Innury And Healing Flashcards
Why does bone break
Trauma-low energy or high energy
Stress-repetitive abnormal force on bone so weakening occurs leading to fractures
Pathological-normal stress on abnormal bone
What conditions lead to pathological insufficiency fractures
Osteopenia and osteoporosis - Soft bone
Malignancy
Vitamin-D deficiency - leads to osteomalacia (adults) or rickets (children)
Osteomyelitis (bone infection)
Osteogenesis Imperfecta - Collagen deficiency
Paget’s disease
Osteopenia/osteoporosis
Loss of bone density
Osteoclasts activity is greater than osteoblasts activity
Primary vs secondary osteoporosis
Primary related to old age
Secondary occurs at any age due to hypogonadism,glucocorticoids in excess as it inhibits insulin growth factor reducing osteoblasts activity
Alcoholism increases pth which leaches calcium from bones
What does osteoporosis do to bone
- Fewer trabeculae
- Thinning of the cortical bone
- Widening of Haversian canals
Vitamin D deficiency
Leads to defects in osteoid mineralization
Causes rickets in children and osteomalacia in adults
Congenital osteoimperfecta
- Decreased type 1 collagen due to decreased secretion and production of abnormal collagen
- Leads to insufficient osteoid production
Affects bones hearing heart and sight
Pagers disease
Excessive bone breakdown and disorganized remodeling
Due to too much or too little osteoblasts and osteoclasts activity
Bone cancers CEOL
- Osteosarcoma- cancers in osteoblasts
- Chondrosarcoma- cancer in chondrocytes
- Ewing Sarcoma
- Lymphoma
Secondary bone cancer
Metastatic bone tumours from other tissue
How do we describe fractures
Open - Fracture in which at least one end of the bone penetrates the skin; presenting potential risk of infection
Closed - A fracture in which the skin remain intact
How do bone tissues heal
Bleeding- blood products involved
2) Inflammation- neutrophils, macrophages involved
3) New tissue formation- blasts involved (fibro-, osteo-, chondro-)
4) Remodelling- macrophages, osteoclasts and osteoblasts involved
What fractures heal more specifically
1) Haematoma forms- bleeding between bone ends
2) Inflammation- cytokines released & there’s granulation (connective/fibrotic) tissue deposited + blood vessel formation
3) Repair- chondroblasts make soft callus (type 2 cartilage collagen) which is converted to hard callus (type 1 collagen which is more like bone), facilitated by increased osteoblast activity
4) Remodelling- callus responds to activity, external forces, functional demands and growth- osteoblasts heavily involved. Excess bone is also removed
Wolffs law
Bone grows and remodels in response to the forces that are placed on it
Primary bone healing
- Intramembranous healing
- Mesenchymal stem cell goes straight to osteoblast and there’s direct formation of woven bone
- Happens when you have a stable fracture (absolute stability) and ends of bone are really close together
Secondary bone healing
- Endochondral healing
- Results in more callus forming
- Involves responses in the periosteum and external soft tissues
- Occurs when you have a relatively stable fracture
- Mesenchymal stem cell goes to chondral precursor which produces bone cells
- takes longer than primary bone healing
Fracture management
- Reduction- bring fracture ends together, (can either be closed or open)
- Hold- the ends in the right position with metal or no metal
- Rehabilitate- once bone has healed, limb will still be weak- needs rehabilitation
What two ways do bones develop in utero? (and which bone class does each development method form)
Intramembranous Ossification - First occurs after conception → flat bones
Endochondral Ossification - Begins 2 months into utero → long bones
Intramembranous ossification
- Clustering/condensation of mesenchymal stem cells which differentiate into osteoblasts
- The ossification centre forms
- Osteoblasts begin to secrete osteoid inwards towards ossification centre
- Osteoblasts become trapped in osteoid (unmineralised organic tissue) causing differentiation into osteocytes
- Osteoid calcifies and hardens after several days
- Trabecular matrix (cancellous bone) and periosteum (outside connective tissue layer) form (Mesenchyme differentiate into periosteum)
- Compact bone/cortical bone develops superficial to cancellous bone and crowded blood vessels (in trabecular spaces) condense into red bone marrow
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Endochondral ossification
- Start with a hyaline cartilage precursor- then forms a ring of tissue around it called perichondrium (perichondrium vascularised and blood vessels supply new nutrients to mesenchymal, causing differentiation)
- Mesenchymal stem cells in cartilage differentiate into osteoblasts
- Osteoblasts gather at diaphysis wall of the bone to form the bone collar
- Chondrocytes within central cavity enlarge, form a calcified matrix, making it impermeable to nutrients, causing cell death
- Primary ossification centre (diaphysis) forms at the centre of the bone
- Periosteal bud (consisting of artery, vein, lymphatics and nerves) invades cavity causing formation of spongy bone, by delivering osteoclasts that break down cartilage and osteoblasts that deposit new spongy bone
- Healthy chondrocytes at ends depositing new cartilage causing bone elongation
- At primary oss. centre, diaphysis continues to enlarge and osteoclasts break down centre of spongy bone to form medullary cavity where yellow bone marrow (fat) will be.
- Secondary ossification centre appears in epiphyses (the ends of long bones)
- Junction between primary and secondary ossification is epiphyseal plate and cartilage at ends of bone only stays at surface to lubricate ends for joints
What is the structure of long bones?
Epiphysis- at joint
Physis- growing area
Diaphysis- long bone
Osteogenic cells
Bone stem cells
Found in periosteum
Osteoblasts
Bone forming cells that secrete osteoid and catalyse osteoid mineralization
Osteoclasts
Bone breaking cells that dissolve and resorb bone by phagocytosis
Entrapped in matrix
