Metabolic bone disease (MBD) encompasses disorders of calcium and phosphorus homeostasis that are often silent until fractures occur. The document discusses several MBDs including osteoporosis, osteomalacia, rickets, and hyperparathyroidism. It provides details on osteoporosis including definitions, classifications, etiology, clinical manifestations, diagnosis through bone densitometry and radiography, assessment methods, and prevention through exercise, nutrition, and drugs.

1. ORTHOPEDIC ASPECTS OFORTHOPEDIC ASPECTS OF
METABOLIC BONEMETABOLIC BONE
DISEASEDISEASE
Presented by DR. ANUBHAV VERMAPresented by DR. ANUBHAV VERMA
30.8.16
Chairperson: Dr. P. Sastry
JSS Medical College and hospital, Mysore

2. Metabolic bone diseaseMetabolic bone disease (MBD)(MBD)
• Encompasses a diverse group of disorders
associated with altered calcium and
phosphorus homeostasis.
• To orthopedic surgeons; MBD is often silent
until the patient presents with fracture.
IntroductionIntroduction

3. Table of contentTable of content
 Osteoporosis.
 Osteomalacia and rickets.
 Hyperparathyroidism.

4. OSTEOPOROSISOSTEOPOROSIS

5. OSTEOPOROSISOSTEOPOROSIS
• Most common metabolic bone disease.
• One of the most prevalent conditions
associated with aging.

6. OSTEOPOROSISOSTEOPOROSIS
Definition : reduced bone mass of normal composition.

7. OSTEOPOROSISOSTEOPOROSIS
• Clinical definition: requires the presence
of a nontraumatic fracture.
• Histologic definition: requires normally
mineralized bone to be present in
reduced quantity.

8. OSTEOPOROSISOSTEOPOROSIS

9. Classification
• PRIMARY-
Postmenopausal osteoporosis (type I)
Caused by lack of estrogen
Causes PTH to overstimulate osteoclasts
Excessive loss of trabecular bone
Age-associated osteoporosis (type II)
Bone loss due to decreased bone turnover
Malabsorption
Mineral and vitamin deficiency

10. • SECONDARY-
1.Hormonal-Hyper parathyroidism, Hypo parathyroidism,
hypogonadism,pituitary tumors, DM-Type 1,Addison’s disease,
cushings syndrome
2.Nutritional
3.Drugs- corticosteroids,Alcohol,Anticonvulsant’s,Vit-d
toxicity
4.Inherited metabolic disorders- Ehler-danlos
syndrome, osteogenesis imperfecta ,marfan’syndrome.
5.Other causes-porphyrinuria, Myeloma, Thalassemia,
Pregnancy,Anorexia nervosa,systemic mastocytosis

11. Concept of peak adult bone mass-

12. ETIOLOGY AND
PTHOGENESIS
• GENETIC FACTORS-The prevalence varies
according to race. Due to difference in peak
bone mass. Adult blacks >bone mass then
whites and asians.
• ESTROGEN STATUS-Estrogen inhibits
osteoclasts and stimulate osteoblasts.It
causes activation of new bone remodeling
sites and exaggerates imbalance between
bone formation and resorption

13. • Endocrine disorders-
1. Hypogonadism-Causes bone loss in both men and
women.Other hypogonadal condition include castration,
panhypopituitarism, klinfelter’s
2. Hypercortisolism- Cushing syndrome
Chronic steroid therapy
This leads to decrease intestinal absorption of calcium
Also stimulates PTH vitD endocrine axis leading to
bone resorption.

14. Hyperthyroidism and Hyperparathyroidism-
They increase bone turnover and remodeling causing a net
increase in bone re absorption.

15. • NUTRITIONAL DEFICIENCY-
CALCIUM-Adequate ca intake is vital for
maintaining peak bone mass.
In response to ca deficiency the body
robs the calcium it needs from skeletal
reserve by increasing PTH and
1,25(OH)2 D.

