Metabolic Bone disease (ch.24)

list most common to least common places to get compression fractures

(m) VERTEBRAE > hips > ribs > radius > femur

is Paget's disease due to a traumatic of insidious onset?

***insidious onset - slowly progressive - variable presentation due to rate of progression

Clinical Management: Treatment: OSTEOMALACIA

*depends on underlying cause - if malnutrition: need more calcium and vitamin D - if is intestinal malabsorption: medications to enhance absorption Physical therapy treatment: similar to that of osteoporosis

"FIRST PHASE" of osteomyelitis:

- Blood supply blocked - subperiosteal abscess forms + pus

Clinical Management: Treatment: OSTEOMYELITIS

- IV and high dose antibiotic therapy - surgery for infections that have spread to the joints or non-healing infections --> goal is drainage and extensive debridement of both bone and involved surrounding soft tissues

"SECOND PHASE" of osteomyelitis:

- Involucrum forms around sequestrum - pus escape

Incidence: OSTEOPOROSIS

- affects more than 10 million people in the U.S. - 34 million ADDITIONAL ppl have OSTEOPENIA (low bone mass) and are at increased risk of osteoporosis as they age - women > men - 1 in 2 women older than 50 will experience fragility fx's SECONDARY to osteoporosis (bc of the dec in estrogen and progesterone)

Clinical Manifestations: PAGET'S DISEASE (musculoskeletal)

- can lead to BONE PAIN (most common symptom), skeletal deformities and osteoarthritis!!! --> most commonly effect axial skeleton @ skull, spine, pelvis femurs, and tibias - in severe cases of paget's it can involve many bones and cause HYPERCALCEMIA (leading to fatigue, weakness, anorexia, abdominal pain, and constipation) - direct pain from peritoneal irritation of bones and is deep/boring, worse at night & reduced with activity but not completely eliminated - BOWING OF THE FEMURS AND TIBIAS!!!

Etiology: PAGET'S DISEASE

- cause unknown - often inherited in autosomal dominant patter, but genetic basis is not well understood - environmental factors including possible viral infection may effect osteoblasts

Clinical Manifestations: PAGET'S DISEASE (neurological)

- due to the fact that it effects the skull and spine - can cause myelopathy (direct impingement of the spinal cord) - can cause ischemia related to pagetic steal syndrome (hyper-vascular pagetic bone stealing blood flow from neural tissue) - enlarged pagetic bones can put pressure on various nerve structures - tinnitus (ringing in the ears), vertigo, and hearing loss

Clinical Management:Prognosis: OSTEOMYELITIS

- earlier tx the better - bc chronic osteomyelitis and necrotic tissue has the chance to build up, reduced blood flow prevents medications from reaching the locus of the infection --> resulting in significant tissue damage and disability

Clinical Management: Prognosis: PAGET'S DISEASE

- generally good, particularly if tx started early (most commonly use biochemical remission with BIOPHOSPHONATES in majority of people) - small risk of OSTEOGENIC SARCOMA, a risk that is must greater in those with paget's than in the general population

Clinical Manifestations: OSTEOMYELITIS in ADULTS

- if the infection extends into the periosteum, increased joint pain, diminished fxn, systemic signs (fever, swelling, malaise) are present - pain described as: deep and constant and increased pain with weight bearing - clinical signs of "sausage toe" can be seen in those with pedal osteomyelitis - spinal osteomyelitis produces: back pain w/ throbbing at rest--> if the abscess becomes too large, it could compress the nerve root and cause radicular symptoms - sacroiliac osteomyelitis: local pain and tenderness and an ANTALGIC GAIT is psoas mm is involved. Painful hip extension

Clinical Manifestations: OSTEOPOROSIS

- loss of height - postural changes: lax abdominal mm, forward head, kyphosis, dowager's hump, loss of lumbar lordosis, posterior pelvic tilt, knee hyperextension, shoulder internal rotation, scapular forward rotation - back pain: spasms can occur in LP and paravertebral mms bc of excess stretch

