1. CALCIUM AND PHOSPHATE
METABOLISM
Karishma.S
II MDS

2. CONTENTS
• INTRODUCTION
• IMPORTANT MINERALS
• CALCIUM & PHOSPHOROUS METABOLISM
• HORMONES INVOLVED IN CALCIUM AND PHOSPHATE HOMEOSTASIS
• APPLIED ASPECTS
• SUMMARY
• CONCLUSION
• REFERENCES

3. IMPORTANT MINERALS
Macro Elements
Calcium
Magnesium
Phosphorus
Sodium
Potassium
Chloride
Sulfur
Trace Elements
Iron
Iodine
Copper
Manganese
Zinc
Molybdenum
Selenium
Fluoride
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.

4.  Most abundant mineral in many animals and in the
human body.
 Ancient Romans prepared lime- calcium oxide. 975 AD
-plaster of Paris (calcium sulfate)was used for setting
broken bones.
 Sir Humphry Davy Isolated calcium(1808)
Calcium

5. It is the second most abundant essential mineral in the human
body after calcium.
In human body Phosphorus is present as phosphates (compounds
containing the phosphate ion, PO4
−3
)
 The first form of elemental phosphorus to be produced was white
phosphorus, in 1669 by Greek .
Hennig Brand(1669) discovered.
PHOSPHORUS

6. ROLE OF CALCIUM IN BODY
 Affects nerve and muscle physiology
 Intracellular signal transduction pathways.
 Co-factor in blood clotting cascade.
 Constituent of bone and teeth.
 Major structural element in the vertebrate skeleton (bones and teeth) in the
form of calcium phosphate (Ca10(PO4)6(OH)2 known as hydroxyapatatite
 Maintain all cells and connective tissues in the body.
 Essential component in production of enzymes and hormones that regulate
metabolism

7. ROLE OF PHOSPHATE
 Key constituent of bone and teeth.
 Component of intra cellular buffering. Forms energy rich bonds in ATP.
 Forms co-enzymes.
 Regulates blood and urinary pH.
 Forms organic molecules like DNA & RNA
 Cellular energy metabolism.
 Constituent of macro molecules like nucleic acids, phospholipids and
phosphoproteins.

8. DISTRIBUTION
1000-1500gm
(1.5% of the body weight)
99%
Bones
1%
ECF
Plasma
500-800gm
80-90%
Bones
Teeth
10%
RBC
Plasma
Total calcium Total phosphorus

9. PLASMA CALCIUM AND PHOSPHATE
Normal plasma levels
9-11mg/dl(calcium)
Normal plasma levels
2.5-4.5mg/dl(phosphorous)
Ionized Unionized
( 5 mg/dl) (4mg/dl)
organic Inorganic
(0.5-1mg/dl)
(Adults:3-4mg/dl)
(children:5-6mg/dl)

10. 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.

11. Best source
Hard cheese
Milk
Dark green leafy vegetables
Good source
Ice-cream
Broccoli
Baked beans
Dried legumes
Dried figs
Fair source
String beans
Eggs
Bread
RDA OF CALCIUM
Average adult-800 mg/ day
Infants: <1yr- 360-540mg
1-10yr- 800mg
11-18yr- 1200mg
During pregnancy & lactation-1200mg/ day
SOURCES OF CALCIUM

12. Rich source
Milk
Meat
Fish
Poultry
Eggs
Moderate sources
Cereals
Pulses
Nuts
Legumes
Meat
RDA OF PHOSPHATES
Adults-800-1200mg/day
Infants-240mg/day
During pregnancy & lactation-1200mg/ day
SOURCES OF PHOSPHATE

13. ABSORPTION AND EXCRETION
OF CALCIUM AND PHOSPHATE
 35-40% of average daily dietary Ca is absorbed from gut, mainly
duodenum and first half of jejunum by a carrier mediated active
transport under the influence of vitamin D
 Additionla 25% of Ca enters the intestine via secreted gastrointestinal
juices and sloughed mucosal cells
 Thus about 90% of daily intake of calcium is excreted in feces

14. PHOSPHORUS ABSORPTION
 50-70%- absorbed
 Small intestine- soluble inorganic phosphate
 Except the portion of phosphate that is excreted in
combination with non absorbed calcium
 Almost all dietary phosphate is absorbed from the
gut and later excreted in urine

15. RENAL EXCRETION OF CALCIUM AND
PHOSPHATE
 10% - urine
 41% - bound to protein and cannot
be filtered
 Rest is filtered through glomeruli

16. PHOSPHOROUS EXCRETION
Is excreted primarily through Urine.
Almost 2/3rd
of the 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.

