This seminar includes sources,daily requirement,metabolism i.e absorption and excretion of calcium and phosphate and various factors associated due to increase or decrease in the levels of calcium and phosphate within the body
4. Most abundant mineral in many animals and in the
Ancient Romans prepared lime- calcium oxide. 975 AD
-plaster of Paris (calcium sulfate)was used for setting
Sir Humphry Davy Isolated calcium(1808)
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
The first form of elemental phosphorus to be produced was white
phosphorus, in 1669 by Greek .
Hennig Brand(1669) discovered.
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
7. ROLE OF PHOSPHATE
Key constituent of bone and teeth.
Component of intra cellular buffering. Forms energy rich bonds in ATP.
Regulates blood and urinary pH.
Forms organic molecules like DNA & RNA
Cellular energy metabolism.
Constituent of macro molecules like nucleic acids, phospholipids and
9. PLASMA CALCIUM AND PHOSPHATE
Normal plasma levels
Normal plasma levels
( 5 mg/dl) (4mg/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
Dark green leafy vegetables
RDA OF CALCIUM
Average adult-800 mg/ day
Infants: <1yr- 360-540mg
During pregnancy & lactation-1200mg/ day
SOURCES OF CALCIUM
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
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
10% - urine
41% - bound to protein and cannot
Rest is filtered through glomeruli
16. PHOSPHOROUS EXCRETION
Is excreted primarily through Urine.
of the total
phosphorous that is excreted is
found in the urine as phosphate of
Phosphorous found in the faeces is
the non absorbed form of
17. When calcium concentration
is low the reabsorption from
the renal tubules is greater
Even minute increase in
calcium increases excretion
Renal phosphate excretion runs
through overflow mechanism
Plasma level <1mmol/litre,all the
phosphate in glomerular filtrate is
Above critical condition phosphate
loss is directly proportional to
18. FACTORS CONTROLLING ABSORPTION
Phylates and oxalates
High dietary phosphate
Free fatty acids
High fiber diet
Para thyroid harmone
Amino acids like lysine and
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
• present in spinach and rhubarb leaves. They form oxalate precipitates
with calcium present in the diet thus decreasing their availability.
• 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
• 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
AMOUNT OF DIETARY CALCIUM AND
Precipitation of calcium in non
osseous tissue under abnormal
Hydroxyapatite does not
precipitate in extracellular
fluid despite super saturation
of calcium and phosphorous
24. HORMONAL CONTROL OF CALCIUM & PHOSPHATE
Three hormones regulate calcium and phosphate
25. VITAMIN D
Cholecalciferol / D3
Ergocalciferol / D2
Can be called as hormone as it is produced in the skin when exposed
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
28. PARATHYROID HORMONE
Parathyroid hormone is one of the
main hormones controlling Ca+2
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
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
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
When plasma calcium level increases to 11mg/dl there is decreased
secretion of PTH
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
33. ACTION OF CALCITONIN
Net effect of calcitonin
decreases Serum Ca
34. OTHER HORMONES ON CALCIUM METABOLISM
TESTOSTERONE & OTHER HORMONES
LACTOGEN & PROLACTIN
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
Testosterone causes differential growth of cartilage resulting to
differential bone development
Acts on cartilage & increase the bone growth.
It is an anabolic hormone which favors bone formation
37. THYROID HORMONE
In infants stimulation of bone growth
increased bone metabolism increased calcium mobilization
Anti vitamin D action, decrease absorption of calcium in
Inhibit protein synthesis and so decrease bone formation
Inhibit new osteoclast formation & decrease the activity of old
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.
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
loss of bone density
Thinning of cortex
Softening of the bones in children potentially leading to fractures and
Due to def. of vit.D causing deficiency in Ca & phosphate
Femoral and tibial bowing
Susceptibility to fracture
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
Phosphate is greatly
Ricket weakness in bones:
increased osteoclastic activity
rapid osteoblastic activity
45. TETANY IN RICKETS:
In early stage if rickets, tetany almost
PTH activates osteoclastic absorption of
Tetanic respiratory spasm
46. Oral manifestation:
Sir Edward Mellanby (1884-1955)- 1st
to report the effect of
rickets on the teeth.
1.Development abnormalities of dentine & enamel,
3.Malalignment of the teeth in the jaws
4.High caries index
5.Abnormally wide predentine zone
Many reports-rickets linked with hypoplasia
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.
Softening & distortion of skeleton
Taylor & day-50% incidence of
severe periodontitis in a series of 22
Def. of enzyme alkaline phophatase
Excretion of phosphoethanolamine in the urine
Failure to thrive
Loss of primary teeth
Rachitic like deformation,
lung., renal, GI disorders
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
High incidence of periodontal disease in natives of India-attributed
in part to their low dietary calcium intake.
Labile for Resorption- Alveolar bone
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
Relatively acid soluble
Highly susceptible to dental decay
1. Textbook of medical biochemistry-DM
2. Textbook of medical physiology-Guyton and Hall
3. Textbook of medical physiology-Sembulingam
4. Essentials of biochemistry,Satyanarayan- 3th
5. Shafer’s oral pathology- 5th
6. Internet sources
Notes de l'éditeur
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.
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 &quot;the Devil&apos;s element&quot;. 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. Brand experimented with urine, which contains considerable quantities of dissolved phosphates from normal metabolism. Working in Hamburg,
IN BONE- HYDROXY APPETITE CRYSTAL
The positive balance is obvious in growing child, about 0.1 gm being retained each day in the growing & 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.
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
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
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
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.
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
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.
(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
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
Individuals with red hair have a decreased risk for rickets due to
their greater production of vitamin D in sunlight.
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.
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
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.
Due accidental surgical removal of parathyroid glands
Auto immune disease