includes the basics of Calcium, its metabolism & disorders associated with Calcium excess and deficiency

1. Good morning!!!
‘LOVE IS BLIND
BUT FRIENDSHIP CLOSES IT’S EYES’
PROVERB

2. Calcium Metabolism &
Disorders
Prepared by,
Dr.Sachin Sunny Otta
1st yr MDS
Rajarajeswari dental
college & hospital,
Bangalore
2

3. CONTENTS
• Introduction
• Flashback Of Calcium
• Properties,occurrence,source & RDA Of Calcium
• Ca:p Ratio
• Functions Of Calcium
• Absorption Of Of Calcium
• Concept Of Calcium Balance
• Factors Controlling Absorption Of Calcium
• Other Hormones Affecting Calcium Metabolism
• Excretion Of Calcium
• Ca-p Imbalance
• Hypocalcemia
• Hypercalcemia
• Dental Considerations
• Conclusion
• Bibliography
3

4. INTRODUCTION
METABOLISM
• It is defined as the chemical and physical process in
an organism by which protoplasm is produced,
sustained, and then decomposed to make energy
available.
• It is the biochemical modification of chemical
compounds in living organisms and cells that
includes the biosynthesis of complex organic
molecules (anabolism) and their breakdown
(catabolism).
Cline J. Calcium and vitamin d metabolism,
deficiency, and excess.
Topics in companion animal medicine. 2012
Nov 30;27(4):159-64.
4

5. • Principal Minerals include - Calcium,
Phosphorous,Magnesium, Sodium, Potassium
and Sulphur.
• Calcium and phosphorous individually have
their own functions and together they are
required for the formation of hydroxyapatite
and physical strength of the skeletal tissue.
5

6. FLASHBACK OF CALCIUM
• Latin- calx or calcis meaning “lime”
• Known as early as first century when ancient
Romans prepared lime as calcium oxide.
• Isolated in 1808 by Englishman
Sir Humphrey Davy through the
electrolysis of a mixture of
lime (CaO) and mercuric oxide (HgO).
• In 1883 Sir Sydney Ringer
demonstrated the biological significance
of calcium.
Sir Humphrey Davy
6

7. PROPERTIES OF CALCIUM
• Fifth most abundant element in Earth´s crust
• Essential for living organisms
• Soft grey alkaline earth metal
• Symbol ‘Ca’
• Atomic Number: 20
• Atomic weight : 40 g/mol
• Single oxidation state : +2
7

8. OCCURRENCE OF CALCIUM
In nature:
• Does not exist freely
• Occurs mostly in soil systems as
limestone (CaCO3), gypsum(CaSO4*2H2O) & fluorite (CaF2)
In the body:
• The most abundant mineral
• Average adult body contains approximately 1 kg
• 99% of total body’s calcium is in the bone.
• 1% in ICF, ECF, & cell membranes.
• Calcium weight is 400mg/kg in infant & 950mg/kg in adult.
8

9. 2.25 – 2.75mmol/l 10 mmol/l
9

10. PLASMA CALCIUM
LEVELS
Diffusible:
• 50% Ca 2+ ionized
• 10% combined with anions
(citrate, phosphate)
Nondiffusible:
• 40% combined with
plasma proteins
10

11. Sources
11

12. RECOMMENDED CALCIUM INTAKE
(RDA)
Age Amount of calcium (per day)
Infants
• Birth to six months 400mg
• 6 months to 1 year 600mg
Children / young adults
• 1 – 10 years 800 – 1200mg
• 11 – 24 years 1200 – 1500mg
12

13. Adult women
• Pregnant and lactating 1200 – 1500mg
• Over 65 yrs old 1500mg
Adult men
• 25 – 64 yrs old 1000mg
• Over 65 yrs old 1500mg
13

14. CALCIUM PHOSPHATE RATIO
• Calcium : Phosphate ratio normally is 2:1.
• Increase in plasma calcium levels causes
corresponding decrease in absorption of phosphate.
• This ratio is always constant.
The serum level of calcium is closely regulated with
normal total calcium of 9-10.5 mg/dL and normal
ionized calcium of 4.5-5.6 mg/dL.
SERUM PHOSPHATE LEVELS
Children - 4 to 7 mg/dL
Adults - 3 to 4.5 mg/dL
14

