METABOLIC BONE DISEASE

metabolic bone diseases and mineral disorders

may arise from deficiency of calciotropic
hormones which are vitamen D and it is
metabolite and parathyroid hormone PTH or of
steroid or peptide hormones that have direct
action on bones or altered in key minerals

*minerals CA-MG-phosphate– genetic or

acquired defect in osteoclast or osteoblasts
functions– bone matrix synthesis mineralasation
turn over or reffered may also called metabolic
bone disease
 OSTEOPOROSIS
*most common metabolic bone disease
*it is disease of diverse etiology characterized by reduction in
the mass of bone per unit of volume to level below that required
for adequate mechanical support function
*it is not accompany by significant decrease in ratio of mineral
to organic matrix this ratio is preserved
HISTOLOGICALLY
*decrease in cortical thickness and in number and size and
trabeculi of cancellous bone
W.H.O definition:
Condition in which the bone mineral density less than minus 2.5
– standard deviation below peak bone mass called T-score
below normal mean of 35 years old women
EPIDEMIOLOGY
Osteoporosis the reduction of mass increase with age with
increase of bone fracture espically in post-menopausal
women most common site of fracture is hip bone vertebrae
and colle's at wrist– bone mass reach it is peak between 40-20
years old after 40 the mass decrease

SOME DEFINTIONS
OSTEOPENIA –which T-score between minus(-1) to minus (
-2.5) bone mineral density (BMD)
NORMAL BMD –when T score above minus (-1) this consider
normal BMD

REMODLING OF BONE
MINERAL BALANCED
Is the balance of key minerals of the bone( ca-mg-po4)
*is affected by PTH and 25,1 hydroxy D3 & through
adjacent to changing mineral acquirement is the end result of
mineral absorption minus faecal and urinary excretion
*might be negative– positive– neutral
*if intake and retention is more than faecal andurinary excretion
positive mineral balance
*when urinary and faecal excretion is more than the intake and
absorption= negative mineral balance
WHAT ARE CAUSES OF OSTEOPOROSIS ?
PRIMARY CAUSES
1-n post menopausal women is the most common single reason
2-senile osteoporosis
SECONDARY CAUSES
1-ENDOCRINE DISEASE
Hypogonadism– hyperthyrodism–
hyperparathyrodism
2-DRUGS
Corticosteroid– osteoporosis induced by
corticosteroid depend on dose and duration of
corticosteroid any patient of do– prednisolone on 7.5
mg daily for more than 3 months– you should expect
that patient having osteoporosis
3-alcohol– smoking– anorexia nervosa– chronic renal
failure– bone metastasis– chronic inflammatory
disease RA-AS
CLINICAL FEATURES
*osteoporosis usually goes silent till the occurance of fractures
at the most common sites-HIP– VERTEBRAE-WRIST
*radiological changes dose not appear till after the loss of %40
-30 of bone mass density so they are late changes
*occurrence of fractures of hip so neck– intertrochantric & get
minimal trauma
CLASSICAL PRESENTION
Post-menopausal female after simple trauma( pain in hip
region )tenderness
*shortening of that lower limb when you examine the lower
limb will elicite shortening in comparism with contral-lateral
side with external rotation of that limb
*wrist– colle's fracture is most important
INVESTIGATIONS
DEXA-dual energy x-ray absorptiometry
*in this study we study hip region or vertebral body– most of
these studies give as T-score and Z-score
*BMD in skeletal sites in the same individuals readings are
different sites
*due to proportion of trabecular cortical bone which are differ
in different body region for example vertebrae have%85
trabecular bone while femoral shaft or neck principly cortical
bone
WHAT ARE INDICATIONS OF BONE DENSITOMETRY?
In addition to
-1. high close.
2-kyphosis
INDICATIONS OF DRUG THERAPY IN OSTEOPOROSIS :
1-T-score minus(-2.5) or below
2-T-score of minus (-1.5) of co icosteroid induced osteoporosis
3-ve ebral body fractures irrespective of bone mineral density
unless they result from sever trauma
MANAGEMENT:
1-general measures or life style advices they include
CA & VITAMEN D ca & vitamen d in isolation have limited
efficiency of osteoporotic fracture so they give poor results
2-vitamen D is given as 100 IU per day, CA 500 MG
DAILY+exposure to sunlight
3 -physical activity important line in general line of treatment
this called life style change– inactivity– immoblization and
paralysis and result in significant bone loss while athletic
patient have more bone density– keep in mind weight bearing
& muscle activity inhance bone mineralization
But note:
Fracture risk is lower in rural area and more common
in community where physical activity is less so more
active individuals are more capable to protect their
skeleton + Stop drinking alcohol
SPECIFIC THERAPIES
BISPHOSPHONATES
*alendronate most used one70 mg tablet taking orally once
weekly
*risedronate 35 mg once weekly
*bisphosphonates– taking orally on empty stomach with plain
water and no food taking for 45 min after that patient should
sit not lie for that period as they are poorly absorbed from GIT
tract +One tab once weekly on empty stomach in morning and
patient continues sitting for 45-60 min and taken with plenty
of water
*alendronate & risedronate should be avoided in patient with
achalasia or esophageal stricture
*calcitonin which osteoclast inhibitor may be give
subcutaneous or I.M or nasal spray mostly used as nasal spray
200 IU PER DAY
*cyclical hormone replacement therapy we use
osterogen– progesterone or both used in
patient with early menopause– should be
avoided in older females because increase risk
of cardiovascular problem and increase risk of
breast cancer
*duration of treatment– for many long time or
life long– one should assess the response to
treatment for 3-2 years after 3-2 years increase
in bone density in % 5-2 of bone mineral
density
*PARATHYROID
PARATHYROID PTH1 34-this
34- is expensive &
rarely used & used for sever osteoporosis when
BMD– T-SCORE of minus-3.5-(minus )4 or below
& duration of treatment 24 months
OSTEOMALACIA & RICKETS
*disorder in which there are defective mineralization of
bones due to vitamen D deficiency