Clinical Management: Treatment: OSTEOPOROSIS

- not curable - intervention can slow or stop progression (by: high Ca2+ intake. smoking cessation, reducing alcohol, physical activity/exercise) - estrogen replacement for women --> Raloxifene (Evista) which has selective estrogen agonist activity in bone but with antagonist activity or no activity in reproductive tissues and breasts) - biophosphate drugs inhibit bone reabsorption and can reverse bone loss - if secondary osteoporosis: treat underlying cause - surgery for patients who are advanced in the disease stages and have neurological deficits OR unstable spines

Clinical Management: Diagnosis: PAGET'S DISEASE

- often delayed bc of slow progression and vague early symptoms - in fact, its often accidentally found (based on x-rays or blood tests) taken for other conditions - alkaline phosphatase is an enzyme that is produced by bone cells and over-produced in pagetic bone --> serum levels are checked

Clinical Management: Diagnosis: OSTEOMYELITIS

- often delayed, particularly in chronic form - any unexplained cellulitis in children should be considered possible underlying osteomyelitis - x-ray - MRI (chronic changes will reveal a weird thickening and modeling of the cortex) - bone scan or PET scan - needle or open biopsy for gram stain and culture --> identification of organism and determination of antibiotic susceptibilities

Clinical Management: Diagnosis: OSTEOMALACIA

- often dx late, since initial sx's are vague - 1st diagnosis often looks for fx - x-ray and bone scan - lab workup (serum for levels of low calcium, low phosphate, inc alkaline phosphatase, and low PTH) (alkaline phosphatase: marker of bone disease and bone metabolism and goes up with injury to the bone) (PTH: will inc Ca2+ reabsorption and stimulate osteoclasts) - urine is also collected to assess calcium and phosphate excretion rates

Clinical Management: Prevention: OSTEOPOROSIS

- prevention and early intervention is critical to long-term outcome (particularly those in high risk groups) - begins in childhood (diet and regular physical activity)

Clinical Management:Prevention: OSTEOMYELITIS

- sterility and would washout and debridement for surgery or open injuries must be cleaned and taken care of - nutritional status to keep out body's immune system up - education of high risk patients (ppl with prosthetics, diabetes, etc)

Clinical Manifestations: OSTEOMALACIA

- vague, diffuse, generalized aching and fatigue (often in the presence of anorexia and weight loss) - bone PAIN and periarticular tenderness - later is disease stages: postural deformities, proximal myopathy which may lead to a waddling gait, and difficulties with transitional movements (e.x. getting out of bed, standing, getting out of a chair, etc)

Clinical Management: Prognosis: OSTEOPOROSIS

- with good prevention and screening, most morbidity and mortality can be avoided with conservative management options - 1st fx has a 2- 4 fold inc risk of 2nd fx - multiple fxs and poor control of progression can lead to death and/or disability

Pathogenesis: OSTEOMYELITIS

--> often starts in METAPHYSIS of long bones since they are very porous, allowing infection to spread rapidly --> can spread to adj tissues and form abscesses in psoas mm, intervertebral disc, paravertebrals, epidural, etc)

Clinical Manifestations: PAGET'S DISEASE (cardiovascular)

--> vasodilation occurs in deformed bones. If 1/3 - 1/2 of the skeleton is involved: - increased cardiac output, which can lead to heart failure (common cause of death in very advanced disease)

5 main Risk Factors: OSTEOPOROSIS

1) Age: - > 50 2) Gender: - females with low estrogen - males who: smoke, alcoholism, steroid therapy, hypogonadism or androgen withdrawal therapy for prostate cancer (androgen withdrawal therapy: The goal is to reduce levels of male hormones, called androgens, in the body, or to stop them from affecting prostate cancer cells) 3) Genetics/ family hx/ethnicity: - Caucasians (bone mass has a direct correlation w/ skin pigmentation) 4) Sedentary lifestyle 5) Poor nutrition/ anorexia/bulemia

Clinical Management: Treatment: PAGET'S DISEASE

1) Biophosphonates (inhibitors of bone reabsorption) - can normalize bone health - may provide long lasting remission in most patients - response followed by serum levels of alkaline phosphatase 2) non-steroidal and other anti-inflammatory agents are used to control pain 3) surgery for some fractures and deformity correction

