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CALCIUM AND PHOSPHATE
METABOLISM
Karishma.S
II MDS
CONTENTS
• INTRODUCTION
• IMPORTANT MINERALS
• CALCIUM & PHOSPHOROUS METABOLISM
• HORMONES INVOLVED IN CALCIUM AND PHOSPHATE HOMEOSTASIS
• APPLIED ASPECTS
• SUMMARY
• CONCLUSION
• REFERENCES
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.
 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
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
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
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.
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
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)
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.
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
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
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
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
RENAL EXCRETION OF CALCIUM AND
PHOSPHATE
 10% - urine
 41% - bound to protein and cannot
be filtered
 Rest is filtered through glomeruli
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.
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
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
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
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.
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.
 
 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
Pregnancy and growth:
HORMONAL CONTROL OF CALCIUM & PHOSPHATE
METABOLISM
Three hormones regulate calcium and phosphate
metabolism.
Vitamin D
PTH
Calcitonin
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
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
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
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)
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
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
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
ACTION OF CALCITONIN
 Net effect of calcitonin 
decreases Serum Ca
 Target site
Bone (osteoclasts)
Kidney
Intestine
OTHER HORMONES ON CALCIUM METABOLISM
 GROWTH HORMONE
 INSULIN
 TESTOSTERONE & OTHER HORMONES
 LACTOGEN & PROLACTIN
 STEROIDS
 THYROID HORMONES
Influence of other harmones:
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
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
THYROID HORMONE
 In infants  stimulation of bone growth
 In adults
increased bone metabolism  increased calcium mobilization
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.
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.
APPLIED ASPECT
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
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
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
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
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
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
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.
OSTEOMALACIA
 Softening & distortion of skeleton
 Oral manifestation:
Taylor & day-50% incidence of
severe periodontitis in a series of 22
Indian women
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
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
 Oral manifestations:
Premature loss of primary teeth
Gingivitis
 Radiographic features:
Hypocalcification
Large pulp chambers
Alveolar bone loss
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
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
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
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
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
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.
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.
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
SUMMARY
HARMONAL INFLUENCE
ON BLOOD CALCIUM
EFFECTS OF HARMONES
ON BLOOD PHOSPHATE
LEVELS
CONCLUSION
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

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Calcium and phosphate metabolism

  • 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
  • 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
  • 26.
  • 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.
  • 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
  • 62. EFFECTS OF HARMONES ON BLOOD PHOSPHATE LEVELS
  • 63.
  • 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