16. VITAMIN D- Dietary source supply 50%
of vit D, the remaining is synthesized in
the skin in response to ultraviolet
irradiation.
The active form of vit D helps maintain
normal levels of calcium and
phosphate.

17. • DRUGS ,ALCOHOL AND SMOKING-
Chronic alcoholism is the most common
cause of bone loss in young men in part
because of poor nutrition.
Tobacco smoking is also linked to a reduction
in bone density and may effect remodeling.
Drugs
corticosteroids,Alcohol,Anticonvulsant’s,hepa
rin ,cytotoxic drugs,lithium are associated
with increased risk of osteoporosis

18. • CHRONIC ILLNESS AND TUMORS-
Chronic illness of almost any kind can lead to
osteopenia, with malnutrition and disuse the major
contributing factors.
Osteopenia is the most common complication of most
bone marrow tumors. Myeloma cells produce
cytokines that potenitially stimulate bone resorption.
Neoplastic disease appears to cause osteoporosis
through osteoclast activating factor ,interleukins and
tumor necrosis factor.

19. • DISUSE-
Disuse osteoporosis is more likely to develop in
sedentary person.
It is not the lack of movement that leads to
osteoporosis but the absence of mechanical
stresses on the bone from wt bearing activity and
from powerful antigravity muscle.
This leads to a progressive thinning and eventual
loss of trabeculae, the loss of trabeculae is most
dramatic in axial skeleton, specially the vertebral
bodies.

20. CLINICAL MANIFESTATION
• Osteoporosis , the silent thief usually remains
asymptomatic until the weakened bone fractures.
• Complications are compression fracture of the
vertebral bodies and fractures of hip,ribs,
humerus,and distal radius.
• Osteoporotic fractures are suspected in-
1. Elderly people(>40)
2. Sudden onset of pain(commonly in back)
3. Stooped posture
4. Shortened stature
5. Fractures of hip with minimal trauma.

21. VERTEBRAL COMPRESSION
FRACTURES-
• The earliest symptom of osteoporosis is often an episode of
acute back pain .
• Spine movement is severely reduced with flexion reduced
more then extension.
• Pain intensifies with sitting or standing and is relieved on
rest.
• Coughing sneezing and straining to move the bowels can
exacerbate the pain.
• Anterior compression fracture may cause thoracic kyphosis.

22. • Stooping posture is characteristic of
osteoporosis.
• Spasm of paravertebral muscle are palpable
and often visible.
• Spontaneous vertebral compression fracture
are stable injuries.

23. Diagnosis OsteoporosisDiagnosis Osteoporosis
Bone densitometryBone densitometry; gold standard
1. Detection osteoporosis before fractures.
2. Determination disease severity.
3. Estimation risk of fracture.
– Serial BMD measurements enable determination
of rate of bone loss or gain and thereby help in
monitoring therapy.
Plain filmPlain film; loss of 30% to 50% of bone is required
before it is detected on conventional
radiographs.

25. Radiological finding (1)Radiological finding (1)
• The m/c radiologic finding is generalized
osteopenia.
– Cortical thinning and accentuation of
weightbearing trabeculae.
– The bone surfaces are well defined, with
sharp margins.

26. Radiological finding (2)Radiological finding (2)
• Fractures - vertebral deformities, which
are also common, include biconcave
end plates (fish vertebrae) and anterior
wedging.

27. Lateral radiograph of the lumbar spine in a 55-year-old woman with postmenopausal osteoporosis shows generalized osteopenia,
compression fractures, and biconcave vertebral endplates ("fish vertebra"). Notice thin, well-defined vertebral cortices ( arrows).

29. Radiological finding (3)Radiological finding (3)
• Patients with osteoporosis secondary to
excess steroids.
– Generalized osteopenia.
– Fractures with exuberant callus
– Steroid-related complications;
• Avascular necrosis.
• Osteomyelitis.

