Chapter 26: Bone Maturation, Fracture, Reactive Flashcards
A child presents with multiple fractures, blue sclera, and hearinga bnormalities.
A radiograph shows bone abnormalities.
Osteogenesis Imperfecta
Autosomal dominant disorders of type I collagen.
Affects skeleton, joints, ears, ligaments, teeth, sclerae, and skin.
A bone biopsy of a fracture is taken from a person with osteogenesis imperfecta. What are the characteristic features?
Thin cortex, hypercellular woven bone.
What are the differences in the four types of osteogenesis imperfecta?
Type I: AD, Mild, reduced severity with aging. Blue sclerae.
Type II: AD, Lethal, stillborn or die a few days after birth. Blue sclerae
Type III: Progressive, severely deforming. Usually AD. Short stature, sclerae go from blue -> white.
Type IV: Mild, sclerae are normal.
Patient presents with numerous cartilaginous masses that lead to bony deformities.
Residual hyaline cartilage, anlage cartilage, or growth plate cartilage does not undergo endochondral ossification and remains in bones.
A radiograph shows the following findings.
Multiple Enchondromatosis (Ollier disease).
Tumors tend to be in metaphyses. Can undergo malignant change to chondrosarcomas.
Solitary rarely undergoes malignant change.
Maffucci syndrome: Multiple enchondromas in cavernous or spindle cell hemangiomas, ocmmon chondrosarcomas.
PTHR1 gene in AD familial disease. cAMP.
A fracture resulting from a force perpendicular to the bone.
A fracture resulting from a force along the long axis of the bone.
A fracture resulting from torsional force.
Perpendicular: Transverse
Along long axis: Compression
Torsion: Spiral
Phases of fracture healing include…
Inflammatory.
Days 1-2: Rupture of blood vessels, hemorrhage, bone necrosis. Dead bone (loss osteocytes and empty lacunae).
Days 2-5: Clot, neovascularizsation, organization.
Days 7+: Woven bone “scar” after 7 days. Granulation tissue called a callus.
Reparative phase:
After 1 week - months. Pluripotential cells make fibroblasts and osteoblasts. Organize and resorb blood clot, neovascularize construction of the callus.
Cutting cones formed by osteoblasts.
Remodeling phase: Ingrowth of callus has sealed the bone ends. Bone is reorganized.
What occurs in primary healing of a fracture?
No bone displacement and soft tissue injury.
This causes no tissue reaction and callus formation. Fracture callus grows directly into the fracture site - rapid reconstitution of the cortex.
If fracture site is held in rigid alignment by metal screws and plates, also little external callus. Cortical cutting cones prominent and heal quickly.
What occurs in nonunion of a fracture?
Fracture site does not heal.
Can include interposition of soft tissues at the fracture site, excessive motion, infection, poor blood supply.
Continued movement at unhealed fracture -> pseudoarthrosis. Joint-like tissue forms. Abnormal tissue must be removed for fracture to heal.
What is a stress fracture?
Repeated microfractures eventually result in a true fracture through the bone cortex.
Cortex has few osteons, forms only when stress is applied to the prepared cortex. Bone produces cutting cones in an attempt to implant osteons. Periosteal and endosteal callus develop to strengthen bone while remodeling takes place. Stress fracture during remodeling.
Callus forms before fracture occurs **.
What is reactive bone? What are some characteristic key words?
Intramembranous bone formed in response to stress on bone or soft tissue. Can be induced by tumors, infections, trauma, or disease.
This picture is sunburst pattern.
Periosteum respond with sunburse pattern or progressive layering (onionlike pattern). On radiograph, cortex appears thickened and coarse cancellous bone is denser.
What is heterotrophic ossification and when does it occur?
Reactive bone formation (woven or lamellar) in extraskeletal sites.
Occurs in genetic, posttraumatic, neurogenic, postsurgical, and specific lesions (myositis ossificans).
Commonly seen: Spicular or trabeculated pattern, no metabolic abnormalities. (Normal calcium and phosphorous).
Genetic disease resulting in massive deposits of bone around multiple joints.
Fibrodysplasia ossificans progressiva.
Deposition of calcium salts in soft tissues.
Irregular, splotchy, amorphous appearance. Occurs in necrotic soft tissue or in cartilage.
Heterotrophic calcification.
Metastatic calcification: Increase in calcium-phosphorous product. Hypercalcemic or hyperphosphatemic conditions.
Dystrophic calcification: Abnormal or damaged soft tissues - tumors, degen diseases, trauma. Loss of neurologic function.
Formation of reactive bone in muscle after injury. In young persons, mimics neoplasm.
Myositis ossificans. Excellent prognosis.
Fibroblasts in center of early lesion atypical and show abundant mytoses, which mimics neoplasm, but bone matures peripherally whereas it is immature or not formed at all in the center of the lesion (zonation effect).
No treatment required, spontaneous regression. Usually blunt trauma to muscle/soft tissue.
In both pictures note ossification that becomes denser at periphery (not a neoplasm!)
Necrotic coarse cancellous bone heals by…
Necrotic cortical bone is healed by…
Cancellous heals by creeping substituion - necrotic marrow replaced by invading or creeping neovascular tissue. Bony trabeculae surrounded by new woven or lamellar bone by osteoblasts or granulation tissue. Intramembranous bone formation.
Cortical bone heals by cutting cone. Forms by preexisting vascular channels in the cortex. Stimulate neovascularization by surrounding pluripotential mesenchymal tissues. Osteoclasts followed by osteoblasts tunnel down, form new lamellar bone.
Osteonecrosis in the femoral head of a child.
Legg-Calve-Perthes disease.
AKA idiopathic osteonecrosis in adults.
Collapse of the femoral head -> joint incongruity, severe osteoarthritis.
Radiograph shows necrotic zone to be radiodense - osteoporosis in surrounding bone, addition of new bone by creeping substitution, or formation of calcium soaps or compaction of dead bone.
Wedge-shaped necrotic zone.
