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221 Cards in this Set

  • Front
  • Back
What gives bone its strength?
its systematic structure
where does the bone meet the joint?
articular cartilage (important for arthritis)
What is the growth plate?
where growth occurs in long bones of children..it fuses in adults and is a thinner line
What is the cylindrical structure of compact bones known as? And why is this helpful?
Haversian Systemosteon-gives bones strength, compact structure, it's like raw spaghetti noodles..one is easy to break but a bunch together is tougher

Note: Bone is made of up two types of bony (osseous) tissue: compact bone (cortical bone) making 85% of bone and spongy bone (cancellous bone) making up remaining 15% of bone. Both are usually present in every bone. Haversian system is only in compact bone.
Is bone vascular?
Yes..very.
What are obsteoblasts?
bone building cells and formation of bone matrix and mineralization of bone matrix with calcium salts (mineralization gives bones strength)
What are the two main general functions of osteoblasts?
1) ossification: formation of osteoid (pre-bone) Collagen and protein matrix

2) Calcification: deposition of calcium salts into osteoid tissue.
-secretes enzyme: alkaline phosphatase:
--locally increases calcium and phosphate levels that promotes precepitation of calcium and phosphate --> mineralization
--increased serum levels following injury/fractures
What are osteocytes-and main function?
osteocytes are mature bone cells that maintain bone matrix

-There are three types of cells in bone: OB, OC, and osteocytes
-OB main function is to lay down new bone-when it does that OB becomes osteocytes
-osteocytes are most plentiful cell in bone
-osteocytes are OB that have become imprisoned within the mineralized bone matrix
-they help maintain bone by signaling ob and oc to form and resorb bone
-osteocytes live within a space in the hardened bony matrix called a lacuna
What are osteoclasts and main functions?
large phagocytic cells, phagocyze bone, resorption of bone matrix (release of calcium and phosphate from bone i.e. when serum needs it)
What is a bone fracture?
Injury to bone and tissue around bone
In general, what does the bone do after a fracture?
a healing process to regenerate itself
Stage I: What happens first after a bone fracture? What are the results?
Hematoma-remember bone is very vascular so bleeding into injury occurs from damaged ends of bones, a clot forms
-clot is good b/c it provides scaffolding for fibroblasts (cells that produce collagen). Collagen is a very strong protein structure.
-hematoma also provides framework for influx of inflammatory cells, ingrowth of fibroblasts, and development of new capillary vessels
-sets of signaling cascade for healing process
-Stage I lasts first week or so..at this time the pt can not bear weight on injured bone
What is fracture healing stage 2 indicated by? Describe..
Fibrocartilaginous Callus Formation
-fibroblasts, osteoblasts, and new capillaries infiltrate hematoma at fx site -> organizes into granulation tissue called procallus
-fibroblasts produce fibrocartilaginous soft callus bridge that connects bone fragments, cartilage is formed as a precursor of bone
-Weeks 2-3..still no weight bearing on injured bone
What is fracture healing stage 3 indicated by? How does this occur? For how long?
Bony Callus Formation:
-ossification: -fibrosteoblasts and osteoclasts mineralize the fibrocartilage into bony callusocartilaginous callus formation of Stage 2 becomes bony callus
-OC and OB mineralize the fibrocartilage which forms bony callus

-process begins 3-4 weeks after injury, continues for months, can begin weight bearing
What is fracture healing stage 4 indicated by?
Remodeling
-excess bony callus remodeling with removal of dead bone tissue by osteoclasts
-important b/c bone that has not been remodeled does not have good mechanical properties for weightbearing and mobility
-healed fracture may have thickened area on bone surface
Complications of bone healing: describe delayed union
Delayed union is failure of fx to heal within predicted time as determined by x-ray
-does not occur until 8-9 months after fx
What are possible contributing factors to delayed union?
-large displaced fx
-inadequate immobilization
-large hematoma
-infx at fx site
-excessive loss of bone
-inadequate circulation
Complications of bone healing: describe malunion
Malunion is the healing of a bone in a nonanatomic position
-deformity at fx site
-deformity or angulation at x-ray
What are possible contributing factors to malunion?
-inadequate reduction
-malalignment of fx at time of immobilization
Complications of bone healing- nonunion: what is it? what are some of the manifestations?
Nonunion is failure of the bone ends to grow together-instead the gap b/w the broken ends fills with dense fibrous and fibrocartilaginous tissue instead of new bone
-failure of bone to heal before the process of bone repair stops
-evidence on x-ray
-motion at fracture site
-pain at weight bearing
Nonunion: what are some possible contributing factors?
-inadequate reduction
-mobility at fracture site
-severe trauma
-bone fragment separation
-soft tissue b/w bone fragments
-infx
-extensive loss of bone
-inadequate circulation
-malignancy
-bone necrosis
-noncompliance with restrictions
What is osteoporosis?
-reduced density of bone mass (bones are very porous)
-structural deterioration of bone
-can be generalized or regional
--common sites: vertebrae, hip, wrists
What are some common manifestations of osteoporosis?
-pain
-bone deformity (bone kyphosis/hump due to vertebral collapse)
-fx due to increased amt of porous bone, compression fx of vertebrae
-decrease in height
What are some primary risk factors for osteoporosis?
-advanced age
-white (fair, thin skin)
-female
-small bone structure
-postmenopausal
family hx
-contributing factors..sedentary lifestyle & long term calcium deficiency
What are some secondary risk factors for osteoporosis?
-cushing disease
-diabetes
-hyperparathyroidism
-hyperthyroidism
-malignancy
-malabsorption disorders
-chronic alcoholism
-medications..
--anticonvulsants
--corticosteroids
--aluminum containing antacids
--heparin
What does RANKL stand for? In a word what is it?
Receptor Activator of Nuclear Factor kB Ligand..it is a receptor
What does RANK stand for? what is its connection with RANKL, in brief terms?
Receptor Activator of Nuclear Factor..
-it is the receptor that RANKL meets up with
-think you want to receive rank
What is OPG? What is its interaction with RANK and RANKL?
osteoprotegerin
-glycoprotein that gets in the middle of the binding of RANK and RANKL
What is apoptosis?
programmed cell death
If something is Proapoptotic what does it do?
promotes apoptosis (cell death)
If something is antiapoptotic what does it do?
slows down apoptosis
What does ERKS stand for?
Extracellular signal Regulated Kinases & it responds to estrogen
The main two contributors to bone maintenance..how does this r/t density?
osteoblasts and osteoclasts

More osteoblast activity--> density increases

More osteoclast activity--> density decreases
What controls osteoclasts?
RANK and RANKL
What happens when RANK and RANKL connect?
decreased apoptosis of osteoclasts -->
increased cell survival of osteoclasts-->
increased bone loss
What happens when RANK and RANKL don't connect? What would get in the way?
OPG gets in the way..like a wad of chewed gum on the key hole.

