Calcium metabolism/ oral surgery courses /certified fixed orthodontic courses by Indian dental academy

SEMINAR
CALCIUM METABOLISM
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

LEARNING OBJECTIVES
At the end of the presentation the learner should be able to;
•Describe regulation of calcium metabolism.
•Identify the role of Parathormone,Calcitonin,1,25 dihydroxy
cholecalciferol in regulation of blood calcium level.
•Enlist clinical features , radiographical features of hyper and
hypo parathyroidism.
•Enlist the clinical features of pseudohypothyroidism.
•Describe the clinical features of vitamin D deficiency
•Outline the causes , signs and symptoms of hypo and
hypercalcemia.
•Describe clinical features and radiographical features of
osteoporosis www.indiandentalacademy.com

CONTENTS
• Distribution of calcium
• Regulation of calcium metabolism
• Parathyroid gland
• Regulation of blood calcium level
• Role of Parathormone,Calcitonin,1,25 dihydroxy cholecalciferol in regulation of blood
calcium level
• Regulation of parathormone secretion
• Hypoparathyroidism
• Hyperparathyroidism
• Radiographic features of hypo &hyperparathyroidism
• Pseudohypoparathyroidism
• Vitamin D deficiency
• Hypocalcemia
• Hypercalcemia
• Osteoporosis
• Medical pitfalls

CALCIUM METABOLISM
• 99% of total body calcium in the bone .
• 1% in ICF ,ECF ,& cell membranes .
• Calcium weight is 400mg/kg in infant &
950mg/kg in adult .
• The 1% can be divided in 3 components :
1) 50% ionized . 2) 40% bound to protein .
3)10% complex /anions

CALCIUM
• physiologic functions :
1.blood coagulation .
2.muscle contraction .
3.neuromuscular transmission .
4.Skeletal growth & mineralization
• Ionized Ca is physiologically important .

PARATHYROID GLAND
Normally there are four parathyroid gland, which are located
immediately behind thyroid gland at the upper and lower poles.
Parathyroid glands are very small gland measuring about 6mm
long, 3mm wide and 2mm thick with dark brown color.
Parathormone secreted by the parathyroid gland is essential for
the maintenance of blood calcium level within very narrow
critical level.

Regulation of blood calcium level
- Calcium taken through dietary substances is absorbed from GIT
into blood and distributed to various parts of body.
- While passing through kidney large quantity of calcium is
filtered in the glomerulous.
- From the filtrate 98-99% of calcium is reabsorbed through
urine.
- Depending upon the blood level the calcium may be deposited
or reabsorbed from bone.
- All these process are regulated by three hormone namely,www.indiandentalacademy.com

• Calcium regulation :mainly by 3 common hormones
:
1}Parathyroid hormone .
2}Vitamin D .
3}Calcitonin .

VITAMIN D
• Vitamin D :provide Ca & PO4 to ECF for
bone mineralization .
• Deficiency in children……..Rickets
• Deficiency in adult……..Osteomalacia
• 7-dehydrocholestrol(skin)…cholecalciferol
25-OH- cholecalciferol(liver)…1- 25-OH-
cholecalciferol(kidney)

VITAMIN D
• Actions:
1)increase Ca absorption from intestine.
2) increase PO4 absorption from intestine.
3) increase renal reabsorption of Ca &PO4.
4) increase bone resorption from old bone
&mineralize new bone{net resorption} .
Overall effect :increase serum Ca & PO4 .

I. Parathormone
- Secreted by chief cells of Parathyroid gland
- Main function is to increase level of blood calcium by mobilizing calcium
from bone.
II. 1,25 Dihydroxy Cholecalciferal
- Steroid hormone synthesized from vitamin D by means of series of
hydroxylation reaction in liver and kidneys.
- Action is to increase blood calcium by increasing calcium absorption from
intestine.
III. Calcitonin
- Secreted by parafollicular cells of thyroid gland.
- It is a calcium lowering hormone. It reduces blood calcium by decreasing
bone resorption.

