2. ⦁ lack of vitamin D, calcium, or
phosphate, which leads to
⦁ softening and weakening of the bones.
⦁ Defective mineralization of bone matrix –
excessive unmineralised osteoid
3. ⦁ Vitamin D helps the body properly control
calcium and phosphate levels in the body.
When the body is deficient in vitamin D, it is
unable to properly control calcium and
phosphate levels
⦁ calcium and phosphorous are found in milk and
green vegetables.
4. ⦁ Defective Vitamin D metabolism –
⦁ lowering of calcitriol -
⦁ intestinal malabsorption of calcium -
⦁ reduction of serum calcium –
⦁ Parathyroid stimulation –
⦁ normalised S.calcium at the expense of
reduced S.Phosphate
6. ultraviolet rays
⦁ 7-Dihydrocholesterol
Cholecalciferol (Vitamin D3)- in dermis
Vit D2 absorbed thru small intestine
Transport in serum- binds with X-globulin
25-Hydroxylation in Liver
1,25- Dihyroxylation in Kidney – active form
8. ⦁ Decrease in effect & amount of Sunlight
⦁ Bread/Chapathi rich in Phytate bind dietary
calcium – reduced absorption
⦁ Infants who are exclusively breastfed may
develop vitamin D deficiency.
⦁ Poor Dietary intake of Ca & Vit D
⦁ Malabsorption disorders – Coeliac d/s, hepatic
osteodystrophy, lactose intolerance
9. ⦁ Renal – Renal osteodystrophy, Nephrectomy,
renal failure, hypoparathyroidism,
X-linked hypophosphatemia/Vit D resistant
rickets
Vitamin dependant Type I (Inability to hydroxylate)
Vitamin dependant Type II (Receptor insensitivity)
⦁ Anticonvulsant therapy( 25OH in liver)
10. ⦁ Failure of deposition of Ca along mature
cartilage cell columns
⦁ Disorderly invasion of cartilage by blood
vessels
⦁ Lack of reabsorption at the zone of
provisional calcification
⦁ Increased thickness of epiphyseal plate
11. ⦁ Abundant osteoid with
⦁ Defective mineralization
⦁ No resorption of uncalcified osteoid by
osteoclasts
⦁ Normal osteoblast – laid irregularly
⦁ Abnormal arrangement of collagen bundles in
compact bone
12. ⦁ Long bones bent when child starts
crawling/walking
22. ⦁Bone pain or tenderness
Arms Legs Spine Pelvis
⦁ Skeletal deformities
o Bowlegs
o pigeon chest
o rachitic rosary
o Frontal bossing
o Spine deformities (spine curves
abnormally, including scoliosis or
kyphosis )
o Pelvic deformities
23. ⦁ Increased tendency toward bone
fractures
⦁ Dental deformities
o Delayed formation of teeth
o Defects in the structure of teeth, holes in
the enamel
o Increased incidence of cavities in the
teeth ( dental caries )
o Decreased muscle tone (loss of muscle
strength)
⦁ Muscle cramps
⦁ Impaired growth
⦁ Short stature
26. ⦁ Dense shadow
⦁ Dense line at the end of metaphysis-
deposition of Ca
⦁ Stage of repair
27. ⦁ Increase in breadth of metaphysis
⦁ Clearly defined bone
⦁ Normal content of Ca salts
⦁ Bone completely repaired
28.
29. ⦁ Serum Ca low or normal.
o Tetany -prolonged muscle spasm.
o Chvostek's sign may be positive (a spasm of
facial muscles occurs when the facial nerve
is tapped)
⦁ S.Phosphorus may be low.
⦁ S.ALP may be high.
⦁ ABG may reveal metabolic acidosis
⦁ Urinary Ca may be low .
30. ⦁ 24-hydroxylase assay – for vitamin D
dependency rickets
⦁ Serum 25-OH vitamin levels
⦁ A bone biopsy is rarely performed but will
confirm rickets.
34. ⦁ Dietary sources of vitamin D include fish, liver,
milk and cheese.
⦁ Exposure to moderate amounts of sunlight is
encouraged.
⦁ Reduce cereal containing phytates
⦁ Supplemention of Calcium and
Vitamin D – 3000 i.u./day
36. ⦁ Control of movements – reduced pressure upon
limbs
⦁ (soft bones easily bent by pressure / muscle
strain)
⦁ Positioning or bracing with ‘rickets’ splints may be
used.
