bones Flashcards
COMPONENTS of the Bone
CELLS Osteoblasts Lay down osteoid PTH, Vit C, Vit D Osteocytes PTH, Vit D, Calcitonin Osteoclasts Howship’s lacunae (microscopic bone concavities due to bone resoprtion) PTH, Vit D, Calcitonin, PG2, etc. MATRIX!!! (first thing) Collagen Glycoproteins Mineral Calcium hydroxyapatite Non-mineralized matrix may be called “osteoid”
3 areas of the bone
epiphysis (end),
metaphisis (inbetween)
diaphysis (middle part of bone (longest part/ shaft
epiphysis
covered by cartlidge- form joint with other bone joint
diaphysis
lenthg and strenghs- center in mostly hollow and bone marrow
metaphysis
blood supply comes in and gives it to other areas
epiphyseal growth plate
the way the long bones growth- lay down the cartiledge (first) that gets converted to the bone
endocontral osification
first step
lay down collagen (osteoite)and sprinkle calcium
osteoid
first step in bone formation where it is just collagen before calcium has been sprinkled
what lays down ca
osteoblast make osteoids
mature osteoblasts
osteocytes (function depends on hormones and vit c, d
osteoclasts
remodeling bone- eat away part of the bone so that osteoblaste replace it
is bone fixed
no-
Achondroplasia
Defect of endochondral ossification
Causes dwarfism
Growth of the long bones is retarded: Short legs, short arms but normal trunk
Autosomal dominant
lack of endocartiocarcitofication- short bones are made by different process so are ok
Osteogenesis Imperfecta(defective bone formation)
Basic problem: Mutations in gene encoding collagen I (which is the principal component of osteoid).
Autosomal recessive or dominant
Age of presentation depends upon the extent of gene defects
Some born with multiple fractures, others develop symptoms in childhood , puberty or later.
Other defects
Blue sclerae (eye whites)
Think skin
Thin dental enamel
weak bones- not enough collagen
Osteopetrosis
don’t need to know
Osteomyelitis
Bacterial infection of bone
Causes
Pyogenic cocci: Staph aureus.
Mixed flora ( drug addicts)
TB
Usually presents as acute infection which may progress to chronic
Starts with hematogenous deposit of Staph in metaphysis
PMN’s attracted, forming pus
Pus spreads into epiphysis, and through compact bone under periosteum
Sequestra: devitalized bone fragments cut off from blood supply
Involucrum: reactive bone formed to wall off infection
can go to diaphysis area (mostly hollow) can take over it
becomes necrotic- sequestral
Osteoporosis(thin bones)
enough calcium and collagen just less so prone to breaks
Bone is normal but thinned out (less than normal tissue density)
Absolute reduction of total bone mass
1/3 of women > 65 years are affected
Causes
Primary – disease of elderly
Secondary
Hormonal problems ( thyroid, cortisol, estrogen)
Dietary (calcium, vitamin C)
Immobilization
Drugs (anticonvulsants, heparin)
Pathogenesis
Loss of bone matrix !!!and mineral
After age 30y, bone loss exceeds formation
After menopause in women, bone loss accelerates 5-fold ( due to loss of estrogen)
Osteoporosis(thin bones)- pathlogy
Pathology Thin, brittle, prone to fracture Type I (postmenopause) Trabecular bone (vertebrae, wrist) Type 2 (old age) Cortical & trabecular bone of long bones (e.g., neck of femur)
Osteoporosis(thin bones)
Clinical Features Vertebral fractures (crush Injury) Back pain, kyphosis Fracture of neck of femur Incapacitation > 1 Million/year in USA
Osteomalacia soft bones
Bone is abnormal (i.e., normal tissue present but not calcified)
Inadequate mineralization of organic matrix
Caused by disturbance of vit. D or PO4 metabolism
Called “rickets”!!!! (word in kids) in young people
Causes
Vitamin D deficiency
Inadequate intake
Inadequate exposure to sunlight
Intestinal malabsorption
Hypophosphatemia
Malabsorption
Excess loss of PO4
enough collagen but not of anything else
enough osteoites
not enough calcium -no sprinkling
Osteomalacia and Rickets
lowAbsorption of calcium + PO4 in intestines leads to increase in Urinary PO4 loss leads to increase Bone resorption
Loss of minerals leads bone softening
compensatory new bone formation (without mineralization) called osteoid
Children: New bone formation is affected in children Growth retardation Including delayed dentition Deformities Bow legs Pigeon breast Rachitic rosary (enlarged costochondral junction – excess osteoid) Adults and Children Fractures Muscle spasms (tetany)
Fractures
Disruption of bony continuity from mechanical stress
Simple – one fracture line; bone not exposed to environment
Compound – one fracture line; bone exposed to environment
Comminuted – several fragments
Complete – Cortex to cortex
Incomplete – part way through bone (also called “greenstick”)
CLOSED fractures are when skin is not broken
simple
one fracture line; bone not exposed to environment
compound
– one fracture line; bone exposed to environment
Comminuted
several fragments
Complete
Cortex to cortex
Incomplete
– part way through bone (also called “greenstick”)
Cause of fracture?