30. Differential considerations forDifferential considerations for
diffuse osteopeniadiffuse osteopenia
1. Osteomalacia.
– indistinct trabeculae and poorly defined interfaces
between cortical and trabecular bone.
– Presence of Looser's zones.
1. Hyperparathyroidism.
– bone resorption at characteristic sites.
1. Multiple myeloma.
– MR imaging may show areas of marrow
replacement.

31. Regional or localizedRegional or localized
osteoporosisosteoporosis
1. Immobilization and disuse
2. Reflex sympathetic dystrophy syndrome
(RSDS)
3. Transient regional osteoporosis
– Transient osteoporosis of the hip.
– Regional migratory osteoporosis.
1. Inflammatory arthritis.
2. Tumors
3. Infection.

32. Radiologic findings in regionalRadiologic findings in regional
osteoporosisosteoporosis (1)
• RSDS : mediated by the sympathetic
nervous system and is characterized by
– aggressive osteoporosis,
– soft tissue swelling.
 The cause is usually traumatic, but the
disease may also be idiopathic.

33. AP radiograph of the hand in a patient with reflex sympathetic dystrophy syndrome shows soft-tissue swelling and periarticular osteopenia.

35. ASSESSMENT OF OSTEOPOROSIS
RADIOGRAPHIC BONE
DENSTIOMETRY
spine-Grading systems for
spine is based on the
appearance and thickness of
cortical shell.
Vertebrae were graded from
6 to 1 as the vertical
trabeculae pattern becomes
more pronounced with the
loss of the horizontal
trabeculae and the cortical
shell becomes progressively
thinned.

36. SINGH’S INDEX-
GRADE 6: All normal trabeculae are
seen.
GRADE 5:Principle tensile and
compressive trabeculae accentuated
GRADE 4:Equivocal evidence with
principal tensile trabeculae reduced
in no but continue to extend from
lateral cortex to femoral neck
GRADE 3:Suggests definite
osteoporosis .Break in continuity of
principle tensile trabeculae
GRADE 2:Marked osteoporosis .
No tensile trabeculae seen.
GRADE 1:Severe osteoporosis
marked reduction even in no of
principle compressive trabeculae

37. QCT-Quantitative
computed tomography
Ultrasound-
• Primarily used to
measure the spine.
• Provides separate
measurements of
cortical and trabecular
bone and may be
especially valuable in
older people.
• Measures bone mass by
calculating the
attenuation of the signal
as it passes through
bone or through the
speed with which it
traverses.
• Mainly used in screening
because of low cost and
mobility.

38. MARKERS-
Markers of bone
formation
Markers of bone
resorption
• Serum alkaline
phosphatase
• Serum osteocalcin
• Serum C-N- propeptide
of type 1 collagen
• Urinary excretion of
pyridinium cross links of
collagen deoxypyridinoline
• Urinary excretion of c-and n-
telopeptides of collagen
• Urinary excretion of
galactosyl hydroxyproline
• Urinary excretion of
hydroxyproline
• Serum tartrate resistant acid
phosphatase

39. PREVENTION OF
OSTEOPOROSIS
Osteoporosis is not an inevitable part of the
ageing process .It can be prevented.
• Increased bone mass by exercise , nutrition during
adolescence to achieve peak bone mass and also at any age
to maintain bone mass.
• Drugs at menopause- Women need drug therapy twice in her
life –Once at perimenopause,2nd
time in old age.
• Yearly BMD measurement especially in females.
• No excessive use of alcohol.
• No smoking.
• Exercise: Aerobic, muscle strengthening , yoga .
• Balanced nutrition.

40. NUTRITIONAL RECOMMENDATION
• Calcium-Optimum ca.
intake reduces bone loss
and suppresses turnover.
• Dairy products ,green leafy
vegetable , juices,cereals are
good source.
• But most patient require
supplements and it should be
taken in dose of >600 mg at
a time as ca absorption
fraction decreases at higher
dose.