OPG stops RANKL it "blocks it" therefore..

increased apoptosis of osteoclasts -->
decreased cell survival of osteoclasts-->
decreased bone loss
What is mature bone made up of?
mature bone is a rigid yet flexible connective tissue consisting of cells, fibers, a gelatinous material termed ground substance, and large amounts of crystallized minerals, mainly calcium, that give bone its rigidity.
What are the steps of bone formation?
-the production of an organic matrix by the bone cells. bone matrix consists of ground substances, collagen, and other proteins that take part in bone formation and maintenance
-then calcification-minerals are deposited and crystallize. Minerals bind tightly to collagen fibers, producing tensile and compressional strength in bone, and withstand pressure and weightbearing
What does resorb mean?
dissolve or digest old tissue
Describe long bones and some of its components
Bones can be classified by shape as long, flat, short (cuboidal), or irregular
-long bones are longer than they are wide and consist of:
-a long narrow tubular MIDportion (diaphysis)
-that merges into a broader neck (metaphysis) and
-a broad end (epiphysis)

-think of a chicken leg..middle is diaphysis, broader neck is metaphysis, broad end is epiphysis
What does the epiphysis allow?
The broadness of the epiphysis allows weightbearing to be distributed over a wide area
-made up of spongy bone covered by compact bone
In a child what exists among the epiphysis?
In a child the epiphysis is separated from the metaphysis by a cartilaginous growth plate, the epiphyseal plate
-after puberty the epiphyseal plate calcifies and the epiphysis and metaphysis merge
-by adulthood the line of demarcation b/w the epiphysis and metaphysis is undetectable
What is a synovial joint?
Synovial joints (diarthroses) are the most movable and most complex joints in the body.
What is a synovial membrane?
The synovial membrane (synovium) is the smooth, delicate inner lining of the joint capsule. It lines the nonarticular portion of the synovial joint and any ligaments or tendons that transverse the joint cavity.
-it is made up of two layers-a vascular layer (subintima) and a thin cellular layer (intima)
What is articular cartilage?
a layer of hyaline cartilage that covers the end of each bone.
-The fibers firmly anchor the cartilage to the bone, and the proteoglycans control the loss of fluid from the cartilage.
--proteoglycans give articular cartilage its stiff quality and regulate the movement of synovial fluid thru the cartilage. W/o proteoglycans, nml weightbearing would push all synovial fluid out.
--proteoglycan is a macromolecule and the CHO component is called glycosaminoglycans
-thickness depends on size of joint, fit of the two bone ends, amount of weight and shearing foice the joint withstands, etc.
-cartilage strength due to extensive network of cross linked collagen fibers and is composed of chondrocytes (cartilage cells)
-it is also composed of an intracellular matrix made up of collagen, protein polysaccharies, proteoglycans,
Glycosaimoglycans, and water
-water makes up 60-80% of the net weight of the cartilage, and individual molecules rapidly enter/exit the articular cartilage to contribute to the resiliency of the tissue
-synovial fluid nourishes the pad of the articular cartilage that covers the ends of the bones..a loss of synovial fluid leads to rapid deterioration of articular cartilage
What are myofibrils?
the functional units of muscle contraction
-each myofibril contains sarcomeres-which appear at intervals
-the sarcomeres are composed of two contractile proteins, actin and myosin
-actin and myosin filaments form cross-bridges that cause the sarcomere to shorten, a process now known as the cross-bridge theory of muscle contraction
The balance between ____ and ____ determine the quality of the bone.
RANKL and OPG.

-RANKL induces osteoclast activation and bone resorption.
-think of RANK as attached to OC ready for RANKL per class illustration
Briefly summarize bone repair
Bone injuries are repaired in stages. Hematoma formation provides the fibrin framework forformation and organization of granulation tissue. The granulation tissue provides a cartilage
model for the formation and crystallization of bone matrix. Remodeling restores the original shape and size to the injured bone.
Joints can be classified by the degree of ____ they allow.
movement:

synarthroses (immovable joint)
amphiarthroses (slightly moveable joint)
diarthroses (freely movable joint)
Joints can also be classified by the type of....
Joints are classified also by the type of connecting tissue holding them together.

-Fibrous joints are connected by dense fibrous tissue, ligaments, or membranes.

-Cartilaginous joints are connected by fibrocartilage or hyaline cartilage.

-Synovial joints are connected by a fibrous joint capsule. Within the capsule is a small fluid-filled space. The fluid in the space nourishes the articular cartilage that covers the ends of the bones meeting in the synovial joint.
What are joints and what do they provide?
A joint is where two or more bones attach. Joints provide stability and mobility to the
skeleton. Joints help move bone and muscle.
What is synovial fluid and what does its loss lead to?
Synovial fluid is superfiltrated plasma from vessels in the synovial membrane
-synovial fluid lubricates the joint surfaces, nourishes the pad of the articular cartilage that covers the ends of the bones, and contains free-floating synovial cells and various leukocytes that phagocytose joint debris and microorganisms
-loss of synovial fluid leads to rapid deterioration of articular cartilage
What do musculoskeletal injuries include? What is the most serious?
musculoskeletal injuries include fractures, dislocations, sprains, and strains.
-fractures are the most serious
-alterations in bones, joints, and muscles may be caused by metabolic d/o, infx, inflammatory or noninflammatory diseases, or tumors
-trauma is the leading cause of death for all persons of ages 1-44
What is a fracture? How can they be classified?
a fracture is a break in the continuity of a bone

-classified as complete or incomplete
--complete: the bone is broken all the way through
--incomplete: the bone is damaged but still in one piece

-or open and closed
--open: (formerly compound)-the skin is broken
--closed: (formerly simple)-skin is not broken
What is a comminuted fx?
a fx in which a bone breaks into more than 2 fragments
A fracture can also be classified according to the ___ of the ___ ___.
direction of the fracture line
-a linear fx runs parallel to the long axis of the bone
-an oblique fx is a slanted fx of the shaft of the bone
-a spiral fx encircles the bone
-transverse occurs straight across the bone
Which fx are children more prone to?
Incomplete fx tend to occur in the more flexible, growing bones of children. 3 main types of incomplete:
-greenstick fx: perforates one cortex and splinters the spongy bone, outer surface is disrupted inner surface intact
-torus fx-the cortex buckles but does not break
-bowing fx-usually occur when longitudinal force is applied to bone
___ fractures are often seen in osteoporosis
fragility fractures
-result from low level trauma
-would not normally cause a fx
What is dislocation?
the temporary displacement of a bone from its normal position in a joint
-generally associated with fractures b/c stress is placed on areas of bone not normally subjected to stress, i.e. shoulder, elbow..
-can be from congenital d/o, arthritis..
What is subluxation?
-if the contact b/w the two surfaces is only partially lost in a dislocation, the injury is called a subluxation
-also generally associated w/ fx for above reasons
___ and ___ injuries can accompany fx and dislocations, describe these two
tendon and ligament

-a tendon is a fibrous connective tissue that attaches skeletal muscle to bone

-a ligament is a band of fibrous connective tissue that connects bones where they meet at a joint

