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OSTEO-


POROSIS

OSTEO-
POROSIS
OSTEOPOROSIS

OSTEOPOROSIS

DEFINITION
WHO Definition 1994:
A skeletal disease characterized by low bone mass and
deterioration of the microarchitecture of bone tissue with a
consequent increase in bone fragility and susceptibility to low
trauma fractures.
Why? Imbalance between osteoblast & osteoclast function
OSTEOPOROSIS
OSTEOPOROSIS

OSTEOPOROSIS

INCIDENCE: 1 in 3 women and 1 in 12 men.


TYPES :
I. (postmenoposal): thin trabicular bone
55-75y
f:m 6:1
II. Senile : thin both trabicular & cortical bone
70-85 y
f : m = 2:1
OSTEOPOROSIS

RISK FACTORS + CAUSES :!


I.POST MENOPOSAL & SENILE (primary)
-sessation of estrogen or androgen
- bad nutritional habits during productive years (15-45yr)
(low calcium content food , smoking,alcohol,soda drinks.
- genetics (inheritance) & race (cocasian female)

II.Secondary :
1.medications: steroids,chronic heparin use,anticonvulsants,chemotherapy.
2.immobilisation
3. Medical conditions: Anorexia Nervosa, RA, Early
menopause,Hyperthyroidism, hyperparathyroidism, hypogonadism
Transplantation, Cushings disease/syndrome, Chronic kidney, lung or GI
diseases
OSTEOPOROSIS
OSTEOPOROSIS

INVESTIGATIONS
1. History for risk factors
2. Physical examination
3. X-ray of lumbar and thoracic spine.
Although >30 % of bone loss required to be visible on X-ray,
there may be some asymptomatic wedge #s
4. Bone mineral Density measurement
5. Blood tests, ESR, serum biochemistry
6. Testosterone and Gonadotrophin levels in men
OSTEOPOROSIS

The Gold standard test in clinical practice is measurement of Bone


Mineral Density (g/cm3), of the vertebral spine and the hip.
This is as recommended by the National Osteoporosis
society. Only vertebral measurements can be used to assess
effectiveness of treatment at present.
1. DEXA scans
2. Radiographic Absorptiometry
3. Single Photon X-ray absorptiometry (SPA)
4. Quantitative Computer tomography
5. Quantitative Ultrasound
OSTEOPOROSIS
OSTEOPOROSIS

PREVENTATIVE MEASURES
Aims- to achieve an adequate peak bone mass, by ?
OSTEOPOROSIS

TREATMENT OF ESTABLISHED OSTEOPOROSIS:


CALCIUM + VIT. D SUPPLEMENTS

Minimum daily intake of calcium should be achieved.


Should only be prescribed if this is not achieved by diet.
Vit D in all elderly institutionalized osteoporotics is
recommended.

RDA Calcium = 1400 mg


RDA Vit. D = 600-800 IU.
OSTEOPOROSIS
HRT (OESTROGEN):
Prevent osteoporosis and slows or reverses progression.
Given at doses equivalent to 0.625mg of Premarin, it will increase
bone density by 2% per year.
Given for 5-10 years almost halves the risk of fractures.
Has a role in corticosteroid induced osteoporosis

Contraindications: Endometrial carcinoma, Breast cancer,


undiagnosed vaginal bleeding.
Other benefits: loss of menopausal symptoms, cardiovascular
protection.
OSTEOPOROSIS
BISPHOSPHONATES:
Synthetic analogues of inorganic pyrophosphate. Inhibit bone
resorption by osteoclasts
Alendronate (Fosamax)
Reduces the incidence of hip, wrist and vertebral fractures in
postmenopausal women (statistically significant)
Contraindications-Abnormalities of oesophagus, renal problems
Dose -10mg daily at least 30 mins before breakfast and sit upright
for at least 30 mins
Disodium Etidronate (Didronel)
Etidronate is effective in reducing vertebral fracture (statistically
significant). Dose- disodium etidronate 400mg once daily.
OSTEOPOROSIS
OESTROGEN RECEPTOR MODULATORS (Raloxifene)
Work like oestrogen at bone without other harmful effects.
Can increase post menopausal symptoms so not to be given within
5 years of menopause
CALCITONIN
Non sex, non steroid hormone
Reduces resorption of bone
Nasal form at dosages of 200 units per day
Can be used for analgesia
CALCITRIOL (1,25 DIHYDROXYCHOLECALCIFEROL)
The active metabolite of vit D. 0.25 microg o.d. may reduce risk
of vertebral #. Need monitoring of plasma calcium
RICKETS & 

OSTEOMALACIA

Def.: reduction in bone mineralization !