15. FUNCTIONS OF CALCIUM
• STRUCTURAL FUNCTION: Supporting material in
bones. Present as calcium phosphate.
• SIGNALLING FUNCTION: Intracellular calcium
functions as a second messenger for the secretion of
some hormones and neurotransmitters.
• ENZYMATIC FUNCTION: Calcium acts as a
coenzyme for clotting factors
• TRANSMISSION FUNCTION:Calcium also causes
the release of Acetylcholine from pre-synaptic
terminals in the transmission of nerve impulses.
• MUSCULAR FUNCTION:Also acts as an
intracellular permeation regulator and mediator of
muscle contraction.
15

16. EXTENDED FUNCTIONS OF
CALCIUM
16

17. ABSORPTION OF CALCIUM
• Calcium is taken through dietary sources as
Calcium Phosphate, Carbonate, Tartrate and
Oxalate.
• It is absorbed from the gastrointestinal tract
into blood and distributed to various parts of
the body
• Two mechanisms have been proposed for the
absorption ofcalcium by gut mucosa:
1. Simple Diffusion.
2. An active transport process, involving energy
and calcium pump.
17

18. • While passing through the kidney, large
quantity of calcium is filtered in the
glomerulus.
• From the filtrate, 98 to 99% of calcium is
reabsorbed in the renal tubules into blood and
only small quantity is excreted through urine.
• In the bone, the calcium may be deposited or
resorbed depending upon the level of calcium
in the plasma.
18

19. 19

20. CONCEPT OF CALCIUM
BALANCE
• Defined as the net gain or loss of calcium by
the body over a specified period of time
• Calculated by deducting calcium in faeces and
urine from the calcium taken in diet.
• Positive calcium balance in growing children
• Negative calcium balance in aging adults.
20

21. FACTORS CONTROLLING
ABSORPTION OF CALCIUM
1. Those Acting On The Mucosal Cells: Vitamin D,
Pregnancy and Growth, PTH, Calcitonin
2. Those affecting the Availability Of Calcium And
Phosphates In The Gut:
• pH of the intestine
• Amount of dietary calcium and phosphates
• Phytic acid and Phytates
• Oxalates
• Fats
• Proteins and amino acids
• Carbohydrates
• Bile salts 21

22. Factors Acting On The Mucosal Cells
• Vitamin D
• Pregnancy & Growth
• PTH
• Calcitonin
22

23. VITAMIN-D
CALCITRIOL (1,25-DHCC)
• It is the biologically active form of Vit-D.
• It regulates plasma levels of Ca and P.
• Calcitriol acts at 3 different levels: intestine, kidney,
bones
Action on Intestine:
• It increases the intestinal absorption of Ca & P in the
intestinal cells. Calcitriol binds with a cytosolic receptor
to form a calcitriol-receptor complex
• This complex then approaches the nucleus and interacts
with a specific DNA leading for synthesis of Ca binding
protein
• This protein increases the Ca uptake by intestine 23

24. Calbindin is a vitamin D-dependent calcium-binding
protein inside intestinal epithelial cells which functions
together with TRPV6 (Transient Receptor Potential
Vanilloid 6) and Calcium pumps (PMCA1- plasma
membrane Ca ATPase pump) in the basal
membrane to actively transport calcium into the body
Action on bone:
• In the osteoblasts of bone Calcitriol stimulates Ca uptake for
deposition as CaPo4
Action on kidney:
• It is involved in minimizing the excretion of Ca & P through
kidney by decreasing their excretion and enhancing
reabsorption
24

25. PREGNANCY AND
GROWTH
• During later stages of pregnancy,
greater amount of calcium absorption is seen.
• 50% of this calcium is used for the development of fetal
skeleton and the rest is stored in the bones to act as a
reserve for lactation.
• This is due to the increased level of placental lactogen
and estrogen which stimulates increased hydroxylation
of vitamin D.
• In growth there is a increased level of growth hormone.
GH acts by increasing calcium absorption.
• It also increases the renal excretion of calcium and
phosphates.
25