REGULATIONOF BLOOD CALCIUM LEVEL
Decreased blood calcium level Increased blood calcium
level
Parathyroid Kidneys
Parathormone 1-25 Dihydroxy
Cholecalciferal
Bone Intestine
Reabsorption
and release of
calcium
Absorption of
calcium
thyroid
Calcitonin
Bone
Deposition of
calcium
Normal blood calcium level

Parathormone
Actions of PTH
Maintain blood calcium level (9-11 mg %) by following mechanisms-
1)
PTH is responsible for resorption of bone by following phase
a) Rapid Phase
Occurs within minutes of release of PTH. PTH gets attached with
receptors of all membrane of osteoblast and osteocytes.
b) Slow Phase
Slow phase of bone resorption is by activation of osteoclasts.
Effect on Bones

2)
PTH increases the reabsorption of calcium from the renal
tubules.
3)
PTH increases absorption of calcium ions from GIT because
of formation of 1, 25 dihydroxy cholecalciferal from
vitaminD.
Effect on Kidneys
Effect on GIT

Role of PTH in activation of vitamin D
Vitamin D is essential for calcium absorption from GIT but it itself is
not active substance, it has to be converted into 1,25 Dihydroxy
cholecalciferal in liver and kidneys.
Activation of vitamin D
- There are various forms of vitamin D but important one is
vitamin D3 (cholecalciferol) which is synthesized in the skin 7
dehydroxy cholestrol by action of UV rays from sunlight.

Step 1.
- Cholecalciferol is converted into 25 hydroxy cholecalciferol in liver, this process is
limited and can be inhibited by 25, hydroxy cholecalciferol itself , this is known as
feedback mechanism.
- Inhibition is necessary for two reasons
-- Regulation of amount of active vitamin D.
-- Storage of vitamin D for months.
-- 25, hydroxy cholecalciferol can be stored in the body for 2-5 days while
vitamin D3 can be stored in liver for months.
Step 2.
25 hydroxy cholecalciferol is converted into 1,25 dihydroxy cholecalciferol in
kidney and it requires presence of parathormone.
Activation of vitamin D occurs in following
phases:-

Role of calcium in regulating 1,25 dihydroxy cholecalciferol
- If more amount of calcium is present it then inhibits formation of
1,25 dihydroxy cholecalciferol in the following ways:
1) It directly supresses 25 hydroxy cholecalciferol conversion into
1,25 dihydroxy cholecalciferol , this effect is mild.
2)Increasing calcium ions causing decrease in PTH secretion hence
supressing the conversion of 25 hydroxy cholecalciferol into 1, 25
dihydroxy cholecalciferol.
-This makes calcium level in plasma to fall back to normal

Cholecalciferal (Vitamin D3)
(inactive form of vitamin D)
25- hydroxy cholecalciferol
1,25 Dihydroxy cholecalciferol
(active form of Vitamin D)
1,25 Dihydroxy cholecalciferol
Calcium
IntestineKidneyLiver
Parathormone
Inhibition
Activation of Vitamin D

Actions of 1,25 Dihydroxy Cholecalciferol
1.It increases absorption of calcium from intestine by formation of
calcium binding proteins, these proteins act as carrier protein for
facilated diffusion by which calcium ions are transported and these
proteins remain in the body even after removal of 1,25 dihydroxy
cholecalciferol.
2.It increases the synthesis of calcium induced adenosine
triphosphate in intestinal epithelium.
3.It increases the synthesis of alkaline phosphate in intestinal
epithelium.

Regulation of Parathormone Secretion
Parathormone secretion is inversely proportional to blood calcium
level. Increase in blood calcium level decreases PTH secretion.
- Condition in which secretion of PTH is decreased
1. Excessive quantities of calcium in the diet.
2. Increased Vitamin D in diet.
3. Increase resorption of calcium from the bones various diseases of
bone.
- Decrease in calcium ion concentration causing increase
Parathormone secretion as in case of rickets, pregnancy.

CALCITONIN
Secreted by parafollicular cells of thyroid gland.
Actions of Calcitonin
- Maintenance of blood calcium level along with PTH. It reduces
calcium level by acting on bones, kidney and intestine.
1. On Bones
Facilitates deposition of calcium on bones. It also suppresses the
activity of osteoclasts .
2. On Kidney
Calcitonin increases excretion of calcium through urine by inhibiting
the reabsorption of calcium from the renal tubules.
3. On Intestine
It prevents absorption of calcium from intestine into the blood.www.indiandentalacademy.com

THREE FORMS OF CIRCULATING CA2+

HYPOPARATHYROIDISM
Hypoparathyroidism causes hypocalcemia by decreasing the
resorption of calcium from bones.
This causes neuromuscular hyperexcitability resulting in
hypocalcemic tetany.
Normally, tetany occurs if the plasma calcium level falls below 6
mg% from its normal value of 9.4mg%.
The four types of hypoparathyroidism are-
1.DiGeorge’s Syndrome
2.Postoperative hypoparathyroidism
3. Idiopathic hypoparathyroidism
4.Pseudohypoparathyroidism
Disorders of Parathyroid gland

SIGNS AND SYMPTOMS OF HYPOPARATHYROIDISM
 Tetany is characteristic, as are paresthesias of the lips, tongue, fingers & feet and
myalgia and spasm of facial musculature.
 The neuromuscular instability associated with hypocalcemia can be proved by
tapping the facial muscles (Chvostek’s sign).
 Another useful test is Trousseau’s sign(carpodeal spasm) which occurs when
blood supply to the hand is reduced by application of a blood pressure cuff above
systolic pressure.
 Other symptoms include muscle weakness, cramps, heart palpitation, and bizzare
behaviour patterns.Abnormalties of skin, nails, and teeth are common.The skin is
coarse, scaly and dry and the nail beds are deformed; hair is thin and alopecia may
be present.

