Bone Flashcards
Functions of bone
Haematopoiesis
Lipid and mineral storage
Support
Protection
Components of bone
Cellular components: Osteoblasts, osteoclasts, osteocytes
Extracellular matrix
Structure of bone
Woven bone (primary bone) Lamellar bone (secondary bone)
Compact bone
Lamellae are organised into osteons
Osteon
Concentric circles of lamellae
Surround vertical Haversian canal (transmits neurovascular and lymphatic vessels)
Connected by horizontal Volkann’s canals
Ostecytes are located between lamellae within cavities called lacunae
Lacunae are interconnected by series of tunnels called canaliculi
Spongy bone
Interior part, deep to compact bone
Honeycombe appearance. 3D network of columns. Crosslink to form trabeculae.
Strong against multidirectional force
Spaces between trabeculae are filled with bone marrow
Bone marrow
Red bone marrow: haematopoietic stem cells
Yellow bone marrow: adipocytes
Periosteum
Layer of connective tissue surrounded external surface
Ossification
Process of producing new bone:
Endochondrial ossification: hyaline cartilage is replaced by osteoblasts secreting osteoid
Intremembranous ossification: mesenchymal tissue is condensed into bone
Both produces primary bone, replaced by mature secondary bone
Remodelling
Mature bone is reabsorbed and new bone formed
Parts of long bones
Epiphysis: joint facing bone
(Metaphysis: growth plate)
Diaphysis: shaft
Parts of long bones
Epiphysis: joint facing bone
Metaphysis:
(Physis: growth plate)
Diaphysis: shaft
Fracture healing stages
Hematoma formation
Fibrocartilaginous callus formation
Bony callus formation
Bone remodeling
Fracture healing: haematoma
Days 0-5
Periosteum and vessels in bone bleed
Damaged bond tissue releases: TNFa, ILs and BMPs (bone morphogenetic proteins)
Attracts macrophages: remove damaged tissue and release VEGF (vascular endothelial growth factor)
Fracture healing: Fibrocartilaginous callus formation
Days 5-11
VEGF stimulates angiogenesis at site
Fibrin-rich granulation tissue develops in haematoma
Mesenchymal stem cells differentiate (driven by BMPs) to fibroblasts, chondroblasts, osteoblasts
Chondogenesis occurs: laying down collagen
Woven bone layer down by osteoprogentior cells
Fracture healing: Bony callus formation
Days 11-28
Cartilaginous callus undergoes endochondrial ossification
Woven bone continues to be laid down
Blood vessels continue to proliferate
Formation of hard calcified immature bone
Fracture healing: bone remodelling
Days 18+
Hard callus undergoes repeated remodelling
Centre of callus is replaced by compact bone
Callus edges replaced by lamellar bone
Salter Harris Classification
I: transverse through physis
II: physis & metaphysis, sparing epiphysis
III: physis & epiphysis, sparing metaphysis
IV: physis, metaphysis, epiphysis
V: compression fracture of physis
(VI-IX additional classifications now also)
Bone tumours
Primary
Secondary (metastasis)
Primary bone tumours: classifications
Bone forming Cartilage forming Fibrous tissue Giant-cell tissues Marrow tumours
Bone forming tumours
Benign: osteoma, osteoid osteoma, osteoblastoma
Malignant: osteosarcoma
Cartilage forming tumours
Benign: chondroma, osteochondroma, chondroblastoma
Malignant: chondrosarcoma
Fibrous tissue bone tumours
Benign: fibroma, fibrzomatosis
Malignant: fibrosarcoma
Giant cell tumours
Benign osteoclastoma
Malignant osteoclastoma
Marrow tumours
Malignant:
Ewing’s tumour
Myeloma
Metastatic bone cancer
Most common cause of bone cancer
Primaries: renal, thyroid, lung, prostate, breast
Most common site: spine
Osteoid osteoma
Benign. Arise from osteoblasts
10-20 years. M>F.
Typically small (<2cm), located around metaphysis of long bones
Sx: localised progressive pain, made better with NSAIDs. Localised swelling, tenderness, limp.
XR: small mass, radiolucent nidus with rim of reactive bone
Rx: conservatively. serial imaging 4-6mnths. resolve spontaneously
Osteochondroma
Benign. Outgrowth from metaphysis covering with cartilagenous cap. 10-20 years. M>F. Sx: usually asymptomatic XR: pedunculate bony outgrowth Rx: conservatively. serial XRs 4-6mnths.
Chondroma
Benign. Arise from chondroblasts
20-50years.
Commonly affecting long bones of hands, femur or humerus
Sx: usually asymptomatic. Can present as pathological fracture
XR: well circumscribed oval lucency with intact cortex
Rx: depending on size and clinical features.
Small risk of transformation into chrondrosarcoma
Giant cell tumour
Benign. Arise from multinucleated giant cells and stroll cells
20-30years
Usually affecting epiphysis of long bones
Sx: pain, swelling, limitation of joint movement
XR: eccentric lytic area, “soap bubble” appearance
Rx: surgical resection w. bone grafting/recon
Osteosarcoma
Malignant. Most common malignant primary bone tumour
Bimodal age: 10-14, >65 (typically with Paget’s disease). RF: Li-Fraumeni syndrome
Most commonly at metaphysis of distal femur or proximal tibia
Sx: localised contact pain. soft tissue mass.
XR: medullary and cortical bone destruction. Significant perisoteal reactions (“Codman’s triangle or “sunburst pattern”)
Tissue biospy required.
Rx: aggressive surgical resection + chemo
Mets: lung and bone
Ewing’s sarcoma
Malignant. Paeds. M>F.
Arise from poorly differentiated neuroectodermal cells.
Commonly affect diaphysis of long bones
Sx: painful, enlarging mass. tenderness.
XR: lytic lesion with periosteal reactions, layers of reactive bone “onion skin” appearance.
Rx: neoadjuvant chemo + surgical excision
Chondrosarcoma
Malignant. Tumour of cartilage.
Commonly primary lesions. Can be malignant change from benign chondromas
40-60
Axial skeleton (pelvis, shoulder, ribs)
Sx: painful enlarging mass.
XR: lytic lesions with calcification, cortical remodelling and endosteal scalloping
Rx: wide en-bloc excision
Diseases of bone structure
Osteogenesis imperfecta
Osteoporosis
Rickets
Osteomalacia
Osteogenesis imperfecta
Abnormal synthesis of collagen from osteoblasts
Sx: fragile bones, bone deformities, blue sclera
Autosomal dominant
Osteoporosis
Reduction in bone density, reducing structural integrity. Osteoclast activity outweighing osteoblasts.
Type 1: postmenopausal (decreased oestrogen)
Type 2: senile (>70yrs)
Type 3: secondary (co-existing disease, e.g. CKD)
Osteoporosis
Reduction in bone density, reducing structural integrity. Osteoclast activity outweighing osteoblasts.
Type 1: postmenopausal (decreased oestrogen)
Type 2: senile (>70yrs)
Type 3: secondary (co-existing disease, e.g. CKD)
Rickets
Vitamin D or Ca deficiency in children with growing bones
Osteoid mineralised poorly and remains pliable. Epiphyseal growth plates become distorted under weight of body
Rickets
Vitamin D or Ca deficiency in children with growing bones
Osteoid mineralised poorly and remains pliable. Epiphyseal growth plates become distorted under weight of body
Osteomalacia
Vitamin D or Ca deficiency in adults with remodelling bones
Osteoid laid down by osteoplasts is poorly mineralised leading to increasingly weak bones and increased susceptibility to fracture