Editor's Notes

  1. Calcium is one of the interesting items that you can find in many products such as cheese, milk, and other types of food. Consuming sufficient calcium is great for the body. The word calcium is derived from the Latin world called as calcis. Calcium is not only found in some important foods like milk and cheese. The buyer can also get this element located on the earth crust. Calcium is as essential element for the plants and animals living surrounding your house. It can strengthen the muscle and form the new skeletal system. Moreover, the animal can form the bio chemical reaction for some purposes. Many people have recognized about the benefit of calcium to the plants, human and animals. In 1808, this element can be purified by the man called as Si Humphrey Davy. He came from England. The benefit of calcium in manufacturing process is big enough. It can be used as a reduction magnet for making other types of metal in the factories. You can also use it to make cheese, making cement, or even eliminating the nonmetallic impurities ingredients in the alloys. he name calcium as I have stated before is derived from Latin word. Can you guess the meaning of calcis. It is lime. That’s why the ancient Roman uses calcium dioxide to make a liquor or a lime drink.
  2. Phosphorus was the 13th element to be discovered. For this reason, and also due to its use in explosives, poisons and nerve agents, it is sometimes referred to as &amp;quot;the Devil&amp;apos;s element&amp;quot;.[34] It was the first element to be discovered that was not known since the ancient times. The discovery of phosphorus is credited to the German alchemist Hennig Brand in 1669, although other chemists might have discovered phosphorus around the same time.[35] Brand experimented with urine, which contains considerable quantities of dissolved phosphates from normal metabolism.[11] Working in Hamburg,
  3. IN BONE- HYDROXY APPETITE CRYSTAL
  4. The positive balance is obvious in growing child, about 0.1 gm being retained each day in the growing &amp; mineralizing skeleton The Negative balance arises in later decades of age 50 yrs or more, this can be detected as a loss of skeletal tissue, not merely a reduction in the proportion of mineralization.
  5. In osteoporosis, the cortex becomes thinner and more brittle, while the inner trabecular bone develops larger holes. Mature adult bone is continually being remodelled. Specialised cells called osteoclasts absorb old bone and other cells called osteoblasts create new, strong, bone. In this way, bone retains its strength and density. Normally in the adult skeleton, about 3%of ‘cortical’ bone – the outer hard part – and 25% of ‘trabecular’ bone – the inner, honeycomb part – is remodelled each year. For this process to work properly we need the minerals calcium and phosphorus from which bone is made (these come from our diet) and a range of hormones and vitamins which drive the process. As we grow, our bone mass steadily increases; more bone is made than is absorbed. By early adulthood, we reach what is known as peak bone mass, which is the maximum density achieved by our bones. After about 35 years of age, even though bone formation still occurs, our bone mass slowly declines as more is absorbed than is added. The cortex becomes thinner and more brittle, while the inner trabecular bone develops larger holes. In women after menopause, absorption and thinning of bones occurs even more rapidly. As bone is lost, the skeleton becomes progressively more and more osteoporotic and prone to bone fracture. While almost everyone loses bone, some people are less likely to suffer from osteoporosis until they are very old (if at all). In some cases, osteoporosis is caused by a deficiency of these hormones or vitamins. Osteoporosis accelerates in women after menopause. That’s because after menopause, levels of the sex hormone oestrogen fall. Oestrogen is thought to play a role in maintaining bone mass by slowing the process of bone breakdown by osteoclasts. People who don’t have enough calcium in the diet are prone to osteoporosis. Failure to absorb calcium properly from the gut can also play a role. This may be due to a disease of the small bowel (where calcium is absorbed) or a deficiency in vitamin D, which is needed for calcium absorption. Osteoporosis isn’t an inherited disease, but it tends to run in families. So it’s more likely if there’s someone else in the family that has it. Symptoms The problem with osteoporosis is that it’s a silent condition; bone loss is gradual and invisible. People may not know they have osteoporosis until their bones become so weak that a sudden strain, bump, or fall causes fracture which wouldn’t have happened in a person with normal strong bones. Fractures are most common in the wrist, hip, spine, pelvis and upper arm – but any bone can fracture. People with smaller, lighter frames are more likely to suffer a fracture than larger, taller people because they have less bone mass to start with, so are more likely to get a fracture for the same degree of bone demineralisation. When a fracture occurs it can be quite serious. It often requires hospitalisation – in the case of a fractured hip for example – and then a prolonged period of rehabilitation. Osteoporosis in the spine may cause collapse of the spinal vertebrae resulting in severe back pain, spinal deformities, loss of height, kyphosis of the spine or ‘dowagers hump.
  6. (Rickets is among the most frequent childhood diseases in many developing countries. The predominant cause is a vitamin D deficiency, but lack of adequate calcium in the diet may also lead to rickets. Although it can occur in adults, the majority of cases occur in children suffering from severe malnutrition, usually resulting from famine or starvation during the early stages of childhood. Osteomalacia is the term used to describe a similar condition occurring in adults, generally due to a deficiency of vitamin D. “rachitis” The “wrist widening” of rickets Epidemiology Those at higher risk for developing rickets include:  Breast-fed infants whose mothers are not exposed to sunlight.  Breast-fed infants who are not exposed to sunlight.  Individuals not consuming fortified milk, such as those who are lactose intolerant Individuals with red hair have a decreased risk for rickets due to their greater production of vitamin D in sunlight. Etiology Vitamin D is required for proper calcium absorption from the gut. In the absence of vitamin D, dietary calcium is not properly absorbed, resulting in hypocalcemia, leading to skeletal and dental deformities and neuromuscular symptoms, e.g. hyperexcitability. Presentation Radiograph of a two-year old rickets sufferer, with a marked genu varum (bowing of the femurs) and decreased bone opacity, suggesting poor bone mineralization. Signs and symptoms of rickets include: 1) Bone pain or tenderness 2) dental problems 3) muscle weakness (rickety myopathy or “floppy baby syndrome”) 4) increased tendency for fractures (easily broken bones),especially greenstick fractures 5) Skeletal deformity *Toddlers: Bowed legs (genu varum) *Older children: Knock-knees (genu valgum) or “windswept knees” *Cranial, spinal, and pelvic deformities 6) Growth disturbance 7) Hypocalcemia (low level of calcium in the blood), and 8) Tetany (uncontrolled muscle spasms all over the body). 9) Craniotabes (soft skull) 10) Costochondral swelling (aka “rickety rosary” or “rachitic rosary”) 11) Harrison’s groove 12) Double malleoli sign due to metaphyseal hyperplasia An X-ray or radiograph of an advanced sufferer from rickets tends to present in a classic way: bow legs (outward curve of long bone of the legs) and a deformed chest. Changes in the skull also occur causing a distinctive “square headed” appearance. These deformities persist into adult life if not treated.
  7. READ SHAFER
  8. SHAFER
  9. Due accidental surgical removal of parathyroid glands Auto immune disease
  10. BURNETTS SYNDROME
  11. Nizel 211