Injury Mechanisms & Healing Bone Flashcards
apophysitis
inflammation of a secondary ossification centre that serves as a tendon attachment eg Sever’s disease & Osgood Schlatter disease. Extremely common in highly active adolescent patients. Self-limiting due to growth plate fusion
Tenoperiostitis
inflammation of tendinous attachment to bone as a result of repetitive muscle pull
Periostitis
inflammation of periosteum, typically as a result of repetitive physical stress
Periosteal contusion bone bruise
disruption of some trabeculae & haematoma beneath the periosteum
Osteopathic Management of Stress Fractures
6 weeks followed by gradual return to activity
Immobilisation can result in mm wasting as well as joint and soft tissue stiffness
rehab program is advised as well as manual therapy for joints and soft tissues
ensure adequate nutritional and calorific intake to support healing
Risk factors of bone mircodamage
Increase in duration, intensity or frequency of physical activity - common in athletic populations, army recruits
Inadequate muscle mass - muscles assist with shock absorption
Training surfaces – hard surfaces, or a recent change in training surfaces
Gait and lower limb mechanics eg pes cavus (high arches) or pes planus (flat arches), leg length discrepancies
Inadequate or a recent change in footwear
Stress Fracture Pathophysology
they develop when excessive mircodamge occurs before the bone can adquwety be romedled.
Stress Fracture
complete or incomplete caused by reptitive physical stress in a localised area of bone
due to reptive application of force, muscle pull, weight bearing shock
Remodelling phase of fracture healing process
Several months
As bone is exposed to external forces and biomechanical demands, immature bone is remodeled.
Trabeculae align along lines of stress, compact bone, spongey bone or medullary cavity is developed and excess bone is remvoed
Repair Stage of the Fracture Healing Process\
week 1-8
end of first week fracture, osteoblasts begin to lay down bone
Bone is immature (not structurally organised) but converts the fibrocartilaginous callus into a bony callus.
Formation of primary callus of the inflammation phase
Fibroblasts produce collagen fibres and chondroblasts secrete cartilage matrix.
Together the fibroblasts and chondroblasts form a fibrocartilaginous (primary) callus which connects the broken bone pieces and splints the bone
Vascular stage of inflammation phase
Network of new vessels grow into the hematoma to provide nutrients for bone repair and inflammatory cells
Fracture Healing Process Inflammation phase (moment of injury to within 1 week post injury)
Cellular Stage
Hemorrhaged blood forms a hematoma (large clot) at the fracture site
Inflammation – Injured cells incite an acute inflammatory response
Inflammatory cells release growth factors – essential for differentiation of osteoprogenitor cells into osteoblasts
Phagocytes remove cell and tissue debris
Displaced fracture Management
Reduction, process of realigning bone fragments
Fixation- stabilisation of bone fragments using internal/external rods, plates
Traction
Fracture Healing Basics
requires immobilisation of bone fragments to heal
6-8 weeks for simple fractures of small-medium sized bones