-tendons and ligaments support the bones and joints and either facilitate or limit motion
-tendons and ligaments can be torn, ruptured, or completely separated from bone at their pts of attachment
A tear in a tendon is commonly known as a ___
Teras in Tendon = Strain (think T)

-major trauma can tear or rupture a tendon at any site in the body
Ligament tears are commonly known as ____
Tears in Legaments = Sprain
a complete separation of a tendon or ligament from its bony attachment site is known as...
avulsion
-an avulsion is the result of abnml stress on the ligament or tendon and is commonly seen in young athletes-esp hard runners
Strains and sprains are classified as..
first degree: least severe

second degree

third degree: most severe

-think like burn..3rd most severe
Patho of tendon or ligament tear
-an extensive cascade of inflammatory processes begin
-inflammatory exudate develops b/w torn ends
-later, granulation tissue containing macrophages, fibroblasts, and capillary buds grows inward f/ surrounding soft tissue and cartilage to begin the repair process
-4-5 days after injury, collagen formation begins, random at first then more organized
-should be strong enough to withstand strong pull 4-5 weeks after injury..if not, at risk for separating again
Trauma and repetitive stress can cause..
-painful degradation of collagen fibers (tendinosis)

-inflammation of tendons (tendonitis)

-or inflammation in bursal sacs (bursitis)
What does tendinopathy include?
-tendonitis-systematic degeneration of the tendon with vascular disruption and inflammatory repair response

-tendinosis-intratendinous degeneration (commonly due to aging, microtrauma, muscular compromise), collagen disorientation

paratendinitis: "inflammation" of the outer layer of the tendon (paratenon) alone, whether or not the paratenon is lined by synovium
--may or may not be accomponied by tendinosis

-other causes of tendinopathy: crystal deposits, postural misalignment, and hypermobility in a joint
What is epicondylitis?
inflammation of a tendon where it attaches to a bone (at its origin)

-however, most tendon pathology, is caused by tissue degeneration rather than inflammation
What are bursae? Where are they located? What are the functions?
small sacs lined with synovial membrane and filled with synovial fluid
-they are located b/w tendons, muscles, and bony prominences
-their primary function is to separate, lubricate, and cushion these structures
-acute buritis-usually middle yrs, caused by trauma
-chronic bursitis-result from repeated trauma
-septic bursitis-caused by would infx or bacterial infx of the skin overlying the bursae
What is bursitis?
an inflammation that is reactive to overuse or excessive pressure
-the inflamed bursal sac becomes engorged, and the inflammation can spread to adjacent tissues
-inflammation may decrease with rest, heat, and aspiration of the fluid
What is rhabdomyolysis?
Rhabdomyolysis, or myoglobinuria, can be a life-threatening complication of severe muscle trauma with muscle cell loss
What is a pysical manifestation of rhabdomyolysis?
myoglobinuria-an excess of myoglobin (an intracellular muscle protein) in the urine
-muscle cell damage releases the myoglobin
-the most severe form is often called crush syndrome
-less severe and more localized forms of muscle damage are called compartment syndromes, which can lead to Volkmann ischemic contracture in the forearm or leg
Who is at risk for Crush Syndrome?
-people found unresponsive and immobile for long periods, i.e. after drug/alcohol OD
What are some causes of rhabdomyolosis?
-injury: immobilization, lightning strike, excessive burns, crush injury, strains, electric shock, ECT
-excessive muscle use, exertion, marathon running,
-etoh, drugs, coke, lsd, x, amphetamines, depressants..
-certain medications (herbal meds, anesthetic agents, cholesterol lowering agent "statins"
-fire ant bites, snake bites, cowfish ingestion
-after viral infx
-medical-malignant hyperthermia, neuroleptic malignant syndrome, heat stroke
Rhabdomyolyosis and renal failure
-if the myoglobinuria is caused by fulminant malignant hyperthermia, severe muscle spasm and rhabdomyolysis can lead to renal failure
Patho of rhabdomyolosis
-muscle injury causes ischemia (the weight of a limp extremity can generate enough pressure to produce muscle ischemia)
-ischemia to muscle leads to edema
-edema increases compression to muscle which furthers edema

Cycle Continues...and eventually leads to cell death

Cell death/damage leads to myoglobin release, increased CK (may be 100x over), increased potassium and phosphate
Urine color with rhabdomyolosis
When myoglobin is released from the muscle cells into the circulation, it can cause a visible, dark, reddish brown pigmentation of te urine
-the renal threshold for myoglobin is low, so little muscle damage is needed before this sx
Labs with rhabdomyolosis and why its problematic
-hyperkalemia (release of cellular potassium into the systemic circulation)
-increased phosphate
-hypocalcemia (b/c inc phosphate which binds to calcium in blood)
-Metabolic acidosis (release of cellular phosphate and sulfate)
-electrolyte inbalances leads to cardiac issue
-liver doesnt like myoglobolin can be damaged
-myogl is also hard on kidneys, 100-200 g muscle damage can damage kidney f/ excess myoglobulin
Sx of rhabdo (local and systemic)
Local – Muscle pain, tenderness, swelling, bruising,
weakness

◦ Systemic – tea-colored urine, fever, malaise, nausea,
emesis, confusion agitation, anuria
Complications of rhabdo (early and latE)
◦ Early – Hyperkalemia, Hypocalcemia (bound to increased
phosphate), hepatic inflammation, cardiac arrhythmia, cardiac arrest
◦ Late – Acute renal failure, Disseminated intravascular coagulation
Osteoporosis: what is osteopenia?
Osteopenia is decreased bone mass
When do women start losing bone?
-bone formation continues at a pace faster than resorption until peak bone mass, or maximum bone density and strength, is reached, around age 30
-after which bone resorbtion slowly exceeds bone formation
What is the number 1 risk for ppl with osteoporosis?
fractures..
vertebral fx are the most common osteoporotic fx but may be asymptomatic
-even if the fx does not cause pain, vertebral fx can cause deformity, reduced pulmonary function, and loss of height
Diet and risk of osteoporosis
-low dietary Ca and Vit D
-low endogenous Mg
-excessive (or low) protein
-excessive sodium intake
-high caffeine intake
-anorexia
-malabsorption
-excessive phosphorus intake (chiefly thru intake of soda and junk food, interferes with ca-phos balance)
What hormone stimulates bone formulation?
androgens (testosterone and dihydrotestosterone)
What is secondary osteoporosis?
sometimes develops temporarily in ppl rec'ving large doses of heparin, perhaps b/c heparin promotes bone resorption by decreasing collagen synthesis or increasing collagen breakdown
-usually stops when therapy stops
-also may occur f/ glucocorticosteroids for RA, lithium, methotrexate, anticonvulsants, cyclophosphamide, cyclosporine
What is transient osteoporosis?
transient osteoporosis of the hip is assoc w/ third trimester preg or immediate post partum
-but typically self limiting syndrome affecting LE joints of middle aged men, unknown cause
Regional osteoporosis..
usually has a known cause
-after 8 wks of immobilization significant osteoporosis is present
-astronauts f/ weightlessness
Patho of osteoporosis-basic
osteoporosis develops when the remodeling cycle-the process of bone resorption and bone formation-is disrupting, leading to imbalance in coupling process
patho of osteoporosis in post menopausal women
increased bone resorption relative to the rate of bone formation, leading to sustained bone loss resulting from estrogen deficiency.
-bone loss resulting from estrogen deficiency also contributes to osteoporosis in men
-the increase in bone resorption results from increased dev of OC and decreased OC apoptosis
Estrogen and ERKS..2 effects
Estrogen activates ERKs or extracellular signal regulated kinases. ERKs has two effects:

1) antiapoptotic effects on OB --> increased cell life of OB --> increased bone

2) proapoptotic of OC --> decreased cell life of OC --> increased bone
Estrogen and OPG
Estrogen stimulates OPG production..which blocks RANK and RANKL
Estrogen and Osteoporosis
Estrogen is decreased with osteoporosis, so low estrogen results in ..