Trosseau’s sign
Chvostek’s sign

ORAL MANIFESTATIONS
Painful muscular spasms affect oral and laryngeal muscles.
Despite low serum calcium levels, the maxilla and mandible are
abnormally dense with well-calcified trabeculae.
If the hypoparathyroidism is part of autoimmune
polyendocrinopathy syndrome, oral mucocutaneous candiasis
may be present in acute or chronic form.
If the hypoparathyroidism occurs in still developing teeth there
will be abnormalities in appearance and eruption pattern.

There may be enamel hypoplasia, single or parallel horizontal
bands on enamel and poorly mineralized dentin.
Other dental findings include malformed teeth, anodontia,
short blunt root apices, elongated pulp chambers, impacted
teeth and mandibular exostoses.
 If hypoparathyroidism occurs after dental development, there
are no abnormalities seen in erupted teeth.

RADIOGRAPHIC FEATURES OF
HYPOPARATHYROIDISM
The principal radiographic change is calcification of basal
ganglia.
On the skull radiographs this calcification appears flocculent
and paired within the cerebral hemispheres on the
posterioranterior view.
Radiographic examination of the jaws may reveal enamel
hypoplasia, external root resorption, delayed eruption, or root
dilaceration.

HYPERPARATHYROIDISM
Hyperparathyroidism is a disease in which there may be a complex
of biochemical, anatomic, and clinical abnormalities resulting from
the increased secretion of PTH.
The primary clinical orofacial signs and symptoms of
hyperparathyroidism are reflections of the systemic effects of
hypercalcemia.
This entity is the most common cause of a generalized rarefaction
of the jaws.
 Bones, stones abdominal groans, psychic moans with fatigue overtones.
Patient complains of weakness, anorexia, nausea, vomiting,
constipation, abdominal pains, muscular and joint pains, polyuria,
polydipsia and emotional instability

 Variety of osseous changes may be present these include metastatic
calcification, subperiosteal erosion, ostetis fibrosa generalisata,
disturbances in jaw bones, brown giant cell lesions and rarely osteoscelrosis.
 Metastatic calcification: ectopic calcification in soft tissue is most common
cause of hyperparathyroidism. 45%-80% patient reports nephrolithiasis and
nephrocalcinosis.
Other soft tissues involved are subcutaneous tissues, walls of blood vessel,
articular cartilages and joint capsules.
 Subperiosteal erosion: especially of middle phalanges, is considered hallmark
of hyperparathyroid dysfunction. Loss of lamina dura has been considered a
type of subperiosteal erosion, likening periodontal ligament to periosteum.

Osetitis fibrosa generalisata(cystica):
The term osteitis fibrosa generalisata refers to pattern of
generalized rarefaction seen in skeletal as a late change in
primary, secondary, or tertiary hyperparathyroidism and
occasionally in pseudohyperparathyroidism.
Early symptoms include vague aches and pains, which may be
uite disseminated later symptoms are severe bone pain and
tenderness followed by fractures and development of
deformities.
On radiographs the bones may appear quite radiolucent with
thin cortices and hazy, indistinct trabeculae. Some bones may be
less homogenous, presenting a moth-eaten image. Regions in
which trabaculae are completely missing have a cystlike
appearance on radiographs.

ORAL MANIFESTATION OF HYPERPARATHYROIDISM
The primary clinical orofacial signs and symptoms of
hyperparathyroidism are reflections of systemic hypercalcemia.
The lytic jaw lesions or jaw tumors can increase in size, causing
the bony cortex to expand, ultimately becoming destroyed.
These tumors rarely expand into periosteum but can produce
gingival swelling.
Due to bony changes teeth become mobile, drift and cause
malocclusion.
With gradual loosening of the dentition periradicular
radiolucencies develop, with increased periodontal pocketing,
root resorption and dental pain.

