑KEY POINTS TO REMEMBER- Simple bone cyst: central, fluid-filled, proximal humerus/femur; ‘fallen fragment’ sign.
- ABC: eccentric, markedly expansile, blood-filled; fluid–fluid levels on MRI.
- Both present in the young, often with pathological fracture.
- Treat by curettage ± adjuvants/grafting (± injection for simple cyst); ABC can recur.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
A pathological fracture is a fracture through abnormal, weakened bone, occurring after trivial or no trauma that would not fracture normal bone. Recognising it matters because the underlying disease must be diagnosed and treated, and because management differs from that of an ordinary fracture.
Causes
Causes are local or generalised. Local: a bone tumour (benign cyst/enchondroma, or malignant — especially metastasis, myeloma or primary sarcoma) or infection. Generalised: osteoporosis (much the commonest overall, e.g. vertebral and hip fragility fractures), osteomalacia, Paget’s disease, and metabolic/genetic disorders such as osteogenesis imperfecta.
⚠️A fracture after trivial injury, or bone pain preceding a fracture, should prompt a search for the underlying cause. In an adult over 40, always exclude metastasis and myeloma before assuming a simple fracture, and biopsy a suspicious lesion (ideally before fixation) so as not to miss a primary sarcoma.Management
Management addresses both the fracture and its cause. Investigate to establish the diagnosis (radiographs, blood tests, bone scan/MRI, biopsy). Stabilise the fracture appropriately — often by internal fixation or prosthetic replacement, since pathological bone heals poorly — and treat the underlying disease (e.g. radiotherapy and systemic therapy for a metastasis, anti-resorptive treatment for osteoporosis). Impending fractures (e.g. Mirels-positive metastases) are best fixed prophylactically.
Clinical Assessment
The clue is a mismatch between the force and the fracture, or bone pain preceding the injury. A careful history (previous cancer, weight loss, constitutional symptoms), examination and targeted investigations (calcium, alkaline phosphatase, renal function, protein electrophoresis, prostate-specific antigen, and imaging of the whole bone) establish the cause. The radiograph is inspected for the tell-tale lesion at the fracture site rather than being read simply as a fracture, since the lesion is easy to overlook once attention fixes on the break.
Never fix without establishing the underlying diagnosis. 🔑KEY POINTS TO REMEMBER- Fracture through weakened bone after trivial/no trauma.
- Causes: local (tumour — esp. metastasis/myeloma, infection) or generalised (osteoporosis commonest).
- In adults >40, exclude metastasis/myeloma; biopsy suspicious lesions before fixation.
- Treat fracture (often fixation/replacement) AND the underlying cause; fix impending fractures prophylactically.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.