26. PARATHYROID HORMONE
• Parathyroid hormone is one of the main hormones
controlling Ca+2 absorption.
• It mainly acts by controlling the formation of Vit. D,
which is responsible for increased Ca+2 absorption.
• Parathormone inhibits renal phosphate re-absorption in
the proximal tubule and therefore increases phosphate
excretion
• Parathormone increases renal Calcium re-absorption in
the distal tubule, which also increases the serum calcium.
Net effect of PTH ↑ serum calcium
↓ serum phosphate
26

27. Stimulation For PTH Secretion:
• Low level of calcium in plasma.
• Maximum secretion occurs when plasma
calcium level falls below 7mg/dl.
• When plasma calcium level increases to
11mg/dl there is decreased secretion of PTH
27

28. CALCITONIN
• Also called as thyrocalcitonin.
• Molecular weight: 3400
• Plasma concentration :10-20ug/ml
• Minor regulator of calcium & phosphate
metabolism
• Secreted by parafollicular cells or C-cells of
thyroid gland.
28

29. Action Of Calcitonin:
• Net effect of calcitonin :Decreases Serum Ca
• Target site
-Bone (suppress osteoclasts)
-Increasing Calcium Excretion through urine
Opposing action to PTH
Calcitonin is a Physiological Antagonist to PTH with respect to
Calcium.
With respect to Phosphate it has the same effect as PTH i.e.
↓ Plasma Phosphate level by inhibiting re-absorption .
29

30. FAST SHORT
TERM
REGULATION –
Deposition &
Resorption from
skeletal system
LONG TERM
REGULATION –
Absorption from gut
& removal via feces
30

31. FACTORS AFFECTING AVAILABILITY OF
CALCIUM AND PHOSPHATES IN GUT
• pH of the intestine
• Amount of dietary calcium
and phosphates
• Phytic acid and Phytates
• Oxalates
• Fats
• Proteins and amino acids
• Carbohydrates
• Bile salts
31

32. ph of Intestine:
• Acidic pH in the upper intestine (deodenum)
increases calcium absorption by keeping
calcium salts in a soluble state(Ca 2+).
• In lower intestine, since pH is more alkaline,
calcium salts undergoes precipitation
32

33. Amount of dietary calcium and phosphates:
• Increased level of calcium and phosphate in
diet increases their absorption however up to a
certain limit.
• This is because the active process of their
absorption can bear with certain amounts of
load beyond which the excess would pass out
into faeces
33

34. Phytic acid and phytates:
• They are present in oatmeal, meat and cereals and
are considered anti-calcifying factors as they
combine with calcium in the diet thus forming
insoluble salts of calcium thus decreasing
absorption
Fats:
• They combines with calcium and form insoluble
calcium,thus decreasing calcium absorption.
Oxalates:
• They are present in spinach and green leafy
vegetables. They form oxalate precipitates with
calcium present in the diet thus decreasing their
availability.
34

35. Bile salts:
• They increases calcium absorption by promoting
metabolism of lipids.
Protein and amino acids:
• High protein diet increases calcium absorption as
protein forms soluble complexes with calcium and
keeps calcium in a form that is easily absorbable.
Carbohydrates:
• Certain carbohydrates like lactose increases calcium
absorption by creating the acidity in the gut as they
favors the growth of acid producing bacteria.
35

36. EFFECTS OF OTHER HORMONES ON
CALCIUM METABOLISM
• Growth Hormone
• Insulin
• Testosterone & Other Hormones
• Lactogen & Prolactin
• Steroids
• Thyroid Hormones
36

37. Growth Hormone:
• Increases the intestinal absorption of calcium
and increases its excretion from urine
• Stimulates production of insulin like growth
factor in bone which stimulates protein
synthesis in bone
• Stimulates somatomedian C which acts on
cartilage to increase the length of bones
37

38. Testosterone:
• Testosterone causes differential growth of
cartilage resulting to differential bone
development
• Acts on cartilage & increase the bone growth.
Insulin:
• It is an anabolic hormone which favors bone
formation
38

39. Thyroid Hormone:
• In infants - stimulation of bone growth
• In adults - increased bone metabolism
- increased calcium mobilization
Glucocorticoids:
• Anti vitamin D action: decreases absorption of
calcium in intestine
• Inhibit protein synthesis and hence decrease
bone formation
• Inhibit new osteoclast formation & decrease the
activity of old osteoclasts.
39

40. EXCRETION OF CALCIUM AND
PHOSPHOROUS
• Calcium is excreted in the Urine, Bile,Sweat
and Digestive secretions.
• The renal threshold for serum Ca is 10 mg/dl.
40