41. VITAMIN-D
• Even though it is called a vitamin, vitamin D acts more
like a hormone in that it helps to increase calcium
absorption and decrease calcium excretion. Vitamin D
can be synthesized in the skin when the skin is exposed
to ultraviolet-B rays from sunlight. A five to ten-minute
exposure of sunlight to the unprotected arms and legs
results in the production of 3000 IU of vitamin D. Proper
intake of calcium and vitamin D may decrease fracture
rates by up to 25% by maintaining good bone health.
• Over the past several years, the recommended daily
dose of vitamin D has increased. The newest
recommendations suggest that 1000 IU of vitamin D is
needed daily

42. OTHER FACTORS-
• Adequate vit –k is required for optimal
carboxylation of osteocalcin.
• Adequate protein and caloric
supplementation reduces the risk of fracture .
• Exercise in young individuals increases
likelihood that they will attain maximal
genetically determined peak bone mass.

43. MEDICAL TREATMENT
Hormonal replacement therapy-
• Estrogen: It reduces turn over , prevents bone loss
and induces small increase in bone mass.
Effective in both surgical and natural menopause.
• Dose for oral route-
Esterified estrogens-0.3mg/day
Conjugated equine estrogen0.625mg/day
Ethinyl estadiol-5microgram/day
• Transdermal-50 microgram estadiol/day

44. • Progestin's-
• In women with a uterus intact, daily
progestin or cyclical progestin at least 12
days per month are prescribed in
combination with estrogen to reduce risk
of uterine cancer.
• HRT should be started early within 5
years of menopause as loss of estrogen
at menopause triggers a period of rapid
bone loss of about 5 years.

45. SERMS
• Selective estrogen receptor modulators have
almost replaced HRT.
• Raloxifene is devoid of action on endometrium and
being extensively used for prevention of
osteoporosis and breast cancer.
• 60 to 120mg/day increases the BMD .
• It reduces the occurrence of vertebral fracture by
30% to 50%

46. BISPHOSPHONATES-
• This group of drugs are
currently the most
potent treatment of
osteoporosis based on
BMD and fracture
studies.
• They inhibit bone
resorption by preventing
protein prenylation in
osteoclast, owing to
inhibition of farnesyl
diphosphate synthase.

47. BISPHOSPHONATES

48. BIPHOSPHONATE
complications-
•Subtrochantric
fracture after
prolong use(more
than 5 years)
•Avascular
necrosis of
mandible
INDICATIONS-
• Osteoporosis
• Postmenopausal
women
• Avascular necrosis of
head of femur
• Perthes disease
• Joint cell tumor of bone
• Total hip replacement to
prevent loosening

49. Usage guideline-
•ALENDRONATE} Patient must
remain upright and refrain from
eating for 30 mins following dose.
•IBANDRONATE}
Oral- Patient must
remain upright and refrain from
eating for 60 mins following dose.
I.V-15 to 30 sec bolus iv injection.
•RESEDRONATE} Patient must
remain upright and refrain from
eating for 30 mins following dose.
•Zolendronic acid}Slow iv infusion
given over a constant infusion rate
the infusion time must be less then
15 min is recommended for patients
with creatinine clearance
>35ml/min.

50. FLUORIDE-
•Has been used in multiple
ostoporosis studies but with
conflicting results.
•So it remains as a experiment
agent.
PTH-
•PTH is associated with
maintenance of
trabecular bone mass.
•It is approved for
treatment of
osteoporosis in patient
with high risk of
fracture.
CALCITONIN-
• Calcitonin can be given as
subcutaneous injection or in
nasal spray.
• Nasal spray containing
calcitonin (200IU/day) is
approved for treatment of
osteoporosis in post
menopausal women.
• The most valid indication is
intractable pain caused by
vertebral fracture.