1) decreased OB stimulation

2) increased OC activity

3) increased OC activity

..based on rationale in previous slides
Rank the severity of osteoporosis..
Normal
Osteopenia-Z score for bone density not that bad
Osteoporosis
Severe Osteoporosis
What is osteomyelitis?
a bone infection most often caused by bacteria..however, fungi, parasites, and viruses can also cause bone infection
Why is bone infection (osteomyelitis) so difficult to treat? 3 reasons, give 1st, r/t permeability
-bones contain multiple microscopic channels that are impermeable to the cells and biochemicals of the body's natural defenses
-once bacteria gains access to these channels, they are able to proliferate unimpeded
Why is bone infx (osteomyelitis) so difficult to treat? 2nd reason..r/t vascularity
-the microcirculation of bone is highly vulnerable to damage and destruction by bacterial toxins
-vessel damage causes local thrombosis (blockage) of the small vessels, which leads to ischemic necrosis (death) of bone
Why is bone infection (osteomyelitis) so difficult to treat? 3rd reason..r/t replacement
-bone cells have a limited capacity to replace bone destroyed by infections
-initially OC are stimulated by infx to resorb bone, which opens up isolated bone channels so that cells of the inflammatory and immune system can gain access to the infected bone
-At the same time, however..resorption weakesn the structural integrity of the bone. New bone formation usually lags behind resorption, and the haversian systems in the new bone are imcomplete
Two types of osteomyelitis- give one
Exogenous osteomyelitis: an infection that enters from outside the body, i.e. thru open fx, penetrating wounds, bite, assault, or sx procedures.
-the infection spreads from soft tissues into adjacent bone
Give the other type of osteomyelitis
Endogenous (hematogenous) osteomyelitis:
-caused by pathogens carried in the blood from sites of infection elsewhere in the body
-the infection spreads from bone to adjacent soft tissues
-common in infants, children, and older adults
-a common complication of sickle cell disease (salmonella) and low oxygen tension
What is the most common cause of hematogenous osteomyelitis?
Staphylococcus aureus
(S. aureus)
common organisms in newborns for hematogenous osteomyeitis
S. aureus, Group B streptococcus,
Gram-negative enteric rods
common organism in infants for hematogenous osteomyelitis
S. aureus, H. Influenzae
common organisms in hematogenous osteomyelitis in older children
S. aureus, Pseudomonas, Salmonella,
N. gonorrhoeae
common organisms in hematogenous osteomyelitis in adolescents and adults
Pseudomonas, M. tuberculosis
organisms in hematogenous osteomyelitis in older adults and immuno compromised
gram negative infections
organisms in hematogenous osteomyelitis in immunocompromised ppl
myobacterial and fungal infx
In adults, what sites are more common in hematogenous osteomyelitis
-spine, pelvis, small bones
-vertebrae, sternoclavicular joint, sacroiliac joint,
symphysis pubis
-microoganisms reach vertebrae thru arteries, veins, or lymphatic vessels
In children, what bones are more commonly involved in hematogenous osteomyelitis
Appendicular skeleton (shoulder girdle, arms, hands,
pelvic girdle, legs, feet)
In osteomyelitis (exogenous), what organisms are common in human and animal bites
human: S aureus
animal: Pasteurella multocida
patho of osteomyelitis (regardless of source)
-first, the invading pathogen provokes an intense inflammatory response
-infl in bone is characterized by vascular engorgement, edema, leukocyte activity, and abscess formation
-once infl is initiated, the small terminal vessels thrombose and exudate seals the bone's canaliculi (microscopic canals between the various lacunae of ossified bone)
-inflammatory exudate extends into the metaphysis and the marrow cavity and thru small metaphyseal openings into the cortex
In children, what might exudate do in osteomyelitis
exudate that reaches the outer surface of the cortex forms abscesses that lift the periosteum off underlying bone
-lifting of the periosteum disrupts blood vessels that enter bone thru the periosteum, which deprives underlying bone of its blood supply
-this leads to necrosis and death of the area of bone infected, producing sequestrum, an area of devitalized bone
-Lifting of the periosteum also stimulats an intense OB response
-OB lay down new bone that can partially or completely surround the infected bone.. this layer of new bone surrounding the infected bone is called an involucrum
-openings in the involucrum allow the exudate to escape into surrounding soft tissue and ultimately thru the skin by way of sinus tracts
Does this occur in adults?
-its rare, bc the periosteum is more firmly attached to the cortex and resists displacement.
-instead, infx disrupts and weakens the cortex, which predisposes the bone to pathologic fx
What is sequestrum? What often occurs with infants?
sequestrum is dead bone