41. PHOSPHOROUS EXCRETION
• Phosphorous is excreted primarily through the
urine.
• Almost 2/3rd of total phosphorous that is
excreted is found in the urine as phosphate of
various cations
• Phosphorous found in the faeces is the non-
absorbed form of phosphorous.
41

42. CALCIUM -PHOSPHORUS IMBALANCE
INCREASED SERUM Ca:
• Hyperparathyroidism.
• Hypervitaminosis (Vit. D)
• Multiple myeloma (breakdown of bone)
• Sarcoidosis (uncontrolled synthesis of Vit.D3)
• Thyrotoxicosis (thyroid hormone affect bone
metabolism)
• Milk alkali syndrome : intake of too much of Ca &
absorbable alkali (common sources- dietary
supplements taken to prevent osteoporosis & antacids)
• Infantile hypercalcemia (William`s Syndrome)
42

43. DECREASED SERUM Ca:
• Renal failure.
• Hypoparathyroidism.
• Vit. D deficiency.
• Tetany.
• Malabsorption syndrome.
43

44. 44

45. HYPOPARATHYROIDISM
• Results from a deficiency in or absence of PTH.
• Hypocalcemia and Hyperphosphatemia and is
often associated with chronic Tetany.
• Hypoparathyroidism usually results from the
accidental removal of or damage to several
parathyroid glands during thyroidectomy.
• Transient hypoparathyroidism is common after
subtotal thyroidectomy.
• Permanent hypoparathyroidism occurs in fewer
than 3% of expertly performed thyroidectomies.
45

46. Causes:
• Accidental removal of gland during surgery
occasionally from autoimmune destruction of the
gland.
• Congenital absence of the gland
• Atrophy of the gland-Idiopathic
• Pseudohypoparathyroidism
Clinical Features:
• Short stature
• Short metacarpal or
metatarsal bones
• Mental retardation
46

47. Oral Manifestations:
• Enamel hypoplasia and dental dysplasia
• Dryness of the mucous membranes
• Angular cheilitis
• Circumoral parasthesia
• Disturbances in tooth eruption
• Root defects
• Hypodontia and impacted teeth
• Large pulp chambers
• Thickening of the lamina dura observed in the
permanent teeth.
47

48. Radiographic features:
• Enamel hypoplasia
• External root resorption
• Delayed eruption
• Root dilaceration
48

49. PSEUDOHYPOPARATHYROIDISM
• It is the result of defective G protein in kidney and
bone, which causes end-organ resistance to PTH.
• There is hypocalcemia and hyperphosphatemia that is
not correctable by administration of exogenous PTH.
• Circulating endogenous PTH levels are elevated.
49

50. Management:
• Administration of extremely large quantities of
vitamin D, to as high as 100,000 units per
day,along with intake of 1 to 2 grams of
calcium, keeps the calcium ion concentration
in a normal range.
50

51. OTHER CAUSES OF HYPOCALCEMIA
1.VITAMIN D DEFICIENCY
• It is an important cause of hypocalcemia.
• Vitamin D deficiency may result from inadequate
dietary intake or decreased absorption due to
hepato-biliary disease or intestinal malabsorption.
• It can also occur because of alterations in vitamin
D metabolism as occurs with certain drugs
(phenytoin, phenobarbital, and rifampin) or lack
of skin exposure to sunlight.
• The latter is an important cause of acquired
vitamin D deficiency in northern climates among
people wearing dress that covers them completely.
51

52. 2.RENAL TUBULAR DISEASE
• Including Fanconi's syndrome due to
nephrotoxins such as heavy metals and distal
renal tubular acidosis, can cause severe
hypocalcemia due to abnormal renal loss of Ca
and decreasing renal conversion to active
vitamin D.
52

53. 3.MAGNESIUM DEPLETION
• Occurring with intestinal malabsorption or dietary deficiency
can cause hypocalcemia.
• Relative PTH deficiency and end-organ resistance to its action
occur with magnesium depletion, resulting in plasma
concentrations of < 1.0 mEq/L (< 0.5 mmol/L)
• Replenishing Magnesium can improve calcium level in body
4.ACUTE PANCREATITIS
• Causes hypocalcemia when Ca is chelated by lipolytic
products released from the inflamed pancreas
53