51. RICKETS ANDRICKETS AND
OSTEOMALACIAOSTEOMALACIA

52. Rickets and osteomalaciaRickets and osteomalacia
• Rickets and osteomalacia are similar
histologically.
• Abnormality in vitamin D metabolism.
• Incomplete mineralization of normal
osteoid tissue.
RicketsRickets
Occurs in childrenOccurs in children
AAffects immatureffects immature bonebone
OsteomalaciaOsteomalacia
Occurs in adultOccurs in adult
Affects mature boneAffects mature bone

53. Rickets and osteomalaciaRickets and osteomalacia
Maintain calcium and phosphate homeostasis.

54. Clinical findings ofClinical findings of
Rickets and OsteomalaciaRickets and Osteomalacia
Rickets:Rickets: stunted skeletal growth.
• Apathetic, Irritable, Hypokinetic.
• Frontal bossing, softening of the skull,
dental caries, rachitic rosary, kyphosis,
joint enlargement, or bowing of long
bones.
• Fractures and slipped capital femoral
epiphyses.
Depend in part on the etiology and severity of the disorder, as well as the
age of the patient at presentation

56. Clinical findings ofClinical findings of
Rickets and OsteomalaciaRickets and Osteomalacia
Osteomalacia:Osteomalacia: more subtle.
• Fatigue, malaise, or bone pain.
• Proximal muscle weakness and
abnormal gait may be present.
Depend in part on the etiology and severity of the disorder, as well as the
age of the patient at presentation

57. Radiologic findings ofRadiologic findings of
OsteomalaciaOsteomalacia
• The M/C radiologic sign is generalized
osteopenia.
• Coarsened and indistinct bony trabeculae.
• Poorly defined interfaces between cortical and
trabecular bone.
• Looser's zone, or pseudofracture. (more
specific but less common)
• End plate deformities and fractures of
vertebral bodies, bowing and fractures of long
bones, and basilar invagination of skull.
The radiologic findings of osteomalacia are often nonspecific, difficult to
confirm the diagnosis with imaging studies

58. Radiologic findings ofRadiologic findings of
OsteomalaciaOsteomalacia
Looser's zone.Looser's zone.
• Linear areas of undermineralized
osteoid that occur in a bilateral and
symmetric distribution.
• Characteristic sites; inner margins of
femoral neck, proximal ulna, axillary
margin of the scapula, pubic rami, and
ribs.
• DDx; Paget's disease or fibrous
dysplasia.

59. AP radiograph of the hip in a 50-year-old man with osteomalacia shows coarsened trabecular pattern with indistinct trabeculae.

60. AP radiograph of the hip in a patient with osteomalacia shows multiple Looser zones ( arrows) in the superior pubic ramus.

62. Osteomalacia. AP radiograph of the pelvis showing osteopenia with bilateral femoral neck pseudofractures (arrows).

63. Radiologic findings ofRadiologic findings of
RicketsRickets
• The M/C radiologic sign is generalized
osteopenia.
• Increased lucency, widening, elongation,
irregularity, and cupping of the metaphyses.
– Earliest; Slight axial widening of the physis
– Next; Increased lucency of the zone of provisional
calcification.
– More advance; The physis widens and its contour
becomes irregular.
• Occasionally, in patients with rickets caused
by chronic renal disease, increased sclerosis
may be seen.

64. Radiologic findings ofRadiologic findings of
RicketsRickets
• The regions of highest yield on
radiologic evaluation of rickets are those
that are undergoing rapid growth.
– Costochondral junctions of middle ribs
(rachitic rosary)
– Distal femur
– Both ends of the tibia
– Distal radius and ulna
– Proximal humerus.

65. Radiologic findings ofRadiologic findings of
RicketsRickets
• The complication of rickets.
– Skeletal deformities.
– In neonates; posterior flattening and squaring of
the skull, or craniotabes, may be seen.
– In early childhood; bowing deformities of arms and
legs are common.
– Older children: scoliosis, vertebral end plate
deformities, basilar invagination of the skull may be
seen.
– Advance disease: Slipped capital femoral
epiphysis.