37. ⦁ Correction by splinting
⦁ In young children below 4 yrs
⦁ Useful in lower limbs
⦁ Continuous supervision needed to prevent
sores
38. ⦁ Correction by osteotomy
⦁ When deformity is near a joint
⦁ At least stage 3 in radiograph
39. ⦁ Chronic skeletal pain
⦁ Skeletal deformities
⦁ Skeletal fractures, may occur without cause
40. ⦁ Rickets of prematurity
⦁ Very premature infants at risk
⦁ Risk factors- hepatobiliary d/s, TPN,
⦁ Diuretic therapy, chest percussion therapy
⦁ Pathologic # in NICU
⦁ Readily heal with treatment
41. ⦁ Antiepileptic medications
⦁ Induce microsomal P-450 enz
⦁ Decreased Vit D
⦁ Should be suspected in neurologic patients
having seizures
⦁ Start having frequent #
42. ⦁ Familial hypophosphatemic rickets
⦁ X-linked dominant (MC)- Mutn in PEX gene
⦁ Aut dominant 12p13 – phosphatonins – fgf
23 – cause phosphaturia
⦁ Aut recessive
43. ⦁ Renal tubule unable to retain PO4
⦁ End organ insensitivity to vit D (AR)
⦁ Kidney unable to perform 2nd hydroxylation
⦁ Renal tubular acidosis (kidney excretes fixed
base and wastes bicarbonate)
⦁ Ca ppt – renal calcinosis
44. ⦁ Older age
⦁ Delayed walking, angular deformities
⦁ Systemic manifestn – irritability and apathy
minimal
⦁ Treatment – Oral Phosphorus , Vit D
⦁ (Compl – nephrocalcinosis)
⦁ Growth hormone – increased height,
increased PO4, reduced Nephrocalcinosis
45. ⦁ Surgery not efficacious – multilevel osteotomy
to correct mechanical axis
⦁ Recurrent deformity common
⦁ Surgery when - gait compromised/severe
pain
46. ⦁ Oncogenic hypophosphatemic
osteomalacia
⦁ Asso with Neurofibromatosis, fibrous
dysplasia
⦁ Osteoblastoma, hemangiopericytoma of
bone, skin tumors
⦁ (disrupts renal tubular abs of po4)
⦁ Secrete phosphatonins
⦁ Resolve with excision of tumor
47. ⦁ C/C pyelonephritis
⦁ Congenital Abnormalities
⦁ Polycystic kidney d/s
⦁ Secondary hyperparathyroidism
⦁ Leads to actvn of osteoclast and resorption of
bone (high turn over d/s)
48. ⦁ Glomerulus unable to excrete Phosphorus
⦁ Vit D prodn reduced
⦁ Ca abs from S.Intestine reduced
⦁ PTH triggered
⦁ Increased S.Ca – bone demineralization
⦁ Precipitate in cornea, skin, blood vessels
49. ⦁ C/F similar to Nutritional.
⦁ Angular deformity, SCFE, AVN
⦁ Radiography – cuppping of physis not
present
⦁ Subperiosteal resorption in phalanges, MC
and ulna (feature of Hyperparathyroidism)
⦁ Osteosclerosis of skull, rugger jersey spine
⦁ Lytic areas in long bones (Brown tumors)
⦁ Treat underlying d/s- Ca, Vit D, growth
hormone, osteotomy, Ilizarov
50. ⦁ Ca Normal or low in all
⦁ Phosphate is reduced in all except Renal
Osteodystrophy
⦁ ALP and PTH high in all
⦁ 25 OH Vit D N or high in all except
nutritional (decreased)
⦁ 1,25 (OH)2 N or low in all except Vit D
dependent typeII (receptor insensitivity)
51. ⦁ Maintain an adequate intake of calcium,
phosphorus, and vitamin D.
⦁ This may require dietary supplements in
people who have gastrointestinal or other
disorders
⦁ Renal causes of vitamin D should be treated
promptly.
52. ⦁ Levels of calcium and phosphorus should be
monitored regularly in people who have renal
disorders .
⦁ Genetic counseling may help people with a family
history of inherited disorders that can cause
rickets.
53. Defining Osteoporosis
⚫“Progressive systemic skeletal disease
characterized by low bone mass and
microarchitectural deterioration of bone
tissue, leading toenhanced bone fragility
and aconsequent increase in fracture risk”
⚫True Definition: bonewith lowerdensity
and higher fracturerisk
⚫WHO: utilizes Bone Mineral Density as
definition (T score <-2.5); surrogate marker
54. Who Gets Osteoporosis?
⚫Age
⚫Estrogen deficiency
⚫Testosteronedeficiency
⚫Family history/genetics
⚫Femalesex
⚫Low calcium/vitamin D intake
⚫Poorexercise
⚫Smoking
⚫Alcohol
55. Who gets osteoporosis?
⚫Low body weight/anorexia
⚫Hyperthyroidism
⚫Hyperparathyroidism
⚫Prednisone use
⚫Liverand renal disease (think aboutvitd
synthesis)
⚫Low sunexposure
⚫Medications (antiepileptics, heparin)
⚫Malignancies (metastaticdisease; multiple
myeloma can presentasosteopenia!)