METABOLIC BONE DISEASES CAN BE BROKEN UP INTO 2 CATEGORIES

1) Disorders of INCREASED bone reabsorption (osteoporosis, osteomalacia, pagets) 2) Infections of the musculoskeletal system that effect bone

Clinical Management: Diagnosis: OSTEOPOROSIS

1) Personal factors and HX: - family hx, hx of fx's, intake of vitamin D, calcium, CORTICOSTEROIDS, risk of falls 2) PE: - height loss 3) BMD testing (dexa scan) 4) x-ray 5) Routine screening - recommended that all men and postmenopausal women age 50+ should be assessed for risk (not necissarily a BMD, but should be asked a series of questions) - BMD testing recommended for women 65+ and men 70+

Etiology: OSTEOPOROSIS

1) Primary osteoporosis: - unknown, but contributing factors: negative calcium balance, declining gonadal and adrenal fxn, estrogen deficiency, and SEDENTARY LIFESTYLE! 2) Secondary form: - prolonged corticosteroid use*** - also heparin, anticonvulsants, alcoholism, malnutrition, endocrine disorders, etc

2 types of osteomyelitis:

1) acute 2) chronic

Risk Factors: OSTEOMYELITIS

1) anyone who is chronically ill (ex. diabetics who present with non-healing ulcers, sausage toes, etc & alcoholics) 2) large dosage of immunosuppressive drugs 3) older adults with additional pre-existing medical conditions: malignancy, malnutrition, renal or hepatic failure 4) hx of prosthetic joints or other implants

bone strength is a function of what 2 components:

1) bone DENSITY 2) bone QUALITY

Pathogenesis: PAGET'S DISEASE

1) initial rapid osteoclastic reabsorption: initial re-absorptive stage with abnormal osteoclast proliferation 2) initial rapid reabsorption: the activity of the osteoclasts is so rapid that osteoblasts cannot keep up and fibrous tissue replaces bone 3) osteoblastic sclerotic phase

Etiology: OSTEOMALACIA (2 primary causes)

1) insufficient INTESTINAL calcium absorption 2) Increased RENAL phosphorus losses

2 fxns of our continuously remodeling skeletal system/bones?

1) maintain the structural integrity of the skeleton 2) act as a storage house of calcium and phosphorus

2 types of osteoporosis:

1) primary osteoporosis 2) secondary osteoporosis

the skeleton is a metabolically active, dynamic organ that does 2 main things:

1) undergoes continuous remodeling throughout life 2) responds to changes in mechanical load on bone (Woff's law)

Individuals with osteoporosis have a high chance of what secondary diagnosis?

FRACTURES (due to insidious onset) - first fracture puts you at high risk for a 2nd - 2nd fx and beyond inc risk of death

Def: OSTEOMYELITIS

Inflammation of bone caused by an infectious organisms (bacteria- the most common, fungi, viruses) 1) can get in thru an open wound or fx, or open sores or overlying soft tissue infections 2) microorganisms travel thru the blood to the bone (hematogenous)

Risk factors: OSTEOMALACIA

Pre-existing conditions that can affect action of vitamin D and decrease absorption of Ca2+: - diseases in sm intestine - liver and kidney disorders - biliary obstruction - pancreatic insufficiency - long term use of antacids which contain aluminum hydroxide (can cause phosphate deficiency) - old age

Def: OSTEOMALACIA

SOFTENING of bones caused by defective bone mineralization, SECONDARY to calcium (hypocalcemia), vitamin D, and/or phosphate deficiency OR overactive reabsorption of calcium as a result of HYPERparathyroidism --> there is a softening of bone, but there is no bone concentration loss --> overall density of the tissue may look normal but the quality of the bone is lacking

Etiology: OSTEOMYELITIS (what is the most common organism which causes osteomyelitis?)