66. A, AP radiograph of the knee in a 2-year-old girl with rickets shows generalized osteopenia and widening of the metaphyses of the proximal tibia and fibula. B, AP radiograph of
the wrist in another child with rickets shows generalized osteopenia, as well as widening and irregularity of the metaphyses of the distal radius and ulna.

67. Rickets in a young child with growth plate widening and irregularity in the wrist (A) and knees (B). Note the small epiphyses in the knees.

68. Rachitic rosary. (A) and lateral (B) radiographs of the chest showing prominence of the costochondral junctions (arrows).

69. Vitamin D-resistant rickets in a 1-year-old child. (A) AP radiograph of the knees showing irregularity and widening of the growth plates. The epiphyses are
small and irregular as well. (B) Three years after high-dose vitamin D therapy, the knees appear normal. There is residual femoral bowing.

71. HOW DO WE TREAT?

72. HYPERPARATHYROIDISHYPERPARATHYROIDIS
MM

73. HYPERPARATHYROIDISHYPERPARATHYROIDIS
MM
• Primary
– Parathyroid adenoma
• Secondary
– chronic renal insufficiency.
Hyperparathyroidism may result in either bone
resorption or bone formation, bone resorption
usually dominates.

75. Radiologic findings ofRadiologic findings of
HYPERPARATHYROIDISMHYPERPARATHYROIDISM
• The M/C radiologic abnormality is generalized
osteopenia.
• Bone resorption, bone sclerosis, brown tumors,
chondrocalcinosis, soft tissue calcification, and
vascular calcification.
• Brown tumors appear as well-defined lytic lesions.
– After resection of parathyroid adenomas, the lesions may
become sclerotic and may mimic blastic metastasis.
• Bone resorption, the most characteristic finding, is
usually classified as
– subchondral, trabecular, endosteal, intracortical,
subperiosteal, subligamentous, and subtendinous.

77. Radiologic findings ofRadiologic findings of
HYPERPARATHYROIDISMHYPERPARATHYROIDISM
• Subperiosteal resorption - M/C
– Usually occurs in the hands and feet.
– M/C affected site: radial aspects of the middle phalanges.
– Acro-osteolysis or phalangeal tufts resoption may also be
present.
• Trabecular resorption
– Often seen in the diploic space of the skull, where it has a
characteristic salt and pepper appearance.
• Subchondral resorption
– May be seen in the sacroiliac joints, sternoclavicular joints,
acromioclavicular joints, symphysis pubis, and discovertebral
junction .

78. AP radiograph of the hand in a 66-year-old woman with primary hyperparathyroidism owing to parathyroid adenoma shows subperiosteal bone
resorption ( arrows) along the radial aspect of 2nd, 3rd, and 4th middle phalanges.

80. AP radiograph of the knee in a child with hyperparathyroidism shows subperiosteal bone resorption ( arrow) along the proximal medial tibia.

81. Lateral radiograph of the skull in a 23-year-old man with secondary hyperparathyroidism shows trabecular resorption of the diploic space ("salt and pepper" appearance).

83. Dental radiograph in another child with hyperparathyroidism shows resorption ( arrow) of the lamina dura of the mandible.

84. Radiologic findings ofRadiologic findings of
HYPERPARATHYROIDISMHYPERPARATHYROIDISM
SecondarySecondary
• Bony sclerosis; focal
or generalized.
• Rugger-jersey
appearance of
spine.
• Soft tissue and
vascular
calcification.
PrimaryPrimary
• Chondrocalcinosis
• usually seen in the
menisci of the
knee, the
triangular
fibrocartilage of
the wrist, and the
pubic symphysis

85. AP radiograph of the wrist in an 83-year-old woman with primary hyperparathyroidism shows
chondrocalcinosis ( arrow) of the triangular fibrocartilage.

87. Secondary HPT. Radiograph of the pelvis and hips showing diffuse osteosclerosis.

88. A, AP radiograph of the spine in a patient with secondary hyperparathyroidism shows generalized bone sclerosis, small kidneys, and left renal calculi. B, Lateral radiograph of the lumbar spine
in another patient with secondary hyperparathyroidism shows horizontal, bandlike ("rugger jersey") sclerosis of the vertebral bodies ( arrows).