OSTEOMALACIA,RICKETS
Normal bone metabolism
■ CALCIUM
99% in bone.
Main functions- muscle /nerve function, clotting.
Plasma calcium- 50% free, 50% bound to albumin.
■ Dietary needs-
Kids- 600mg/day,
Adolesc.-1300mg/day,
Adult-750mg/day,
Pregnancy-1500mg/day,
Breastfeeding-2g/day,
Fractures- 1500mg/day
■ Absorbed in duodenum (active transport) and jejunum
(diffusion), 98% reabsorbed in kidney prox. tubule, may be
excreted in stool.
OSTEOMALACIA,RICKETS
Normal bone metabolism

■ PHOSPHATE 85%
in bone. Functions-
metabolite and buffer in enzyme systems.
■ Plasma phosphate mainly unbound.
Daily requ. 1-1.5g/day
OSTEOMALACIA,RICKETS
Regulation of Calcium & Phosphate Metabolism:
Peak bone mass at 16-25 years.
Bone loss 0.3- 0.5% per year (2-3% per year after 6th decade).
1. Parathyroid Hormone (PTH)
2. Vitamin D3
3. Calcitonin
4. Other Hormones:
Estrogen: Prevents bone loss
Corticosteroids: Increases bone loss
Thyroid hormones: Leads to osteoporosis
Growth hormones: Cause positive calcium balance
Growth factors
RICKETS, OSTEOMALACIA

PATHOLOGY:
Sufficient osteoid, poor mineralization
(Rickets is found only in children prior to the closure of the
growth plates, while OSTEOMALACIA occurs in persons of
any age. Any child with rickets also has osteomalacia, while the
reverse is not necessarily true).
RICKETS, OSTEOMALACIA

CAUSES:
1. Nutritional deficiency
1. Vit D
2. chelators of calcium- phytates, oxalates, phosphorous
3. Antacid abuse, causing reduced dietary phosphate binding
2. GI Absorption defects
1. Post gastrectomy
2. Biliary disease (reduced absorption of Vitamins )
3. Small bowel disease
4. liver disease
3. Renal tubular defects
4. Renal osteodystrophy
5. Miscellaneous causes
RICKETS, OSTEOMALACIA

CLINICAL FEATURES:
■ Rickets -
Tetany , convulsions, failure to thrive,
restlessness, muscular flaccidity.
Flattening of skull (craniotabes),
Thickening of wrists from epiphyseal overgrowth,
Stunted growth,
Rickety rosary, spinal curvature,
Coxa vara, bowing, # of long bones

■ Osteomalacia, - Aches and pains, muscle weakness loss of


height, stress #s.
RICKETS, OSTEOMALACIA

XRAY FINDINGS:

RICKETS
Thickening and widening of
physes,
Cupping of metaphysis,
Wide metaphysis,
Bowing of diaphysis,
Blurred trabeculae.
RICKETS, OSTEOMALACIA

XRAY FINDINGS:

OSTEOMALACIA
Loosers zones - incomplete
stress # with healing lacking
calcium, on compression
side of long bones.
Codfish vertebrae due to
pressure of discs
Trefoil pelvis, due to
indentation of acetabulae
stress #s
RICKETS, OSTEOMALACIA

INVESTIGATIONS:

BLOOD TESTS
Calcium Reduced,
Phosphate reduced
Alkalline Phosphatase increased
Urinary excretion of calcium diminished

Calcium phosphate products (= serum [Ca] x serum [PO4])


normally 30. In rickets and osteomalacia is less than 24
RICKETS, OSTEOMALACIA

MANAGEMENT:
Depends on the cause

Nutritional Vitamin
D deficiency Dietary
chelators of calcium
Phytates
Oxalates
Phosphorus deficiency (unusual)
Antacid abuse
• Treatment- vitamin D (5000u) and Calcium (3g/day)
RICKETS, OSTEOMALACIA

MANAGEMENT:
Depends on the cause

Gastro-intestinal absorption defects


Post-gastrectomy
Biliary disease
Enteric absorption defects
Short bowel syndrome
Rapid onset (gluten-sensitive enteropathy)
Inflammatory bowel disease
Crohns
Celiac
RICKETS, OSTEOMALACIA

MANAGEMENT:
Depends on the cause
Renal tubular defects
Vitamin D dependant
type I
type II
Treatment; High levels of vit D

Vitamin D resistant (familial hypophosphatemic rickets)


Treatment; Phosphate 1-3 gm daily, Vit D3 high dose
Fanconi syndrome I, II, III
Renal tubular acidosis
RICKETS, OSTEOMALACIA

MANAGEMENT:
Depends on the cause

Renal Osteodystrophy – in chronic renal failure


Miscellaneous
Hypophosphatasia
Anticonvulsant therapy

SURGERY
For deformities

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