-infants under 1: sequetrum can leak
out to joint, can lead to septic arthritis(vessels cross into epiphysis)
What about sequestrum in older kids?
>1 to adolescent: sequestrum
can leak to adjoining tissue
(vessels do not cross into
epiphysis)
What are arthropathies?
Joint disease-there are 2 major types: noninflammatory joint disease and inflammatory joint disease
What is OA? What is it characterized by?
Osteoarthritis-a common age-related disorder of synovial joints.
-characterized by local areas of loss and damage of articular cartilage, new bone formation of joint margins (osteophytosis), subchondral bone changes, variable degrees of mild synovitis and thickening of the joint capsule.
Inflammatory or non?
OA has been commonly classified as non-inflammatory joint disease
-However..new info has made it clear that specific markers of infl are present in OA
-reclassified as inflammatory joint disease
advancing disease of OA reveals what?
-advancing disease reveals narrowing of the joint space b/c of cartilage loss, bone spurs (osteophytes), and sometimes changes in the subchondral bone
What is the cause of OA?
Unknown, but involve
-low grade inflammation
-calcification of articular cartilage
-genetic alterations
-metabolic d/o
What are risk factors to OA?
-any condition that damages cartilage directly, subjects the joint surfaces or underlying bone to chronic, excessive, or abnml forces, or causes instability in the joint
-trauma-sprains, strains, dislocation, fx
-LT stress-athletes, obesity,
-inflammation in joint structures-during which infl cells release enzymes capable of digesting cartilage cells
-joint instability
-neurological d/o-which pain and propioceptive reflexes diminished/loss, increasing tendency for abnml movement
-congenital or acquired skeletal deformities
-hematologic or end d/o-ie hemophilia-which causes chronic bleeding into the joints, or hyperparathyroidism-bone loses Ca
-drugs that stimulate activity of collagen digesting enzymes in synovial membrane
-obesity
What is the primary defect in OA? What happens early in the disease and then late?
loss of articular cartilage
-early: the articular cartilage loses the glistening appearance, becoming yellow/brownish gray
-later: surface areas of the articular cartilage flake off and deeper layers develop longitudinal fissures (fibrillation)
-the cartilage becomes thin and may be absent over some areas, leaving the underlying bone (subchondal bone) protecting
-then the unprotected subchondral bone becomes sclerotic (dense and hard)
-cysts sometimes develop within the subchondral bone and communicate with the longitudinal fissures in the cartilage
What can happen with these cysts in OA?
-pressure builds in the cysts until the cystic contents are forced into the synovial cavity, breaking thru the articular cartilage on the way
-as the articular cartilage erodes, cartilage-coated osteophytes may grow outward from the underlying bone and alter the bone contours and joint anatomy
-these spur like bony projections enlarge until small pieces, called joint mice, break off into synovial cavity
-if osteophyte fragments irritate the synovial membrane, synovitis and joint effusion result
-the joint capsule also becomes thickened and at times adheres to the deformed underlying bone, which may contribute to the limitation of movement
How is articular cartilage probably lost?
probably lost thru enzymatic breakdown of the cartilage matrix (the proteoglycans, glycosaminoglycans, and collagen)
-first, the enzymes break down the macromolecules of proteoglycans, glycosaminoglycans, and collagen into large, diffusible fragments
-then the fragments are taken up by the large cartilage cells (chondrocytes) and digested by the cell's own lysosomal enzymes
-the loss of proteoglycans from articular cartilage is a hallmark of the OA process
What enzymes are markedly elevated in OA? and why?
-stromelysin and and acid metalloproteinase
-because they affect proteoglycans by interfering with assembly of the proteoglycan subunit or the proteoglycan aggregate
-these changes in the conformation of the proteoglycans disrupt the pumping action that regulates movement of water and synovial fluid in/out of the cartilage
-without this, cartilage imbibes (absorbs) too much fluid and becomes less able to withstand the stresses of weightbearing, and synovial fluid less able to move
-enzymatic destruction of articular cartilage begins in the matrix, with destruction of proteoglycans and collagen fibers
What are some of the enzymes that degrade collagen?
-chemokines and metalloproteinases - and are produced by the synovium
-collagenase breaks down collagen
-chondrocyte apoptosis is increased in OA cartilage and is directly correlated with hydroxyaptite crystal deposition
-collagen breakdown destroys the fibrils that give articular cartilage its tensile strength and exposes the chondrocytes to mechanical stress and enzyme attack
-thus a vicious cycle begins that involves all components of articular cartilage-proteoglycans, collagen fibers, and chondrocytes
What are some symptoms of OA?
Main two are pain and stiffness
-usually weightbearing or load bearing joints
-use related joint pain relieved by rest is a key feature
-also enlargement/swelling, tenderness, limited ROM, muscle wasting, partial dislocation, and deformity
-nocturnal pain usually not relieved by rest and may involve parathsesis (numbness, tingling, prickling)
-pain may be referred to another part of body
Joint stiffness in OA
the origin is unknown
-joint stiffness is difficulty initiating joint movement, immobility, or loss of ROM.
-usually occurs as joint movement begins and dissipates within 30 min
-may be accompanied enlargement and bulging of joint contour, commonly described as swelling
What are some probably causes of swelling in OA?
-bone enlargement or the proliferation of osteophytes around the margins of the joint
-inflammatory exudate or blood enters the joint cavity, thereby increaseing the volume of synovial fluid..this condition is called joint effusion
-picture on slide 29 has nice summary of OA patho
What is joint effusion caused by?
1) the presence of osteophyte fragments in the synovial cavity
2) drainage of cysts from diseased subchondral bone
3) acute trauma to joint structures, resulting in hemorrhage and inflammatory exudation into the synovial cavity
What is a procedure that is done mostly from OA? Why is it done? What are more conservative treatments?
hip replacements-sx is used to improve joint movement, correct deformity or malalignment, or create a new joint w/ implants
-rest
-ROM to prevent joint capsule contraction
-cane/walker/crutches to decrease weightbearing
-weight loss
analgesic/anti inflammatory drug therapy to control pain and swelling
-glucosamine to reduce pain and progression of OA
-alternative..magnetic bracelets, accupressure
-intra-articular INJ in knee of high molecular weight vicrosupplements, particularly hyaluronic acid
In summary..result of OA
-degeneration and loss of articular cartilage
-damage to bone underneath cartilage
-formation of bone spurs (osteophytes)
-slide 29 depicts patho
What is RA?
a systemic inflammatory autoimmune disease associated with swelling and pain in multiple joints
What is the first joint to be affected in RA?
the synovial membrane, which lines the joint cavity.
What contributes to joint damage in RA?
multiple immunoregulatory cytokines (such as interleukins, B-cells, and matrix metalloproteinases) contribute to joint damage
-eventually, inflammation may spread to the articular cartilage, fibrous joint capsule, and surrounding ligaments and tendons, causing pain, joint deformity, and loss of function
Which joints are most commonly affected by RA?
fingers, feet, wrists, elbows, ankles, knees..but others are common too
What can RA cause?
Besides inflammation of the joints, RA can cause
-fever
-malaise
-rash
-lymph node or spleen enlargement
-and Raynaud phenomenon (transient lack of circulation to the fingertips and toes)
Cause of RA?
unknown..many probably factors
-environmental exposure-ie infectious agent
-genetic
-hormonal
-reproductive factors
What is RF
Rheumatoid factors
-with LT or intensive exposure to the antigen (infectious microorganisms that may play a role in RA), normal antibodies (immunoglobulins [Ig]) become autoantibodies
-these are antibodies that attack host tissues (self-antigens)
-b/c they are usually present in individuals w/ rheumatoid arthritis, the transformed antibodies are termed RFs
What do the RFs usually consist of
-two classes of immunoglobulin antibodies (antibodies for IgM and IgG) but occasionally involve antibodies for IgA
-their main antigenic targets are portions of the immunoglobulin molecules
-RF binds with their target self-antigens in blood and synovial membrane, forming immune complexes (antigen-antibody complexes)
What is an antibody?