54. 5.HYPOPROTEINEMIA
(Factitious Hypocalcemia)
• Reduced protein-bound fraction of plasma Ca.
• Hypocalcemia due to diminished protein
binding is asymptomatic.
• The ionized Ca fraction is unaltered
6.HYPERPHOSPHATEMIA
• Also causes hypocalcemia by one or a variety of
poorly understood mechanisms.
• Patients with renal failure and subsequent
phosphate retention are particularly prone to this
form of hypocalcemia
54

55. 7.SEPTIC SHOCK
• May be associated with hypocalcemia due to
suppression of PTH release and conversion of
25(OH)D3 to 1,25(OH)2D3.
8.DRUGS
• Associated with hypocalcemia include those
generally used to treat hypercalcemia
anticonvulsants (phenytoin, phenobarbital) and
rifampin, which alter vitamin D metabolism.
55

56. SYMPTOMS
56

57. 57

58. Manifestations of
Hypocalcemia
58

59. RICKETS
• Occurs in children between 6 months to 2
years of age.
• Affects long bones
• Lack of calcium causes failure of
mineralization resulting into formation of
cartilagenous form of bone.
• Most critical area that gets affected is the
central endochondral ossification at the
epiphyseal plates.
59

60. Clinical features:
60

61. Radiographic features:
Cupping of proximal
tibia Bowing of lower
limbs
Cupping of metaphysis of
distal radius/ulna
Flaring of metaphysis
61

62. Oral Manifestations:
• Developmental abnormalities of dentin and enamel
• Delayed eruption
• Misalignment of teeth in the jaw
• High caries index
• Enamel hypoplasia
62

63. TYPES OF RICKETS:
1) Nutritional Rickets
2) Vitamin D Resistant Rickets.
3) Vitamin Dependent Rickets.
4) Oncogenous Rickets.
63

64. NUTRITIONAL RICKETS
• Primarily, Vitamin D deficiency due to poor dietary
intake
* Vegetarian diet(cereals, vegetables, fruits).
* Non-Vit.D supplimented formulations for children.
• Children with chronic diarrhea or malabsorption
disorders, e.g cystic fibrosis.
• Exclusive breast-fed infants, in mothers with poor
UV light exposure or mothers with vit D deficiency
• Dark skin infants at higher risk.
• Premature infants on parenteral nutrition.
64

65. VITAMIN D RESISTANT RICKETS
• Also referred as X-linked hypophosphatemia.
• Non-nutritional rickets.
• Some mothers of affected siblings manifest the
disease features.
• Autosomal dominant and sporadic case may occur.
• Defect in the proximal tubular reabsorption of
phosphate.
• Defect in conversion of 25-(OH)D to 1,25D(OH)
• Abnormal gene in this disorder is on X-
chromosome 22p(PHEX) or Phosphate regulating
gene.
65

66. Clinical Features:
• Rachitic rosary
• Tetany
• Genu Varum (Bow Leggedness)
RACHITIC ROSARY
66

67. Radiographic findings:
• Metaphyseal widening and fraying.
• Cupping of metaphysis of proximal and distal
tibia,distal femur, radius and ulna
• Dental radiographs reveal hypocalcification of teeth
and the presence of large pulp chambers and alveolar
bone loss.
Cupping of metaphysis of
proximal and distal tibia 67

68. Oral manifestations:
• Histological evidence of widespread formation of
globular, hypocalcified dentin, with clefts and tubular
defects occuring in the region of pulp horns.
• Periapical involvement of grossly normal appearing
deciduous and permanent teeth, followed by the
development of multiple gingival fistulas.
• Abnormal cementum and the alveolar bone pattern
• Lamina dura is frequently absent or poorly defined
68

69. VITAMIN D DEPENDENT RICKETS
• Pseudo vitamin D deficiency
• Two types exist:
Type 1.( VDDR1): deficiency of renal 25(OH)D-
1 alpha-hydroxylase
Type 2.(VDDR2): intracellular Vit.D receptor
defect
69