*resistant to effect of vitamen D or hypophosphetemia–

osteomalacia occur in adult afterclosure of epiphyseal
growth plate

*ricket occur in children involve bone & cartilage matrix

growth plate withinadequate mineralization of matrix–
there is variable cupping of epiphysis
CAUSES OF OSTEOMALACIA & RICKETS

1-vitamen D de ciency either by inadequate ultraviolet

sunlight exposure or inadequate
vitamen D taking & also malabsorption syndrome
–celiac disease
–gluten enteropathy
2-failure of 1,25 hydroxy vitamen D synthesis it occur in
chronic renal failure as type 1 vitamen D resistance due to
inactivity of enzyme
3-vitamen D receptor defect called type 2 vitamen D
resisitant (VDRR)
4-defect in phosphate &progesterone metabolism defect in
renal tubular phosphate reabsorption

5-iatrogenic
–medically induce due bisphosphonate therapy
–anti-convulsant
–phenobarbital
–phenetoin
– carbamazepine

6-Lack of sunlight exposure most common (2 thirds from it,

one third from food)
 CLINICAL FEATURES:

1-ricket in children lead to delay development of child

– muscle hypotonia
– craniotabes
– unossify membrane of skull of child
– possing of frontal parital bone
– delay closure of anterior fontanelle
– enlarge distal end of radius
– swelling of costochondral junction called ricketic rosary
2 -osteomalacia in adult might be insidiousslowly progressive
may be asymptomatic

– in more sever cases

– sever osteomalacia present with muscle & bone pain
– proximal muscle weakness is prominent and patient walk with
a waddling gait and has difficulty in get up from chair
– there may be muscle tenderness and bone tenderness on
pressure and focal bone pain can occur due to fissure fractures
of the ribs and pelvis
 INVESTIGATIONS
1-serum alkaline phosphate increase
2-serum ca & phosphate level may be low but normal
level not exclude diagnosis
3-serum,25 hydroxyl vitamen D decrease (Low D3 and
absence of other abnormalities, unlikely to be
significant and might be d.t abnormalities in vit D.
Binding protein)
4-PTH increase (indicate hyperparathyrodism )
5-X-RAY FINDINGS:
*plain radiograph negative usually normal unless
we have fissure fractures
– also called psedofracture involve ribs
– pelvis& long bone
*in children thick & widening of epiphyseal plate
– radiographical osteopenia is common
*wedging of vertebrae due to cracke fracture
may cause confusion with osteoporosis
 TREATMENT
*vitamen D supplement 800 mg orally
– vitamen d it is fat soluble vitamen present in fatty food
– meet
-fish
-liver
– synthysis by skin by ultraviolet light

*calicium found in milk dieta product

–yough . –soya beans
–egg. –rice bran
–wheat our –apple
–beef. –shrimp
–dates
*duration of treatment for few months (3-4m)
*for vitamen D resistance rickets active metabolite
–vitamen D
–alpha 1
(renal failure give active metabolite )
*patient with chronic renal failure use alpha 1

WHAT is difference between osteomalacia &

ricket
 VITAMEN D SYNTHYSIS
*ultraviolet sunlight exposure to catalyse synthesis of
cholecalciferol from-7 dehydrocholesterol in the skin
*lack of cholecalciferol results in reduced hepatic
production of(25 OH)D3& reduced renal production of
biologically active metabolite(25,1 OH)D3
*lack of(25,1 OH)D3 impaires intestinal calcium absorption
and lowers serum calcium which stimulate PTH secretion
*this causes phosphate wasting and increase bone
resorption in an attempt to maintain serum calcium levels
whithen normal range causing progressive demineralization
of bone