What are cytokines
An antibody, or immunoglobulin, is a serum glycoprotein produced by plasma cells in response to a challenge by an immunogen

Cytokines are glycoproteins that function as chemical signals between the cells
Evidence for ___ involvement in RA
endocrine:
1) presence of androgen and estrogen receptors
2) high concentrations of biologically active steroids
3) key enzymes of steroid metabolism
4) significant changes of estrogen to androgen ratio

-data strongly suggests that individual immune cells, including synovial macrophages, may behave as steroid sensitive cells

-like most autoimmune diseases, more common in women, sx lessen during preg and worsen post partum
Antigen activates ___ which causes what?
Antigen activates T helper cells
--> cytokines
--> T helper cells and cytokines stimulate synovial macrophages and neutrophils and fibroblasts
What does this stimulation cause?
1) phagocytosis of immune complexes
2) enzyme release--> synovial tissue and articular cartilage degredation
3) T & B cell activation
--T cell --> increased immune response
--B cell --> RF
4) RANKL release and OC activation
In RA, several types of __ enter ___. Give examples and implications
Several types of leukocytes are attracted out of the circulation and into the synovial membrane
-the phagocytes of inflammation (neutrophils and macrophages) ingest the immune complexes and thus, release powerful enzymes that degrade synovial tissue and articular cartilage
-the immune system's B and T lymphocytes are also activated
-B lymphocytes are stimulated to produce more RFs
-T lymphocytes eventually cause release of enzymes that amplify and perpetuate the inflammatory response
In addition, __ is expressed..
In addition, RANKL is expressed by various cells in the synovium and induces OC maturation and activation, thus producing increased bone resorption
Damage to synovial membrane..and loong chain of events that result
-swelling caused by leukocyte infiltration damages synovial membrane
-the synovial membrane also undergoes hyperplastic thickening as its cells proliferate and enlarge abnormally
synovial inflammation--> vascular occlusion, gets clogged by infl response and decreased circulation to synovial tissue
--> hypoxia and metabolic acidosis
acidosis stimulates --> release of hydrolytic enzymes from synovial cells into the surrounding tissue
--> initiating erosion of the articular cartilage and inflammation in the supporting ligaments and tendons
infl --> hemorrhage, coagulation, and fibrin deposition on the synovial membrane, in the intracellular matrix, and in the synovial fluid
--over denuded areas of the synovial membrane, fibrin develops into granulation tissue called pannus
What is pannus composed of?
several different cells, but 2 most common:
-OC & synovial fibroblasts
-granulation tissue is the tissue produced earliest in the process of healing
-synovial fibroblasts also produce additional pro-infl cells, cytokines, natrix metalloproteinases, and other cells involved in cartilage damage
Sx that RA begin with..
General systemic manifestations of infl, including
-fever
-fatigue
-weakness
-anorexia
-weight loss
-generalized aching and stiffness
Local manifestations of RA
also appear gradually ove weeks or months
-typically the joints become painful, tender, and stiff
-pain early in the disease caused by pressure from swelling
-later it is caused by sclerosis of subchondral bone and new bone formation
-stiffness usually lasts for about 1 hour after arising in the morning and is thought to be r/t synovitis
What is joint swelling in RA caused by?
-joint swelling is widespread and symmetric
-caused by increasing amounts of inflammatory exudate (leukocytes, plasma, plasma proteins) in the synovial membrane, hyperplasia of inflamed tissues, and formation of new bone
What does RA look/feel like?
palpation-swollen joint feels warm and the synovial membrane feels "boggy"
-skin over the joint may have a ruddy, cyanotic hue and may look thin and shiny
Quality of life with RA
-inflamed joint may lose some of its mobility and ROM
-this can lead to atrophy, joint instability, permanent deformities, deviation, and flexion contractures
Two complications, what are they, what are they caused by?
Two complications of chronic RA are caused by an excessive amt of inflammatory exudate in the synovial cavity
1) formation of cysts in the articular cartilage or subchondral bone
--occasionally cysts communicate with the skin surface (us sole of foot) and can drain thru passages called fistulae
2) rupture of a cyst or of the synovial joint itself, us caused by strenuous physical activity that places excessive pressure on the joint. Rupture releases inflammatory exudate into adjacent tissues, thereby spreading inflammation
nodules with RA
extrasynovial rheumatoid nodules, or swellings, are observed in areas of pressure or trauma in 20% of ppl with RA
-each nodule is an aggregate of inflammatory cells surrounding a central core of a fibrinoid and cullular debris
-nodules found most often in SUBQ tissue over the extensor surfaces of elbows and fingers
-rheumatoid nodules may also invade the skin, cardiac valves, pericardium, pleura, lung parenvhyma, and spleen and cause problems in those respective areas
-these nodules are identical to those encountered in some individuals with rheumatic fever and are characterized by central tissue necrosis surrounded by proliferating connective tissue
Nodules and pulmonary involvement with RA
the occurence of pulmonary nodules and pneumoconiosis (chronic infl of the lungs f inhalation of dust) creates Caplan syndrome
Conservative tx with RA
-rest
-hot/cold packs
-PT
-antineoplastic meds
-high cal/vitamin diet
-corticosteroids
-antiinflammatory drugs
-immunosuppressents
-disease modifying antirheumatic drugs (DMARDS) taken PO or INJ
Surgery in RA
-to decrease inflammatory effusion and remove pannus
-to correct deformity or mechanical deficiency
What is gout?
gout is a syndrome caused by an inflammatory response to uric acid production or excretion resulting in high levels of uric acid in the blood (hyperuricemia) and in other body fluids, including the synovial fluid.
Is hyperuricemia necessary for gout? Are there other factors?
Yes-hyperuricemia is necessary for gout.
Other factors include:
-age (rare before 30 y/o)
-genetic predisposition (X-linked alteration of enzyme HGPRT)
-excessive ETOH consumption
-obesity
-certain drugs (esp thiazides)
-lead toxicity
When the uric acid reaches a certain concentration in fluids, what happens?
When the uric acid reaches a certain concentration in fluids:
-it crystallizes, forming insoluble precipates that are deposited in connective tissues throughout the body
What is gouty arthritis?
Crystallization in synovial fluid causes acute, painful inflammation of the joint, a condition known as gouty arthritis
What are tophi?
With time, crystal deposition in SQ tissues causes the formation of small, white nodules, or tophi, that are visible through the skin
Crystal aggregates deposited in the kidneys can..
Crystal aggregates deposited in the kidneys can form urate renal stones that can lead to renal failure
What is the difference between uric acid and urate?
Uric acid-Uric acid is a byproduct of protein metabolism that normally assists with removal of nitrogen waste from the body. Uric acid is created when the body breaks down purine nucleotides.

Urate-the salts of uric acid
What are purines?
Two of the four deoxyribonucleotides and two of the four ribonucleotides, the respective building-blocks of DNA and RNA, are purines.

Purines are synthesized to purine nucleotides, whiched are used in the synthesis of nucleic acids, adenosine triphosphate, cyclic adenosine monophosphate (cAMP), and cyclic guanosine monophosphate (GMP)
Difference and similarities between classic gouty arthritis and pseudogout
Classic gouty arthritis-monosodium urate crystals form and cause joint inflammation

Pseudogout-is caused by the formation of calcium pyrophosphate dihydrate (CPPD) crystals

The effect of either crystal is the same: the onset of a cytokine-mediated acute inflammatory response
Briefly, what are the possible causes of elevated uric acid production?
increased uric acid production

OR

decreased uric acid elimination
Increased uric acid production:
Increased uric acid production will result from either an increase in purine synthesis or an increase in purine breakdown

-Some individuals with gout have an accelerated rate of purine synthesis accompanied by an overproduction of uric acid.

