Bone Injury + Repair Flashcards
Why does bone not scar?
Unlike repair of soft tissues such as the skin, wound healing in bone does not form a scar. Therefore bone ‘repair’ does not biologically occur. Bone is damaged daily by repetitive cyclic, loading resulting in ‘fatigue microdamage’. To repair the damaged site and restore mechanical integrity, targeted remodelling is initiated at the sites of microcracks. Bone senses areas of microdamage by the disruption of the canalicular network of osteocytes. The osteocytes undergo apoptosis which stimulates osteoclasts to migrate to the site and resorb the damaged area of bone, initiating a remodelling cycle.
Furthermore the microstructural discontinuities caused by the microcracks increase the local strain by up to four times the normal tissue range, stimulating bone formation to restore the strength to the damaged site. Thirty percent of all bone remodelling is damage
initiated.
Research has indicated that targeted remodelling of bone microdamage is initiated by what stimuli?
Bone senses areas of microdamage by the disruption of the canalicular network of osteocytes. The osteocytes undergo apoptosis which stimulates osteoclasts to migrate to the site and resorb the damaged area of bone, initiating a remodelling cycle.
What determines whether intramembranous or endochondral ossification occurs in fracture healing?
Low interfragmentary strain results in intramembranous dominated bone formation; moderate interfragmentary movements leads to endochondral ossification; and high interfragmentary strain results in
non-union due to the inability of bone to form.
Rigid fracture fixation has been shown to have negative effects on fracture healing. What are these negative effects and why do they occur?
Rigid fixation can limit the formation of callus because it restricts the relative movement of fracture fragments. Some degree of callus formation is essential for proper healing, and reduced callus formation can lead to delayed or impaired healing.
Delayed union is a condition where the fracture takes longer to heal than expected. Rigid fixation may impede the natural motion at the fracture site, which is essential for the bone’s response to mechanical stress and the stimulation of bone remodelling. This can prolong the healing process. In severe cases, rigid fixation can lead to non-union, where the fractured bone fails to heal. This occurs when the fracture site becomes biologically inactive and does not progress toward healing. Non-union is more likely to occur when there is inadequate blood supply, infection, or excessive rigidity at the fracture site.
What is the purpose of the formation of the periosteal callus in fracture healing and what event signals consolidation of the callus?
During fracture healing woven bone is essential in establishing a stable bridge across the fracture gap to restrict the movement of the two fractured ends. The outer periosteal callus braces the fracture fragments and more importantly through an increase in diameter, enhances structural integrity across the fracture site as the fractured fragments are bridged by new bone. This increase in cross-sectional area or callus formation is needed to compensate for the lack in material strength of the woven bone callus associated with its random collagen organisation and initial low mineral content.
Similar to the repair of a complete cortical crack during fracture healing, periosteal calluses are also formed in response to internal damage to the bone matrix, such as an accumulation of microdamage with age. As the microcracks are remodelled and repaired, a periosteal callus forms to increase the stiffness of the bone whilst the internal bone matrix regains its own strength
Why does a soft callus form before a hard callus in fracture healing?
The earlier ‘soft’ callus is transformed into a harder material through a process of mineralisation and remodelling. As this internal
remodelling progresses and improves matrix strength, the size of the callus reduces proportionately through external remodelling until a size has been reached where efficient and safe locomotion or movement becomes optimal. Therefore internal remodelling precedes external remodelling
Why does bone often resorb at sites adjacent to metal implants? What is this phenomenon called?
Stress shielding can also occur during fracture healing. Resorption will occur under the fixation plate if the plate is too stiff or is making contact with the cortical bone. The bone resorption will reduce the diameter of the bone through cortical thinning and the cortical bone is seen to undergo trabecularisation ie. changes its architecture.
Following a bone fracture, a callus forms to attempt to restore mechanical integrity. Why does the callus consist of woven bone tissue if it is inferior to lamellar bone tissue in terms of material strength? Why does a callus form rather than the new bone tissue just forming in the gap between the fractured ends of the bone?