70. ONCOGENOUS RICKETS
(Primary hypophosphatemic Rickets)
• Rickets due to a mesenchymal tumor .
• Mostly benign.
• Occur in sites difficult to detect.e.g nasal antrum,
pharynx,small bones of the hands etc.
• May be associated with other syndromes like
Neurofibromatosis.
• They elaborate massive amounts of F6F23
gene,which impairs hydroxylation of 25-(OH)D
• Also impairing Phosphate reabsorption.
• Remission occurs on tumor excision.
70

71. Management of Rickets:
Treatment:
• Oral therapy:
Vitamin D - 0.5-1g/24 hr for children 2-4 yrs
- 1-4g/24 hr for children > 4 yrs.
• Corrective osteotomy for deformed limbs should be delayed till
radiological healed rickets is noted and serum alkaline phosphatase
levels are normal. 71

72. 72

73. OSTEOMALACIA
• Bone defect in adults
• Common cause is Vit.D deficiency.
• Also due to excessive resorption of bones in
hyperparathyroidism.
• Softening of bones due to defective
mineralization (Ca and PO4).
73

74. Main causes:
• Inadequate Ca absorption
• Phosphate deficiency due to renal loss
Other causes:
• Renal tubular acidosis
• Malabsorption syndrome.
• Malnutrition during pregnancy.
• Hypophosphatemia.
• Tumor induced osteomalacia.
• Drugs-anticonvulsants, anti TB, Steroids,
glucocorticoids
74

75. Clinical features:
• Pain and Chronic fatigue, starting insidiously.
• Proximal muscles weakness.
• Waddling gait.
• Deformed pelvis and exaggerated lordosis.
• Bowing of Lower limbs
• Biochemical features are similar to Rickets except
in renal osteodystrophy where serum phosphate is
high.
75

76. Radiographic features:
• Pseudofractures - Common on scapula, medial
femoral cortex and pubic rami.
• Biconcave vertebral bodies.(fish vertebra)
• Femoral neck fractures.
76

77. Lab Investigations:
77

78. TETANY
A condition marked by intermittent
muscular spasms, caused by malfunction
of parathyroid gland and a consequent deficiency of
calcium.
Clinical features:
• Paresthesias of the lips,tongue, fingers and feet
• Carpopedal spasm, which may be prolonged and
painful
• Generalized muscle aching
• Spasm of facial musculature.
• Latent tetany generally occurs at less severely
decreased plasma Ca concentrations: 7 to 8 mg/dL
(1.75 to 2.20 mmol/L). 78

79. • CHVOSTEK’S SIGN
79

80. • TROUSSEAU’S SIGN (ACCOUCHER’S
HAND or OBSTETRICIAN HAND)
80

81. TREATMENT OF HYPOCALCEMIA
81

82. 82

83. HYPERCALCEMIA
83

84. HYPERCALCEMIA
• Elevated serum calcium level up to 12- 15
mg/dl
Conditions leading to hypercalcemia:
• Hyperparathyroidism
• Acute osteoporosis
• Thyrotoxicosis
• Vitamin D intoxication
84

85. SYMPTOMS
85

86. CAUSES OF HYPERCALCEMIAA) PTH related
i) Primarily hyperparathyroidism
a) Solitary adenoma
b) Multiple endocrine neoplasia
ii) Lithium therapy
iii) Familial hypocalcuric hypercalcemia
B) Vit D related
i) Vit D intoxication
ii) Increased 1,25 DHCC, sarcoidosis.
iii) Idiopathic hypercalcemia of infancy
C) Malignancy related
i) Solid tumor with metastasis
ii) Solid tumor with humoral mediation of hypercalcemia
D) Associated with High bone turn over
i) Hyperthyroidism
ii) Immobilization
iii) Thiazide
E) Association with renal failure
i) Severe secondary hyperparathyroidism
ii) Milk alkali syndrome
86

87. HYPERPARATHYROIDISM
• Primary hyperparathyroidism
• Secondary hyperparathyroidism
• Tertiary hyperparathyroidism
87

88. PRIMARY
HYPERPARATHYROIDISM
• Tumor of one of PTH gland – Single adenoma
• Adenomas are located at inferior portion of
parathyroid gland
• Mostly seen in women than men & children
• Extreme osteoclastic activity in bones
• Elevates Ca ion concentration in ECF which
depresses phosphate ions.
88