17. When calcium concentration
is low the reabsorption from
the renal tubules is greater
Even minute increase in
calcium increases excretion
markedly
Renal phosphate excretion runs
through overflow mechanism
Plasma level <1mmol/litre,all the
phosphate in glomerular filtrate is
reabsorbed
Above critical condition phosphate
loss is directly proportional to
additional increase

18. FACTORS CONTROLLING ABSORPTION
Factors inhibiting:
Phylates and oxalates
High dietary phosphate
Free fatty acids
High pH
High fiber diet
Factors promoting:
Vitamin D
Para thyroid harmone
Low pH
Lactose
Amino acids like lysine and
arginine

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

20. Phytic acid and phytates:
• 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
Oxalates:
• present in spinach and rhubarb leaves. They form oxalate precipitates
with calcium present in the diet thus decreasing their availability.
Fats:
• combines with calcium and form insoluble calcium , thus
decreasing calcium absorption.

21. Bile salts:
• increases calcium absorption by promoting metabolism of lipids.
Protein and aminoacids:
• increases calcium absorption as protein forms soluble complexes
with calcium and keeps calcium in a form that is easily
absorbable.
Carbohydrates:
• lactose promotes calcium absorption by creating the acidity in
the gut as they favours the growth of acid producing bacteria.

22.  Rottenson -1938-amount of calcium stored in body is directly
proportional to amount of calcium absorbed in body
 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
AMOUNT OF DIETARY CALCIUM AND
PHOSPHATES:
Precipitation of calcium in non
osseous tissue under abnormal
conditions
Hydroxyapatite does not
precipitate in extracellular
fluid despite super saturation
of calcium and phosphorous

23. Pregnancy and growth:

24. HORMONAL CONTROL OF CALCIUM & PHOSPHATE
METABOLISM
Three hormones regulate calcium and phosphate
metabolism.
Vitamin D
PTH
Calcitonin

25. VITAMIN D
 Cholecalciferol / D3
 Ergocalciferol / D2
 Can be called as hormone as it is produced in the skin when exposed
to sunlight.
 Vitamin D has very little intrinsic biological activity.
 Vitamin D itself is not a active substance, instead it must be first
converted through a succession of reaction in the liver and the kidneys
to the final active product 1, 25 di hydroxycholecalciferol

27. 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

28. PARATHYROID HORMONE
Parathyroid hormone is one of the
main hormones controlling Ca+2
absorption.
It mainly acts by controlling the
formation of 1,25 DHCC, which is
active form of Vit. D, which is
responsible for, increased Ca+2
absorption.
NORMAL PTH LEVEL IN SERUM – 10-60ng/L

29. PARATHYROID HORMONE (PTH)
 Secreted by parathyroid gland
 Glands are four in number
 Present posterior to the thyroid gland
 Formed from third and fourth branchial pouches
 Histologically – two types of cells
1)Chief cells (forming PTH)
2)Oxyphilic cells (replaces the chief cells
stores hormone)

30. ACTIONS OF PTH
 The main function is to increase the level of Ca in plasma within
the critical range of 9 to 11 mg.
Parathormone inhibits renal phosphate reabsorption in the
proximal tubule and therefore increases phosphate excretion.
( Mg,H and Na,K)
 Parathormone increases renal Calcium reabsorption in the distal
tubule, which also increases the serum calcium.
 Net effect of PTH  ↑ serum calcium
↓ serum phosphate

31. STIMULATION FOR PTH SECRETION
 The stimulatory effect for PTH secretion is low level of calcium in
plasma. (Rapid phase,Slow phase)
 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

32. CALCITONIN
 Minor regulator of calcium & phosphate metabolism
 Secreted by parafollicular cells or C-cells of thyroid gland.
 Single chain polypeptide
 Plasma concentration – 10-20ug/ml
 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

33. ACTION OF CALCITONIN
 Net effect of calcitonin 
decreases Serum Ca
 Target site
Bone (osteoclasts)
Kidney
Intestine

34. OTHER HORMONES ON CALCIUM METABOLISM
 GROWTH HORMONE
 INSULIN
 TESTOSTERONE & OTHER HORMONES
 LACTOGEN & PROLACTIN
 STEROIDS
 THYROID HORMONES
Influence of other harmones:

35. 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
GROWTH HORMONE

36. 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

37. THYROID HORMONE
 In infants  stimulation of bone growth
 In adults
increased bone metabolism  increased calcium mobilization

38. GLUCOCORTICOIDS
Anti vitamin D action, decrease absorption of calcium in
intestine
Inhibit protein synthesis and so decrease bone formation
Inhibit new osteoclast formation & decrease the activity of old
osteoclasts.