During fracture healing woven bone is essential in establishing a stable bridge across the fracture gap to restrict the movement of the two fractured ends. The outer periosteal callus braces the fracture fragments and more importantly through an increase in diameter, enhances structural integrity across the fracture site as the
fractured fragments are bridged by new bone. This increase in cross-sectional area or callus formation is needed to compensate for the lack in material strength of the woven bone callus associated with its random collagen organisation and initial low mineral content.
What do we mean by woven bone consolidation and how does this occur? When does the bone ‘know’ when to start consolidation of woven bone tissue following a fracture?
Woven bone consolidation is the process by which newly formed “woven” bone tissue, which is initially deposited at the site of a fracture, is gradually transformed into mature, lamellar bone during the bone healing process. Woven bone is an early, immature form of bone tissue that has a disorganized, random arrangement of collagen fibres. It is less mechanically stable than lamellar bone, which has a more organized, layered structure with aligned collagen fibres. The consolidation of woven bone involves the remodelling of this tissue into lamellar bone, which is stronger and better suited for long-term structural support.
i. Haematoma formation. A bone fracture ruptures blood vessels inside the bone and surrounding tissues, causing bleeding. The fracture haematoma is the mass of clotted blood at the fracture site.
ii. Soft callus formation. Neutrophils and macrophages infiltrate the haematoma and phagocytose debris and haematoma. The haematoma is first remodelled into a fibrous connective tissue zone called the procallus. Fibroblasts produce collagen fibres that help to connect the broken ends of the bones and chondroblasts form a dense regular connective tissue which starts to resemble cartilaginous tissue. Note that the interfragmentary strain (degree of movement between the fractured ends) dictates whether cartilaginous tissue is formed or whether the fibrous tissue is directly converted to bone tissue.
iii. Bony callus formation. This stage mimics endochondral ossification during development. Angiogenesis allows new blood vessels to infiltrate the soft callus to supply osteoprogenitor cells to the site. Osteoclasts begin to resorb the cartilaginous matrix. Osteoblasts deposit osteoid on the soft callus matrix to start forming woven bone; cartilaginous tissue is eventually completely resorbed and replaced with bone tissue. At this stage the fracture gap has been bridged with bone tissue and is stabilised; weight-bearing can commence without risk of re-fracture.
iv. Callus remodelling. The hard callus persists for at least 3-4 months as osteoclasts remove excess bony material externally and internally. Lamellar bone replaces woven bone.
A complex network of signalling molecules and growth factors, such as bone morphogenetic proteins (BMPs) and transforming growth factor-beta (TGF-β), are released at the fracture site. These signals help coordinate the activities of different cell types involved in the healing process.
Concerning fracture fixation:
if the strain rate is high, intramembranous ossification occurs
flexible fixation results in low strain rates between the fractured end
fracture fixation may result in stress shielding if the plate is too rigid
if the strain rate is very low, the bone may not heal resulting in a non-union
c, d
Concerning bone healing:
a periosteal callus increases the diameter of the bone to increase the structural strength of the bone by increasing the polar moment of inertia
the soft callus consists of woven bone tissue
high strain rates at the fracture site will induce endochondral ossification and the formation of cartilaginous tissue
osteocyte apoptosis stimulates targeted bone remodelling to repair microdamage
a, d
Concerning classification of fractures:
a simple fracture occurs when the fracture traverses the entire bone
A hairline fracture is a type of compound fracture.
a fracture that occurs in bone that has been weakened by disease such as osteoporosis is called a stress fracture
when the bone splinters into more than two pieces it is called a comminuted fracture
d
Concerning callus remodelling and consolidation:
the soft callus is converted into a bony callus when strain levels have decreased at the fracture site
consolidation of the callus refers to the reduction in size of the callus
external remodelling precedes internal remodelling
remodelling of the callus involves the replacement of woven bone tissue with lamellar bone tissue
a, b, d
Place these stages of fracture healing into the correct order from earliest event to latest event:
bony callus formation
soft callus formation
callus consolidation
haematoma formation
haematoma formation
soft callus formation
bony callus formation
callus consolidation
