- bone is broken entirely

1. Comminuted

- 2 or more fragments present

2. According to direction of break:

- spiral - encircles the bone

- transverse - straight across

- oblique - at an angle

- linear - along the length of the bone

- bone is damaged but still in one piece (tend to occur in children)

1. greenstick - only one side is broken

2. torus - the outer portion of the bone buckles but doesn't break

3. bowing - bone pairs (tibia/fibula, radius/ulna) - one bone breaks, but the other only bends

- difficult to treat, as have two diff. situations

1. Open - compound; skin is broken

2. Closed - simple; skin is intact

1. Transchondral

- occurs at end of bone: fragmentation of articular cartilage (tends to occur in adolescents)

2. Pathologic

- due to a prior disease that weakens a bone eg. tumors, infections

3. Stress

- in normal bone: 

- due to repeated stress

- eg. new spot, muscle gains strength before bone, and can get microfractures w/ repeated stress

- in abnormal bone:

- bones has lost ability to deform and recover and injury occurs w/ normal use

- eg. rheumatoid arthritis, osteoporosis

- can overlap w/ pathologic

- osteoclasts move across space fr. each side, dissolving into bone on other side of break, followed by osteoblasts that fill in bone behind the osteoclasts (cutting cones)

- no callus formation

- occurs when adjacent bone surfaces are in contact w/ each other

- eg. ends of bone held in place by plates/pins

- similar to endochondral bone formation

- involves formation of callus, w/ subsequent bone remodeling

- often observed w/ use of cast or other non-surgical treatment

- bone tissue is unique, in that new bone tissue is actually made during healing (not scar tissue)

- hepatic tissue does not form new tissue but regenerates

1. clot formation

- in the medullary cavity, under the periosteum, and bet. the ends of the bone fragments

2. necrosis

- adjacent bone tissue dies b/c the torn blood vessels are unable to perform exchange of nutrients/waste, gases to site

3. inflammation

- necrosis stimulates inflammation (vasodilation, infiltration of plasma, wbc, growth factors and mast cells)

4. fibrocartilaginous callus = procallus

- phagocytic cells move in and remove dead tissue

- fibroblasts and chondroblasts also arrive

- lay down collagen fibers and cartilage on the network formed by the fibrin of the clot

- this forms an initial bridge called fibrocartilaginous callus bet. the bone ends

5. bony callus

- osteoblasts w/in the procallus (fr. the periosteum & endosteum) synthesize collagen and matrix, w/c then calcifies, forming a bony callus

6. remodelling

- during subsequent months, the callus is remodelled by osteoblasts and osteoclasts (excess callus is resorbed and trabeculae are formed along lines of stress)

- displacement of one or more bones in a joint in w/c opposing surfaces lose all contact

- most joints of the shoulder, elbow, wrist, finger, hip and knee

- displacement of one or more bones in a joint in w/c opposing surfaces lose only some contact

- same joints as dislocation

- increased curvature of upper spine

- can be caused by:

- diseases causing loss of bone density in vertebrae (osteoarthritis, etc.)

- fusion of joints bet. vertebrae (ankylosing spondylitis, etc.)

- loss of curvature of lower spine

- can be caused by:

- ankylosing spondylitis, for eg.

- rotational curvature of the spine

- can be caused by:

- idiopathic (perhaps genetic)

- due to systemic conditions (cerebral palsy)

- conditions not directly affecting spine (leg length discrepancy)

- tearing of ligament

- most common in wrist, ankle, elbow and knee

- avulsion

- sprain, complete separation commonly seen in young athletes 

- tearing or stretching of a muscle or tendon

- can occur anywhere in the body, but most in leg, hand, upper arm

- decrease in bone mass, leading to fragile bones

- can be present for decades - not known until fracture occurs; not always a disease of age

- general process is that old bone is being reabsorbed faster than new bone is being deposited, resulting in bones losing density (thinner and more porous)

- eventually fractures can occur spontaneously

- most severe in femoral neck, thoracic and lumbar spine and wrist

- can be localized, involving one segment of the appendicular skeleton

- or generalized, involving major portions of the axial skeleton

1. PTH

2. cortisol

3. thyroid hormone

4. growth hormone

- peak bone mass occurs at around age 30, and then declines (resorption slowly exceeds formation)

- it is linked to estrogen deficiency

- can arise thru stress, excessive exercise and low body weight

- one effect is that:

- it aids in maintaining bone density thru helping osteoclast apoptosis, so a decrease in estrogen results in more survival of bone resorbing cells

- in women, bone mass decline is fastest in several years after menopause

- due to advanced age, but this type of osteoporosis is linked to estrogen deficiency

1. the decrease in bone protecting hormones (testosterone, estrogen) in men is more gradual than in women, so that there's slower loss of bone in men than women during aging

2. men also begin w/ denser bones, so osteoporotic levels are reached at an older age

1. low levels of androgens

2. insufficient intake/absorption of minerals

- calcium absorption decreases w/ age

3. excessive intake of caffeine, phosphorus, alcohol, and nicotine

4. small stature/thin build

1. kyphosis: hunched back due to vertebral collapse

2. fractures common due to thin and sparse trabeculae in spongy bone and porous compact bone