39. 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.

40. APPLIED ASPECT

41. OSTEOPOROSIS
 An atrophy of bone
 Bone resorption>bone deposition
 Calcium or hormonal deficiencies
 Older people- women>60yrs
 c/f: loss of height- shortening of the trunk &collapse of the vertebrae
Deformed thoracic cage
Bone pain-due to fracture

42. Common causes:
Lack of physical stress
Lack of vitamin c
Post menopausal lack of estrogen
Old age
Cushing’s syndrome
Malnutrition
Radiographically:
 loss of bone density
 Thinning of cortex
 Trabaculae-reduced

43. RICKETS
 Softening of the bones in children potentially leading to fractures and
deformity.
 Due to def. of vit.D causing deficiency in Ca & phosphate
 CLINICAL FEATURES
 Femoral and tibial bowing
 Growth retardation
 weakness
 tetany
 Susceptibility to fracture
 Irritability
 Some studies shown that rickets during the
time of tooth formation is the most
common cause of enamel hypoplasia.
 Shelling & Anderson- in rachitic
children:43% of teeth showed hypoplasia.
 Type- pitting variety

44. Plasma concentration of
calcium and phosphate
decrease in rickets:
Calcium is slightly
depressed(PTH)
 Phosphate is greatly
depressed
Ricket weakness in bones:
Prolonged rickets
increased PTH
increased osteoclastic activity
rapid osteoblastic activity

45. TETANY IN RICKETS:
 In early stage if rickets, tetany almost
never occurs
 PTH activates osteoclastic absorption of
bone
 <7ml/dl
 Tetanic respiratory spasm
 IV calcium

46. Oral manifestation:
Sir Edward Mellanby (1884-1955)- 1st
to report the effect of
rickets on the teeth.
1.Development abnormalities of dentine & enamel,
2.Delayed eruption
3.Malalignment of the teeth in the jaws
4.High caries index
5.Abnormally wide predentine zone
6.Interglobular dentine
Many reports-rickets linked with hypoplasia

47. TREATMENT:
Diet and sunlight
Recommendations are for 400 international units (IU) of vitamin D a day for
infants and children. Children who do not get adequate amounts of vitamin D are at
increased risk of rickets. Vitamin D is essential for allowing the body to uptake
calcium for use in proper bone calcification and maintenance.
According to the American academy of paediatrics (AAP),
all infants, including those who are exclusively breast-
fed, may need Vitamin D supplementation until they
start drinking at least 17 US fluid ounces (500 ml) of
vitamin D-fortified milk or formula a day.

48. OSTEOMALACIA
 Softening & distortion of skeleton
 Oral manifestation:
Taylor & day-50% incidence of
severe periodontitis in a series of 22
Indian women

49. Oral manifestation:
Severe Periodontitis
Thin or absent trabeculae
Loosened teeth
Weakened jaw bones
Clinical features:
Bone pain and tenderness
Peculiar waddling or “penguin”gait
Tetany
Greenstick bone fractures
Myopathy

50. HYPOPHOSPHATASIA:
 Def. of enzyme alkaline phophatase
 Excretion of phosphoethanolamine in the urine
 C/F:
Infantile form
Severe rickets
Bone abnormalities
Failure to thrive
Childhood
Loss of primary teeth
Increased infection
Growth retardation
Rachitic like deformation,
lung., renal, GI disorders
Adult
Spontaneous fracture

51.  Oral manifestations:
Premature loss of primary teeth
Gingivitis
 Radiographic features:
Hypocalcification
Large pulp chambers
Alveolar bone loss

52. HYPOCALCEMIA
<8.8 mg/dl
<8.5mg/dl- mild tremors
<7.5mg/dl- life threatening
condition will result- TETANY
Symptoms
muscle cramps
Paresthesia
Neuromuscular irritability
muscle twitching
Tetany
Seizures
Bradycardia
Causes
Hypoparathyroidism
Vit. D deficiency
Increased calcitonin
Deficiency of calcium, magnesium
Hypoalbuminemia