Traumatic – obvious physical cause
Pathologic – Fracture through pre-existing disease in bone (e.g., tumour, osteoporosis)- don’t need a lot of force to break
Fracture Healing
Hematoma fills and surrounds injured area
Clotted blood seals off farcture site
Clot organizes to soft tissue pro-callus
Conversion to new formed fibrocartilaginous callus by one week)
Replacement by bony provisional callus – this creates spindle-shaped splint maximum at 2-3 weeks
Callus strengthened by widening of bone spicuels
Remodeling (final stage)with osteoclastic and osteoblastic activity
get a callus- healy of the fracture
fracture treatment
Treatment Immobilization of Fracture Reconstruction of any gap Debridement (removal of necrotic tissue) Immobilization (pins +/or plates) Factors that delay healing Nutrition Vitamins C & D, Calcium, PO4 Infection Foreign Bodies Failure of immobilization leads to Fibrous non-union leads to Pseudoarthrosis (false joint)
Bone Tumors
know osteosarcoma
seen in younger men and not good tumor
osteosarcoma
Most Common Metaphysis of long bones of extremities (50% in Knee) Young persons (rare in adults) Rx: surgery & chemotherapy 5 year survival: 30%
Osteoarthritis
Degenerative joint disease Wear and tear of the articular cartilage Cartilage shows Softening Surface defects Irregular thinning -> fibrillation & vertical clefts Denuded bone -> eburnation (polished bone) Bone degeneration -> bone cysts Spicules of new bone (osteophytes)
affects the joint
without the cartilidge there is rubbing which may lead to broken down bones
try to regrown = sclerotic bone
3 main
thinkening of the bone
thinned cartelidge
bone defect
broken down fragments of cartiledge
osteophytes
new bones forming
Clinical Features
osteoarthristis
Clinical Features
Weight-bearing (hip, knees, spine) and small joints of hands are affected
Pain & stiffness (in morning especially) (lasting 15 - 20 min)
Mobility & deformity
Crepitus (grating on movement can hear about it)
Swelling & warmth (2º Inflammation)
Heberden’s nodes: osteophytes ( bony spicules)- bumpy on hands
ULNAR DRIFT IS NOT SEEN
Heberden’s nodes
osteoarthritis
Rheumatoid Arthritis
Chronic systemic disease of unknown etiology
Systemic autoimmune disease affecting synovial joints
Chronic symmetric inflammation
Affects women more (M:F::1:4)
Affects 1% of population
Synovitis – exudation of fluid & inflammatory cells into joint
Ingrowth of vessels & synovial cells-> granulation tissue (pannus)
Pannus secretes lytic enzymes & inflammatory mediators -> destruction of cartilage & erosion of bone
Joints immobilized
Intra-articular space obliterated -> ankylosis
Insidious onset Systemic disease with fever, malaise, anemia etc. Symmetrical involvement of small joints Hand: PIP, MP Wrist Elbow & ankle also common May be juvenile or adult 10% of adults severe disability 50% of children severe disability
Complications Joint deformities Contractures E.g., ULNAR DRIFT Subcutaneous nodules Fibrinoid necrosis surrounded by macrophages and lymphocytes Lungs Interstitial & pleural fibrosis Eyes, heart, vasculature