3. fractures of long bones, radius, ribs and vertebrae most common

- fat or pulmonary embolism

- pneumonia

- hemorrhage

- shock

- infectious bone disease

2 types of osteomyelitis

and one source for each

1. exogenous osteomyelitis (most common)

- caused by:

- pathogens entering joint (fractures, penetrating wounds (bites), surgery)

- eg. diabetic foot infection

2. endogenous osteomyelitis

- pathogens are carried in the blood fr. site of infection elsewhere in the body

- eg. hematogenous osteomyelitis, usually found in infants, children and elderly

- Staphylococcus aureus

- but other bacteria, fungi, parasites and viruses can also cause bone infection

1. inflammatory response

- intense vascular engorgement, edema, leukocyte activity, abscess formation

2. sequestrum

- in children:

- exudate fr. infection can lift off periosteum, thereby disrupting blood supply to area of the bone leading to necrosis of area (sequestrum)

3. involucrum

- lifting of periosteum stimulates osteoblasts, w/c lay down layer of bone on top of sequestrum (involucrum)

4. in adults:

- periosteum is more firmly attached to bone, so exudate doesn't cause this problem

- instead, it can disrupt and weaken the cortex, increasing susceptibility to fracture

1. appear during 5th/6th decade of life

2. pain in one or more joints (heavy use, load bearing)

3. primary signs include pain, stiffness, enlargement (swelling), deformity of joints

4. range of motion is limited due to cartilage degeneration

1. articular cartilage changes structure

- the surface flakes off and underlying layers develop cracks

2. exposed articular bone

- becomes hardened and may develop cysts

3. osteophytes

- are the cartilage coated projections of bone at the edges of the joint

- these may grow out and alter the anatomy of the joint

4. joint mice

- small pieces of osteophytes may break off and go into the synovial cavity

5. synovitis and joint effusion

- develops fr. joint mice irritating the synovial membrane

6. joint capsule

- becomes thickened and may stick to the underlying bone, therefore restricting movement

1. due to bone enlargement around the joint

2. due to inflammatory exudate or blood entering the joint cavity, thereby increasing the volume of synovial fluid (joint effusion)

- caused by presence of bone fragments in the synovial cavity, drainage of cysts, etc.

- age-related disorder of synovial joints

- characterized by:

- local areas of loss of articular cartilage

- new bone formation of joint margins (osteophytosis)

- subchondral bone changes

- variable degrees of mild synovitis

- thickening of the joint capsule

- characterized by:

- inflammatory damage in the synovial membrane or articular cartilage

- and by systemic signs of inflammation (fever, leukocytosis, malaise, anorexia)

- can be:

- infectious

- caused by introduction of pathogens thru wound or the bloodstream

- noninfectious (most common)

- caused by immune rxns (rheumatoid arthritis and ankylosing spondylitis) or deposition of monosodium urate crystals (gouty arthritis)

- chronic, systemic, inflammatory autoimmune disease distinguished by joint swelling and tenderness, AND destruction of synovial joint leading to disability and premature death

- synovial memb. get affected first then articular cartilage, joint capsule, and surrounding tissue

- common affected are fingers, wrists, elbow, feet, ankles, knees

- cause is unknown but probably due to interaction of genetic factors w/ inflammatory mediators

- rheumatoid factors are antibodies that react to portions of host antibodies present in the synovial membrane

1. production of RFs

- unknown antigen in the synovial tissue triggers the immune system, activating T & B cells, & macrophages

- B cells produce antibodies (RFs) agnst the Fc portion of IgG

- these RFs then form complexes w/the IgG, and activate complement protein w/c further stimulates the immune response

2. edema & production of granulation tissue

- stimulated by a dense population of immune cells and the resultant large production of cytokines

3. pannus

- tissue produced by the granulation tissue

- consists of lymphocytes, macrophages, fibroblasts, mast cells

4. destruction of the joint

- pannus can grow over and erode articular cartilage and bone, expanding and destroying the joint

1. begins w/ general systemic signs of inflammation

- fever, fatigue, weakness, etc.

2. stiffness lasts for about 1 hr after rising whereas osteoarthritis stiffness only in first few mins of use

3. loss of mobility leads to atrophy of surrounding muscles

- chronic inflammatory joint disease

- characterized by:

- ankylosing: stiffening & fusion of the spine & sacroiliac joints

- spondylitis: systemic, autoimmune inflammatory disease

- area that is affected:

- Ankylosing spondylitis

- excessive bone formation occurs at the point at w/c ligaments, tendons & the joint capsule are inserted into bone

- leading to fusion of the joint, primarily the sacroiliac joint & vertebral column

- Rheumatoid arthritis

- primary site of inflammation is the synovial memb. thus affecting synovial joints

1. fibrocartilage in vertebral joints becomes inflamed

2. damage occurs fr. macrophages & lymphocytes

3. fibroblasts repair the damage, secreting collagen that eventually becomes ossified

4. final result is fusion of the joints

- clubfoot

- one or both feet turn inward and downward

- can be positional, idiopathic or as a result of another syndrome eg. spina bifida

- can be corrected by manipulation and casing begun soon after birth

- imperfect development of the hip joint

- may be idiopathic or teratologic eg. spina bifida

- may be correctable w/ Pavlik harness

- if not successful, require surgery and body casting

- attributable to another cause