-Other individuals break down purine nucleotides at an accelerated rate that also results in an overproduction of uric acid

-Production of uric acid can be the rsult of an increased turnover of nucleic acids, which is associated with an increased turnover of cells in other body sites

-The increased turnover of nucleic acids leads to increased levels of uric acid with a compensatory increase in purine synthesis
HGPRT
A deficiency of the enzyme HGPRT can lead to an increased production of uric acid

-A complete absence of HGPRT is uncommon but can occur in the X-linked Lesche-Nyhan syndrome, with males at risk for hyperuricemia, neurologic alterations, and sometimes gouty arthritis
What is primary gout?
The majority of individuals with gout have an unknown metabolic defect, which is referred to as primary gout
What is secondary gout?
When the etiology is unknown, it is referred to as secondary gout
How is most uric acid eliminated?
Most uric acid is eliminated from the body through the kidneys
Where is urate filtered?
Urate is filtered at the glomerulus and undergoes reabsorption and excretion within the renal tubules.
Urate excretion in primary gout
-In primary gout, urate excretion by the kidneys is sluggish

-The sluggish excretion may be the result of a decrease in glomerular filtration of urate or an acceleration in urate reabsorption

-In addition, monosodium urate crystals are deposited in renal interstitial tissues, causing impaired urine flow
Process by which crystals of monosodium urate are deposited in joints and induce gouty arthritis..
is uknown. However, several mechanisms may be involved:

1) monosodium urate precipitates at the periphery of the body, where lower body temp may reduce the solubility of monosodium urate
2) decreased albumin or glycosaminoglycan levels, which cause decreased urate solubility
3) changes in ion concentration and decreases of pH that enhance urate deposition
4) trauma that promotes urate crystal precipitation
Monosodium urate crystals can..the inflammatory response.
Monosodium urate crystals can stimulate and perpetuate the inflammatory response. The presence of the crystals triggers the acute inflammatory response

Inflammation:
-leukocytes to the area -->
-phagocytosis of crystals -->
-death of leukocyte -->
-release of inflammatory mediators -->
-PAIN and inflammation
Gout is manifested by...(5 total manifestations)
1) an increase in serum urate concentration (hyperuricemia)
2) recurrent attacks of a monoarticular arthritis (inflammation of a single joint)
3) deposits of monosodium urate monohydrate (tophi) in and around the joints
4) renal disease involving glomerular, tubular, and interstitial tissues and blood vessels
5) the formation of renal stones
The 5 manifestations appear in 3 clinical stages.

The 1st clinical stage of gout..
Asymptomatic hyperuricemia- the serum urate level is elevated bur arthritic symptoms, tophi, and renal stones are not present; may persist throughout life
The 2nd clinical stage of gout..
Acute gouty arthritis-attacks develop with increased serum urate concentrations; tend to occur with sudden or sustained increases of hyperuricemia but can also be triggered by trauma, drugs, and alcohol
The 3rd clinical stage of gout..
tophaceous gout: the third and chronic stage of disease; can beegin as early as 3 years or as late as 40 years after the initial attack of gouty arhritis. Progressive inability to excrete uric acid expands the urate pool until urate crystal deposits (tophi) appear in the cartilage, synovial membranes, tendons, and soft tissue
What is the most common aggravating factor?
Trauma.

The great toe is subject to chronic strain in walking, and subsequently an acute gout attack may follow long walks. Trauma associated with occupations, such as truck driving, also may precipitate an attack
Attacks of gouty arthritis occur ___. Most common sites?
Attacks of gouty arthritis occur abruptly, usually in a peripheral joint.

-the primary sx is severe pain
-approx 50% of the initial attacks occur in the metatarsophalangeal joint of the great toe
-the other 50% involve the heel, ankle, wrist, or elbow
Pain in a gouty arthritis attack
-primary sx is severe pain
-pain is usually noticed at night
-within a few hours the affected joint becomes hot, red, and extremely tender and may be slightly swollen
Systemic signs in gouty arthritis attack?
Lymphangitis and systemic signs of inflammation (leukocytosis, fevor, elevated sedimentation rate) occasionally are present
How long to gouty arthritis attacks last?
Untreated, mild attacks usually subside in several hours but may persist for 1-2 days. Severe attacks may persist for several days or weeks
What is intercritical periods? How long does it last?
-After recovery, the symptoms of gouty arthritis attacks resolve completely

-Intervals between attacks of gouty arthritis are called intercritical periods

-Some individuals never have a second attack, others experience subsequent attacks within days to as long as 5-10 years after the first
What is the most common site of tophi?
The helix of the ear is the most common site of tophi, which are the chracteristic diagnostic lesions of chronic gout.
What does each tophus consist of?
Each tophus consists of a deposit of urate crystals, surrounded by a granuloma made up of mononuclear phagocytes (macrophages) that have developed into epithelial and giant cells.
Complications of tophaceous deposits?
-Tophaceous deposits produce irregular swellings of the fingers, hands, knees, and feet

-Tophi commonly forms lumps along the ulnar surface of the forearm, the tibial surface of the leg, the Achilles tendon, and the olecranon bursa

-tophi may produce marked limitation of joint movement and eventually cause grotesque deformities of the hands and feet

-Although the tophi themselves are painless, they often cause progressive stiffness and persistent aching of the affected joint

-Tophi in the upper extremities may cause tarsal tunnel syndrome.

-Tophi may also erode and drain through the skin
-
All about Renal stones
-renal stones are 1000 more prevalent in individuals with primary gout than in the general population b/c they might be made of uric acid, or the uric acid may promote other types of stones

-the stones can be the size of a grain of sand or a piece of gravel, or they can accumulate in massive deposits called staghorn calculi

-they range from pale yellow to brown or reddish black, depending on composition

-some stones are pure monosodium urate, others are calcium oxalate or calcium phosphate

-renal stones can form in the collecting tubules, pelvis, or ureters, causing obstruction, dilation, and atrophy of the more proximal tubules and leading eventually to acute renal failure.

-stones deposited directly in renal interstitial tissue initiate an inflammatory reaction that leads to chronic renal disease and progressive renal failure
General aims of gout treatment
The aims of gout tx are to:
-terminate the acute gouty attack as promptly as possible
-prevent recurring attacks
-prevent or reverse complications associated with urate deposits in the joints and kidneys
-and prevent formation of kidney stones
Drugs for acute gouty arthritis
antiinflammatory drugs

-drug of choice are NSAIDs and xanthine oxidase inhibitors such as allopurinol and febuxostat

-Colchicine is used in individuals unable to tolerate NSAIDS

-Hydrocortisone may be injected into the joint to relieve pain

-Drugs that block IL-1 have shown promise

-antihyperuricemic drugs are given to reduce serum urate concentrations
Non pharm tx for acute gouty arthritis
-Ice also may relieve some of the inflammation of the joint

-weightbearing on the involved joint is avoided until the acute attack subsides

-the individual is put on a low purine diet with high fluid intake to increase urinary output
SCOLIOSIS..what the fuck is it?
scoliosis is a rotational curvature of the spine over 30 degrees, most obvious in the anteroposterior plane.
It can be characterized as either...
Nonstructural or Structural

Nonstructural scoliosis-results from a cause other than the spine itself, such as posture, leg length discrepancy, or pain

Structural scoliosis is curvature of the spine associated with vertebral rotation.