90. AP radiograph of the hand in a 50-year-old man with renal osteodystrophy shows acro-osteolysis ( short arrows), subperiosteal bone
resorption ( long arrows), and vascular calcifications.

91. Secondary HPT. Radiograph of the hand showing resorption of the first to third tufts with soft tissue calcification (1). There is articular
calcification (2), and subperiosteal and subligamentous resorption (3).

92. The differential diagnosis ofThe differential diagnosis of
HYPERPARATHYROIDISMHYPERPARATHYROIDISM
• Focal subperiosteal resorption involving a single bone
– Neoplasms or osteomyelitis.
• Bone sclerosis in patients with secondary
hyperparathyroidism.
– Metastatic disease, radiation-induced bone disease,
hypoparathyroidism, myelofibrosis, mastocytosis, sickle-cell
disease, and Paget's disease.
• Chondrocalcinosis
– Pyrophosphate arthropathy (CPPD) or hemochromatosis.
• Brown tumors
– includes other focal lytic lesions, such as giant cell tumor
and fibrous dysplasia.

93. TREATMENT
1. Management of acute hypercalcemia by
rehydration with normal
saline,bisphosphonates,haemodialysis.
2. Medical line : -Monitor serum creatinine
levels and calcium levels every 6
months.DEXA scan on an annual basis.
-Avoid thiazide diuretics.
-Maintain high oral fluid intake.
-Improving bone mineral density and
achieving calcium homeostasis by
calcimimetics and HRT.

94. 3. Surgery : -Is indicated in patients
with complications and in younger
age group.
-Minimally invasive surgery to excise
solitary adenoma,
Subtotal parathyroidectomy in case
of diffuse hyperplasia are being done.

95. SECONDARY
HYPERPARATHYROIDISM
• It occurs when PTH secretion is increased to
compensate for prolonged hypocalcemia.
• It is seen in patients with chronic renal
failure where the failing kidneys do not
convert vitamin D to its active form and
they do not excrete phosphate.
Excess phosphate combines with calcium to
form calcium phosphate.
• Both processes lead to hypocalcemia,cause
hyperplasia of all parathyroid tissue and
hence secondary hyperparathyroidism.

97. • Secondary hyperparathyroidism can
also result from malabsorption of
vitamin D due to chronic
pancreatitis,small bowel
disease,bariatric surgery.
• CLINICAL FEATURES : are mostly
of renal failure.If it is due to vitamin D
deficiency,limb
deformities,pathological fractures
occur.

98. • INVESTIGATIONS : Serum calcium levels are
low.PTH levels are raised. Phosphate levels
depend on etiology (e.g. high in renal disease,
low in vitamin D deficiency).
Radiology shows evidence of bone disease.
• TREATMENT : Medical line is the mainstay.
The underlying condition needs to be
treated
-correcting vitamin D deficiency.
-treatment of chronic kidney disease
(Calcium supplementation.
Treatment with vitamin D and its analogues.
Calcimimetics)

99. TERTIARY
HYPERPARATHYROIDISM
• In a small proportion of cases of
secondary
hyperparathyroidism,continuous
stimulation of the parathyroids results in
adenoma formation and unregulated PTH
secretion.
• Even correction of the underlying cause
will not stop excess PTH secretion i.e
parathyroid gland hypertrophy becomes
irreversible.

100. • CLINICAL FEATURES : Symptoms and
signs are due to hypercalcemia so
presentation is similar to primary
hyperparathyroidism.
• INVESTIGATIONS : Serum calcium and
PTH levels are raised.
Phosphate levels are often high.
• TREATMENT : Total or subtotal
parathyroidectomy is the recommended
treatment.
Autotransplantation of parathyroid tissue in
the forearm is also commonly carried out.

101. THANK YOU