metabolic bone diseases refer to:
- diseases that have an imbalance of bone anabolism (construction) and bone catabolism (destruction)
metabolic bone diseases include conditions of:
- decreased bone density and strength such as: osteoporosis, osteomalacia, and paget disease of the bone
what is osteoporosis?
- abnormal loss of bone mineral density and deterioration of bone tissue through the decrease of both mineral and matrix
If the bone decreases to the point it cannot maintain structural integrity risk of what increases?
- fractures
what percentage of patients w/ osteoporotic hip fractures die within one year?
- 20%
Type I/primary osteoporosis results from what?
- hormonal changes: estrogen deficiency in women, testosterone deficiency in men
type I/primary osteoporosis is often considered what type of disorder?
- endocrine
what is actually abnormal in type I/primary osteoporosis
- bone resorption (loss) is increased, rate of bone formation is often normal
what is the most common cause of estrogen deficiency in women?
- menopause
what does testosterone deficiency (in men) usually result from?
- a gradual decline with age
F:M type I/primary osteoporosis ratio
- 6:1
Type II/secondary osteoporosis usually affects what population
- patients > 70 y/o
what is type II/secondary osteoporosis related to
- a disease process or medication that alters calcium metabolism, decreasing new bone formation
men with osteoporosis usually have what type?
- type II/secondary
patient w/ osteoporosis may present with:
- back pain, fracture, loss of height, or spinal deformity
common fractures related to osteoporosis include:
- vertebral compression fractures
- distal radius
- hip and pelvis
- any fx resulting from a low-impact or non-traumatic event
spinal deformity in osteoporosis is usually characterized by?
- thoracic kyphosis w/ abdominal distention
laboratory findings in primary osteoporosis
- normal levels of serum calcium, phosphorus, and parathyroid hormone (PTH) and alkaline phosphatase
vitamin D level in primary osteoporisis
- is usually low, considered a comorbid condition
- order a 25-hydroxyvitamin D serum level 25(OH)D while pt is fasting
is laboratory work-up necessary to diagnose osteoporosis?
- no, definitive dx via DEXA
when is a lab work-up in osteoporosis definitely necessary
- if you suspect the osteoporosis to be secondary and you are looking for the disease causing the osteoporosis
gold standard for bone mineral density measurement
- DEXA (dual-energy x-ray absorptiometry) of the hip and lumbar spine
- used to dx osteoporosis and monitor success/failure of treatment
how are results of a DEXA scan reported
- as a T score, comparing the pt bone density to that of young normal individuals
- T score is expressed as a standard deviation above or below
T score of 0 to -1.0
- normal
T score of -1.01 to -2.49
- low bone mass (osteopenia)
T score of -2.5 or less
- osteoporosis
Z scores
- may be used to evaluate younger patients
- they provide a comparison to the same age, race, and gender of the pt
The national osteoporosis foundation & USPSTF agree that screening for osteoporosis should be done in this population:
- women >/= 65 y/o
for women < 65 y/o, when should screening for osteoporosis be done?
- if fracture risk is >/= to 65 y/o woman, determined by FRAX
should men be screened for osteoporosis according to USPSTF?
- no
RF for osteoporosis
- parental hx of hip fracture
- lifestyle factors: alcohol abuse, smoking, low calcium, low vitamin D, excessive thinness
- disease or medication known to cause bone loss
when is treatment of osteoporosis indicated?
- when T scores </= -2.5
in women with T score between -1.0 and -2.49 when should treatment be initiated?
- if their FRAX score is >/= 20% for osteoporotic fracture OR >/= 3% for hip fracture
in post-menopausal women with history of vertebral or hip fracture when is treatment for osteoporosis indicated?
- always, regardless of T score
calcium daily requirements
- 1200 mg/day
vitamin D daily requirements
- 800 IU/day
how is osteoporosis treated
- antiresorptive agents or anabolic agents
when are antiresorptive agents used?
- for high-turnover osteoporosis where a lot of bone breakdown products are found in blood
- this is the most common
when are anabolic agents used?
- for pt w/ decreased rate of bone formation
bisphosphonates
- best evidence is for alendoronate or risedronate (both oral) or zoledronic acid (IV)
alendronate and risedronate dosing
- generally q week
- other options are available
- have to take on empty stomach and remain upright for at least 30 minutes
zoledronic acid (IV) dosing
- 5mg IV q year
side effects of bisphosphantes
- GI disturbances, bone pain
- jaw osteonecrosis w/ IV form, prevalence of jaw osteonecrosis very small w/ oral form
- atypical femur fracture
contraindications for bisphosphonates
- pregnancy
- esophagitis
RANK-ligand inhibitor
- denosumab
- dosed as SQ injection 2x/yr
- SE include jaw osteonecrosis and lowering serum calcium
- contraindications include hypocalcemia
when can bisphosphonates be discontinued?
- low risk pt after 3-5 yr of use
- rescreen 1-2 yr after stopping
osteoporosis prevention
- estrogen
- bazedoxifene/conjugated estrogen (Duavee)
how does bazedoxifine/conjugated estrogen work?
- combination selective estrogen receptor modulator and an estrogen replacement
- FDA approved for vasomotor sx AND osteoporosis prevention
when is peak bone mass reached?
- age 28
how is bone formation maximized?
- through adequate calcium, vitamin D, exercise, and avoidance of tobacco and alcohol abuse
if the initial DEXA screen is normal how long can a pt wait until having a second screening?
- 5 years
what is osteomalacia?
- defective mineralization of bone resulting from inadequate amount of phosphorus and calcium available in the blood
what is the most common cause of osteomalacia?
- vitamin D deficiency resulting in decreased intestinal absorption of calcium
other causes of osteomalacia include
- deficient calcium intake
- phosphate deficiency d/t malignancy
- renal disease or alcoholism
labs in osteomalacia
- often abnormal
- hypocalcemia
- hypophosphatemia
- and/or increase in alkaline phosphatase
clinical presentation of osteomalacia
- initially asx
- eventually will have bone pain and muscle weakness
- possible pathologic fracture
- children may show bowing of legs and epiphyseal widening
treatment of osteomalacia
- vitamin D w/ calcium supplementation
- sunshine for vitamin D = 15 min 2x a week on face, arms, hands, or back
- food sources of vitamin D = fish and fortified milk
what is paget disease of the bone
- excessive bone destruction and unorganized bone repair
- increased vascularization occurs over affected bone
cause of paget disease of the bone
- unknown
- genetic component
labs in paget disease of the bone
- calcium and phosphate normal
- alkaline phosphatase is markedly elevated
clinical presentation of paget disease of the bone
- often asx
- bone pain first sx
- affected bones become soft, leading to bowed tibias, kyphosis, increase in hat size, or deafness
treatment of paget disease of the bone
- if asx possibly no tx
- bisphosphonates are tx of choice for sxatic patients
how long are bisphosphonates indicated in symptomatic pt w/ paget disease of the bone
- until alkaline phosphatase levels return to normal
- restart when levels begin to rise
prognosis of paget disease of the bone
- good
- more complications are seen if the disease begins early in life