-nonstructural scoliosis can become structural if the underlying cause is not found and treated
Structural scoliosis can be caused by..
a great variety of conditions

-congenital skeletal abnormalities-fetuses 6th-8th wk (15%)
-neuromuscular disease-scoliosis occurs as part of neuropathic or myopathric disease (ie with cerebral palsy) (15%)
-trauma
-extraspinal contractures
-bone infections that involve the vertebrae
-metabolic bone d/o (rickets, osteoporosis, osteogenesis imperfecta)
-joint disease
-tumors

-Structural scoliosis with no known cause, termed idiopathic scoliosis, accounts for at least 65% of cases. Most are healthy, neurologically normal children
Idiopathic scoliosis is classified as..
infantile, juvenile, or adolescent, depending on the child's age at time of onset.
-infantile: spinal curvature develops during the first 3 years of life
-juvenile: curvature develops b/w skeletal age of 4-adolescence
-adolescent-develops after the skeletal age of 10
___ is the most common type of scoliosis
adolescent idiopathic
Gender and scoliosis
scoliosis in milder forms occurs equally in boys and girls once curves measures more than 15 degrees; however girls are 5 times more likely to have scoliosis than boys
Scoliosis may or may not..
may or may not include rotation or deformity of the vertebrae
Scoliosis genetic component
A genetic component is suggested because 30% occur within families
CNS and scoliosis
-Hypothesized that with adolescent scoliosis, there is an abnormality of the central nervous system involving the balance mechanism (reticular system) in the midbrain

-experimentally it has also been shown that individuals with adolescent idiopathic scoliosis have an abnormality in the function of the posterior columns in the spinal cord. This results in abnormal proprioception.

-the exact cause of scoliosis tho remains elusive
earliest pathologic changes in scoliosis..
The earliest pathologic changes, which are probably secondary changes, occur in the soft tissues

-the muscles, ligaments, and other soft tissues become shortened on the concave side of the curve

-with time, progressive deformities of the vertebral column and rib develop

-In growing kids, lateral deviation of the spinal column ceases, and one-sided compression of the vertebral bodies on the concave side of the curve begin

-vertebral deformity occurs as assymetric forces are applied to the ephiphyseal center of the ossification by shortened and tight soft tissues on the concave side of the curve

-the degree of compression and twisting varies according to the position of the vertebrae in the curve. The compression force is greatest on the vertebrae in the apex of the concavity, so that the apical vertebrae become most deformed
In scoliosis, the curves increase most rapidly during..
periods of rapid skeletal growth.

-if the curve is less than 40 degrees at skeletal maturity, the risk of progression is quite small.

-in curves greater than 50 degrees, the spine is biomechanically unstable, and the curve will in all likelihood continue to progress even after the cessation of growth at an average rate of 1 degree/year.
complications of scoliosis by part of spine affected
curves in the thoracic spine greater than 80 degrees result in decreased pulmonary function, whereas the most common complication of large curves in the lumbar spine is back pain
Clinical manifestation of nonstructural scoliosis
-mild spinal curvature with prominence of one hip or rounded shoulders
-the curvature disappears with forward flexion of the spine, lying down, or traction of the head
-treatment is correction of the underlying disorder
Clinical manifestation of structural scoliosis
-assymetry of hip height
-assemetry of shoulder height
-assymetry of leg length
-shoulder and scapular (shoulder blade) prominence
-rib prominence
in scoliosis, spinal curvature is usually..
visible or palpable, and muscles on one side of the lower back (the convex side) may be prominent or bulging.
Diagnosis of scoliosis
-most cases of idiopathic adolescent scoliosis are noticed during school screening programs
-in girls, the deformity may be noticed because clothing does not "hang" properly on the body
-dx is made by roentgenographic examinations
treatment: 25-35 degrees in skeletally immature child:
treatment for 25-35 deree curves in skeletally immature children:
-in most cases the low profile brace is used
-occasionally milwaukee brace, which has a metal upper structure and neck ring, is needed for curves with an apex higher than mid thoracic level
-both of the above are worn for 23 hours/day until skeletal maturity
-bracing will only prevent progression of the curve, it will not correct the curvature
-bracing is not effective in curves greater than 40 degrees or in skeletally mature individuals-the most effective time for bracing is in a young child (less than 12) w/ a small curve

-Charleston-only at night and less effective
chiropractor with scoliosis?
extensive chiropractic manipulations and electrical stimulation have not been shown to change natural history
sx with scoliosis?
surgical treatment with spinal fusion with instrumentation is recommended for curves greater than 40-50 degrees

-if sx is indicated, it is better performed during the adolescent yrs while there is greater flexibility of the curves and less risk for complications
Juvenile rheumatoid arthritis: what kind of disease is this?
A rheumatic disease-the rheumatic diseases are a group of diverse conditions having in common the inflammation of connective tissues. They include RA, systemic lupus erythematosus, dermatomyositis, scleroderma, and polyarthritis.
What is JRA?
JRA is the childhood form of RA. Like adult onset RA, JRA is a syndrome that is often accompanied by systemic manifestations.
How many cases of RA begin in childhood?
About 5%
Similarities and differences between JRA and RA:
-The basic pathophysiology of JRA is the same as that of adult RA.

-the clinical manifestations of JRA may differ, however, beginning with mode of onset

-unlike adult RA, which begins insidiously with systematic signs of inflammation and generalized aches, JRA has 3 distinct modes of onset: arthritis in fewer than 5 joints (pauciarticular arthritis), arthritis in more than 5 joints (polyarticular arthritis), and systemic disease. Onset is less gradual in JRA than in adult RA.
JRA also differs from the adult form in the following respects: (7)
1) predominantly the large joints are affected
2) subluxation and ankylosis of the cervical spine are common if the disease progresses
3) joint pain may not be severe as in the adult time
4) serologic tests often detect antinuclear antibody (ANA)
5) chronic uveitis (inflammation of middle eye) is common, esp if ANA positive
6) serologic tests seldom detect rheumatoid factor
7) rheumatoid nodules are not limited to SQ tissue but are found in the heart, lungs, eyes, and other organs
Does JRA progress to adulthood RA?
-many children with pauciarticular arthritis who are seronegative for ANA will resolve their sx over time

-however, with systemic onset (Stills disease) or seropositivity, JRA may progress to true adult RA
Treatment for children with JRA
is supportive but not curative

-the aims of tx are to control inflammation and other clinical manifestations of the disease and to minimize deformity