53. TETANY
Manifestations: Carpopedal spasm
Laryngismus stridor
Trousseu’s sign
Treatment:
Oral calcium with vitamin d
supplementation.
Underlying cause should be
treated.
Tetany needs IV calcium.
Chvotske’s sign

54. HYPERCALCEMIA
Causes
•Hyperparathyoidism
•Thyrotoxicosis, addison’s disease
•Paget’s disease
•Dehydration
•Milk- alkali syndrome
•Drugs- thiazides
symptoms
•Anorexia, nausea, vomiting
•Polyuria, polydypsia
•Confusion, depression, psychosis
•Osteoporosis & pathological fracture
•Renal stones
•Ectopic calcification & pancreatitis
•Increased serum alkaline phosphatase
BONES
STONES
GROANS
MOANS
Parathyroid poisioning:
Ca >15 mg/dl – Ca-p crystals

55. MANAGEMENT OF HYPERCALCEMIA
 Adequate hydration, IV normal saline
 Furosemide IV to promote calcium excretion
 Steroids, if there is calcitriol excess
 Definitive treatment for the underlying disorder

56. PERIODONTAL DISEASE DUE TO DIETARY CALCIUM
DEFICIENCY AND/ OR DIETARY PHOSPHOROUS EXCESS
 Henrickson suggested:
High incidence of periodontal disease in natives of India-attributed
in part to their low dietary calcium intake.
 Labile for Resorption- Alveolar bone
Vertebrae
Ribs
Long bones
Nutrition and Immunology: Principles and Practice edited by M. Eric Gershwin, J. Bruce German, Carl L. Keen

57. CASE REPORT:
A 19-month-old girl was referred to a University of Minnesota pediatric dental clinic for consultation due to the unexplained,
nontraumatic, premature loss of the patient’s lower central incisors. At the initial consult, the patient presented with an
unremarkable medical history and was in good general health. She was growing along the 14th percentile for length and 34th
percentile for weight. She lost her first tooth at 10 months of age, and a second tooth at 12 months. At 15 months, she was
found to have four loose teeth. Although there was no family history of skeletal abnormalities, her maternal grandfather and
his mother started losing teeth in their 50s. The patient’s 6-year-old brother had no history of premature tooth loss.

58. Biochemical and Radiographic Evaluation — The patient’s vitamin D, intact parathyroid hormone, calcium
and phosphorus levels were all within normal range, however. In addition, her bone alkaline phosphatase
level was low (30.1 ug/L, compared to a normal range of 33.4 to 145.3 ug/L). Radiographic imaging showed
no skeletal abnormalities.
Oral Evaluation — Initial interpretation and assessment by a
general dentist attributed the premature loss of her first
primary incisor to unwitnessed orofacial trauma. After the loss
of her second primary incisor and presence of four loose
maxillary incisors, the patient was evaluated by a pediatric
dentist, who suspected HPP and referred her to a medical
provider. Subsequent evaluations of alkaline phosphatase levels
were also low at 18 months, and again two weeks later. She
subsequently exfoliated a third primary tooth — a lower lateral
incisor. The third exfoliated tooth was submitted to the
University of Minnesota Oral Pathology Laboratories for
histologic assessment. The lab confirmed a lack of cementum ,
which is consistent with a potential diagnosis of HPP.

59. EFFECT OF CALCIUM, PHOSPHORUS IMBALANCES &
VITAMIN D DEFICIENCY ON DENTAL CARIES INCIDENCE
Variation in Ca:P Ratios in experimental diets
Quite cariogenic, because the carbonate level of the tooth was
increased.
Relatively acid soluble
Highly susceptible to dental decay

60. SUMMARY

61. HARMONAL INFLUENCE
ON BLOOD CALCIUM

62. EFFECTS OF HARMONES
ON BLOOD PHOSPHATE
LEVELS

64. CONCLUSION

65. REFERENCES
1. Textbook of medical biochemistry-DM
Vasudevan
2. Textbook of medical physiology-Guyton and Hall
3. Textbook of medical physiology-Sembulingam
4. Essentials of biochemistry,Satyanarayan- 3th
edition
5. Shafer’s oral pathology- 5th
edition
6. Internet sources