STAPHYLOCOCCUS AUREUS --> Forms a protective glycocalyx and biofilm that helps invade the immune system (glycocalyx = glycoprotein and polysaccaride covering) --> other organisms that can cause infection: - group B strep - pneumococcus - pseudomonas - hemophilus influenza - E. coli - salmonella in sickle cell disease

Def:

a chronic, progressive disease characterized by LOW bone mass, impaired bone QUALITY, decreased bone STRENGTH --> LOSS of bone mass making "brittle bones" --> ALL OF WHICH RESULT IN A SUSCEPTIBILITY TO FX

Bone remodeling (deF)

a process in which bone constantly renews itself where osteoclasts (reabsorb) and osteoblasts (lay down/form) bone ---> purpose of remodeling is to maintain the strength and integrity of the skeleton by replacing fatigue-damaged older bone with new bone and to act as a source of vital minerals (ex. calcium) necessary for the maintenance of mineral homeostasis

osteoblastic sclerotic phase (def)

abnormal regeneration in which normal architecture is replaced by coarse, thickened lines of trabecular bone and cortical bone becomes irregularly thickened, rough, and pitted

Def: PAGET'S DISEASE

aka oseotis deformity increased activity of osteoclasts and bone reabsorption which results in area of increased rapid activity of osteoblasts that are moving at such a fast pace, where we get deformity --> characterized by an abnormal bone remodeling and unorganized new bone formation --> normal bone marrow slowly replaced by vascular and fibrous tissue --> although its a state of high bone turnover, the excess bone that is formed lacks the structural stability of a normal bone. --> FORMS THICK, BUT UNSTABLE BONES

Pathogenesis: OSTEOMALACIA

although the bone matrix remains intact (bone structure remains unchanged) due to UNCALCIFICATION of the matrix, which usually makes the bones hard, and a decrease in deposition of calcified salts

2) secondary osteoporosis

associated with medications, or linked to other diseases

you CANNOT measure quality of bone, but you can measure DENSITY, how?

bone mineral density (BMD)

osteoid (def)

bone that has not matured or calcified --> as the osteoid accumulates, bone strength declines --> osteoids appear radiographically as radiolucent stripes/patches --> most commonly occur on CONCAVE sides of long bones!!

"INITIAL INFECTION" of osteomyelitis:

initial infection is present

1) acute osteomyelitis:

meaning, its a new infection in bone that can develop RAPIDLY into chronic when/if treatment is delayed or inadequate --> typically effects children, older adults, and IV drug users

Clinical Manifestations: OSTEOMYELITIS in CHILDREN

more likely to present with acute, severe complaints --> high fever, intense pain --> local symptoms such as edema, erythema, and tenderness

sequestrum (def)

necrotic tissue --> involucrum forms AROUND the sequestrum

2) chronic osteomyelitis:

often the result of acute osteomyelitis going undiagnosed, relapse, or slowly evolving bone infection

exogenous osteomyelitis (def)

refers to etiology caused by invasion by a direct extension of: penetrating injuries, open fx's, open sores or overlying soft tissue infections

hematogenous osteomyelitis (def)

refers to etiology caused by microorganisms traveling thru the blood to the bone --> acquired from pre-existing infection in distant tissue

involucrum (def)

sheath of new bone formed by the osteoblasts

what is the process of infectious material in the Haversian canals?

the canals contain blood, lymph vessels and nerves- the flow rate within the bone being much slower than even terminal arterioles --> once bacteria are in these channels, they are able to proliferate and form a SUBPERIOSTEAL ABSCESS (with pus) that deprives the bone of its blood supply and eventually becomes NECROTIC --> necrotic bone are a perfect place for the organisms to multiply (and there are no sensory nerve endings in the cancellous bone, so this process can occur without pain) --> Once necrosis is present in the bone, it stimulates the osteoblasts to form new bone

1) primary osteoporosis

the most common form, which is due to 1) post-menopausal/estrogen deficient women 2) age-related

vertebral compression fractures (def)

the most common osteoporosis related spinal fx's --> presnt with: back pain, posture changes, loss of height, functional impairment, disability and overall diminished quality of life --> can be "SILENT" Can be comminuted VCF (comminuted = burst)

Pathogenesis: OSTEOPOROSIS

when new bone formation falls behind reabsorption --> over time the density of the trabecular arches and trusses diminishes and the spaces between them become LARGER --> weakening the bone structure (and potentially leading to fx) (Too much bone demineralization can lead to osteopenia- low bone mass)

At what age (range) do we have our peak bone mass?

~ 25-35 yrs old