89. Multiple Endocrine Neoplasia:
MEN I (Wermer's syndrome)
• Consists of hyperparathyroidism and tumors of
pituitary and pancreatic islet cells, often
associated with peptic ulcer and gastric
hypersecretion (Zollinger – Ellison syndrome)
MEN II - Carcinoma of the thyroid
89

90. Oral Manifestations:
• Dehydration
• Mandibular or maxillary tumors of the bone, which
on biopsy display a Brown tumor of von
Recklinghausen
• Increased incidence of tori
• Reduction in cortical bone content leading to
osteoporosis
90

91. Radiographic features:
• Normal trabecular pattern is lost & replaced by
granular or ground glass appearance.
• Moth-eaten like appearance of jaw bones
• Teeth are mobile and migrate.
MOTH EATEN
APPERANCE
91

92. Brown Tumor
• Bone lesion due to increased osteoclastic activity
(hyperparathyroidism)
• Results in disorders of bone and mineral metabolism.
• Diffuse and focal lesions may arise in multiple bones &
may mimic true neoplasm
• On occasion, a patient with undiagnosed
hyperparathyroidism presents with a lytic lesion that may
be mistaken for a tumor.
• These lesions are termed
"Brown Tumors" due to
the presence of old hemorrhage
in the lesion.
92

93. Rib is expanded by a brown tumor. The mass
is reddish brown, well circumscribed, and
delineated into multiple nodules by
numerous septa
Primary hyperparathyroidism
having multiple Brown tumors
mimicking malignancy
93

94. Osteitis Fibrosa Cystica
• The unique bone involvement in hyperparathyroidism
is osteitis fibrosa cystica.
• In the past osteitis fibrosa cystica occurred in 10 to 25
percent of patients with hyperparathyroidism.
• Histologically the pathognomonic features are :
1. Reduction in the number of trabeculae and increase in
the giant multinucleated osteoclasts in scalloped areas
on the surface of the bone. (Howship’s lacunae)
2. Replacement of the normal cellular and marrow
elements by fibrous tissues.
3. Loss of lamina dura of the teeth is less specific.
4. Tiny “punched out” lesions may be present in the
skull, producing the so called salt and pepper
appearance. 94

95. Salt And Pepper Appearance
95

96. SECONDARY
HYPERPARATHYROIDISM
• Excessive secretion of PTH in response to
hypocalcemia & associated hyperplasia of
gland.
• Often seen in Vitamin D deficiency,Chronic
renal disease, Hypocalcemia &
hyperphosphatemia
• Management: Attention to underlying
cause,Dietary restriction of
phosphorous,calcium,vitamin D & Extended
Release Calcifediol
96

97. TERTIARY
HYPERPARATHYROIDISM
• Parathyroid tumor develop from long standing
secondary hyperparathyroidism.
• When SHPT is corrected & parathyroid gland
remain hyper functioning, it become Tertiary
Hyperparathyroidism
• Management : surgical removal of three & one
half of parathyroid gland.
97

98. TREATMENT OF
HYPERCALCEAMIA
• Reduction of dietary Calcium & Vitamin D
intake
• Bisphosphonates therapy
• Calcitonin i.m or s.c
• Xgeva(Denosumab) for malignancy refractory
to bisphosphonate therapy
• Surgical – Parathyroidectomy
98

99. 99

100. DENTAL CONSIDERATIONS
HYPERPARATHYROIDISM
• The clinical management of these patients does not require
any special consideration.
• Higher risk of bone fracture : take precaution in surgical
treatments.
HYPOPARATHYROIDISM
• These patients have more susceptibility to caries because of
dental anomalies.
• Dental management will be the prevention of caries with
periodic reviews, advice regarding diet and oral hygiene
instructions.
• Before performing dental treatment, serum calcium levels
should be determined. They must be above 8mg/100ml to
prevent cardiac arrhythmias, seizures, laryngospasms or
bronchospasms. 100

101. THE
CONCLUSION
Disturbances in calcium and phosphate intake,
excretion and trans cellular shift result in deranged
metabolism accounting for abnormal serum levels.
As a result of the essential role played by these
minerals in intra and extracellular metabolism, the
clinical manifestations of related disease states are
extensive.
Thus, an understanding of the basic mechanism of
calcium, phosphate metabolism and pathophysiology
of various related disorders is helpful in guiding
therapeutic decisions.
101

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102

103. 103