⚫Hemiplegia s/p CVA/ immobility
56. Back pain, which can be severe if fractured or collapsed
vertebra
Loss of height over time, with an accompanying stooped
posture
Fractureof thevertebrae, wrists, hipsorother bones
59. T-Score
WHO, Guidelines for Preclinical Evaluation and Clinical Trials in Osteoporosis, 1998.
World Health Organization (WHO)
Osteoporosis Guidelines
1.4
1.3
1.2
1.1
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
20 30 40 50 60 70 80
Age
BMD
Mean
–2 SD
Considerpreventive interventio
Considertherapeutic interventio
Mean LumbarSpineBMD:
Decades 3 to 9 of a Woman’s Life
Bone Mineral Density Values
60. Osteoporosis
⚫PATHOGENESIS
⚫1. Peak bone mass : about 20 yearsold
- genetic, hormone, nutrition, lifestyle
⚫2. Rateof bone loss : afterage 30-45, bone resorption
(osteoclast)> formation (osteoblast) and become
exaggerated after menopause
(50 yearsold)
⚫3. Boneremodeling : keep balanceat 20-30 yearsold,
afterthat become negative balance
9
61. Singh Index
•grade 1: only thin principal
compression trabeculae visible
•grade 2: principle compression
trabeculae present, other
resorbed
•grade 3: principle tensile
trabeculae thinned and breakage in
present
•grade 4: principal tensile
trabeculae thinned without loss of
•grade 5: principle tensile and
compression trabeculae readily
prominence of Ward triangle
•grade 6: all trabeculae visible and
of normal thickness
63. Osteoporosis
⚫ Type 1
Postmenopausal
Type 2
Senile
Type 3
secondary
⚫Age 55 -70 years
⚫Sex(F/M)
⚫Fxsite
6:1
vertebrae
70-90 years
2 :1
vertebrae
distal forearm hip
all
1:1
vertebrae
hip
distal forearm
⚫The threshold for Fx is reduced forosteoporotic
bone
11
65. Lab Investigations
CBC
ESR
Serum calcium (8.6 – 10.4 mg/dl)
Serum phosphorus (3.00 – 4.5 mg/dl) Children 4-6 mg/dl
Serum alkaline phosphatase (44 – 147 Iu/lit.) Children 1.5 -
2.5 times more
Liver function tests
Renal function tests
T3,T4, TSH
Para thyroid hormones
Vitamin D 25 (25 – 80 ng/ml)
Protein electrophoresis (M band)
Anti endomysial antibody (Coeliacdisease)
66. Osteoporosis Treatment: Calcium and
Vitamin D
⚫Fewerthan half adults take recommended
amounts
⚫Higher risk: malabsorption, renal disease, liver
disease
⚫Calcium and vit D supplementation shown to
decrease risk of hip fracture in olderadults
⚫1000 mg/day standard; 1500 mg/day in
postmenopausal women/osteoporosis
⚫Vitamin D (25 and 1,25): 400 IU day at least;
⚫Frail older patients with limited sun exposure may need
up to 800 IU/day
67. Osteoporosis Treatment: Calcitonin
⚫Likely notas effectiveas
bisphosphonates
⚫200 IU nasally/day (alternating
nares)
⚫Decrease pain with acutevertebral
compression fracture
68. Osteoporosis Treatment: Bisphosphonates
⚫Decrease bone resorption
⚫Multiple studies demonstratedecrease in hipand
vertebral fractures
⚫Alendronate, risodronate
⚫IV: pamidronate, zolendronate (usually used for
hypercalcemiaof malignancy, malignancy related
fractures, and multiple myeloma related
osteopenia)
⚫Ibandronate (boniva): once/month
⚫Thoseat highest risk of fracture (pre-existing
vertebral fractures) had greatest benefitwith
treatment
71. A study of disease management in
a rural healthcare population
demonstrated that a preventive
program was able to reduce hip
fractures and save money.
98% of a woman’s skeletal mass is acquired byage 20
Optimal strategies for building strong bonesoccurs during childhood and
adolescence
1. A balanced dietrich in calciumand
vitamin D
2. Weight-bearingand resistance-
training exercises
3. A healthy lifestylewith nosmoking
orexcessivealcohol intake
4. Talking toone’s healthcare
professional about bone health
5. Bone density testing and
medicationwhen appropriate
Five Steps Toward Prevention