PRIMARY HYPERPARATHYROIDISM
When excessive secretion arises from one or more parathyroid
gland it is referred as primary hyperparathyroidism.
 It is result of a primary hyperplasia or a benign or malignant
tumor of the parathyroid glands.
Postmenopausal women are most commonly affected by
hyperparathyroidism.
Pathologic hyperparathyroidism may affect one or more
members of the family, resulting in familial hyperparathyroidism.
This type may also be associated with MEN syndrome types1, 2A
& 2B or the hyperparathyroid jaw tumor syndrome(HPT-JT)
 In advanced cases the classic serum changes of increased levels
of calcium and alkaline phosphatase and decreased levels of
phosphorous are usually present.www.indiandentalacademy.com

SECONDARY HYPERPARATHYROIDISM
Occurs when the parathyroid glands are stimulated to produce
increased amount of PTH to correct abnormally low serum
calcium levels.
May also occur due to compensatory glandular enlargement in
response to unusual hypocalcemia induced by metabolic
disorders such as renal failure, deficiency of 1,25 dihydroxy
vitamin D or malabsorption of calcium found in rickets, and some
forms of osteomalacia.
The low serum calcium levels stimulate increased production and
secretion of PTH, which then induce bone resorption with
liberation of calcium and phosphate ions.
Contrary to the situation to primary hyperparathyroidism, in
secondary hyperparathyroidism there is an inverse relationship
between the levels of serum PTH and serum calcium.

TERTIARY HYPERPARATHYROIDISM
Parathyroid tumor develop due to long standing secondary
hyperparathyroidism this is known as tertiary
The increased PTH levels produced increased bone resorption and
a resultant hypercalcemia.

RADIOGRAPHIC FEATURES
General radiographic features:
Subtle erosion of bone from the subperiosteal surfaces of
phalanges of the hand.
Demineralization of the skeleton results in an unusual
radiolucent appearnce.
Osteitis fibrosa cystica resulting in apparent bone structure.
Brown tumor are peripheral or central tumors of bone are
radiolucent.
Pathologic calcifications of soft tissues is seen in kidneys and
joint.
In prominent hyperparathyroidism, the entire calvarium has a
grannular appearance caused by the loss of central (diplopic)
trabaculae and thinning of cortical tables.www.indiandentalacademy.com

RADIOGRAPHIC FEATURES OF THE
JAWS
Demineralization and thinning of cortical boundaries often
occur in the jaws in cortical boundaries such as inferior
border, mandibular canal and the cortical outlines of maxillary
sinuses.
 The density of the jaws is decreased.
A change in the normal trabecular pattern may occur resulting
in a ground-glass appearance of numerous, small, randomly
oriented trabaculae.
Brown tumors may appear in any bone but are more common
in facial bones and jaws, lesions may be multiple within single
bone.

RADIOGRAPHIC FEATURES OF THE TEETH AND ASSOCIATED
STRUCTURE
Periapical radiographs reveal loss of lamina dura in patients (only
about 10%) with hyperparathyroidism.
The loss of lamina dura may either be complete or partial around
a particular tooth.
The result of loss of lamina dura may give the root a tapered
appearance because decreased image contrast.
Fully developed teeth are not affected except that they appear
more radiopaque.

PSEUDOHYPOPARATHYROIDISM
• Symptoms and signs
• Hypocalcemia
• Hyperphosphatemia
• Characteristic physical appearance: short stature, round face,
short thick neck, obesity, shortening of the metacarpals
• Autosomal dominant
• Resistance to parathyroid hormone
• The patients have normal parathyroid glands, but they fail to respond
to parathyroid hormone or PTH injections
• The rise in urinary cAMP after parathyroid hormone fails to occur
• Symptoms begin in children of about 8 years
• Tetany and seizures
• Hypoplasia of dentin or enamel and delay or absence of eruption
occurs in 50% of people with the disorder
• Rx: vitamin D and calcium

PSEUDOHYPOPARATHYROIDISM
Elfin facies, short stature,
enamel hypoplasia

VITAMIN D DEFICIENCY
• Inadequate intake and absence of sunlight
• Osteoblasts contain the vitamin D receptor
• Vitamin D deficiency in children produces rickets
• The most prominent clinical effect of Vitamin D
deficiency is osteomalacia, or the defective
mineralization of the bone matrix
• A deficiency of renal 1α-hydroxylase produces
vitamin D-resistant rickets
• Sex linked gene on the X chromosome
• Renal tubular defect of phosphate resorption
• Teeth may be hypoplastic and eruption may be
retarded

RICKETS

VITAMIN D-RESISTANT
RICKETS
• Above: Hypoplastic teeth
• Below: Minimal caries can
produce pulpitis; periapical
abscesses are thus common
• Lack 1-hydroxylase in kidney
• Rx: Respond well to 1, 25-
dihydroxyD3

CAUSES OF HYPOCALCEMIA
Hypoparathyroid Nonparathyroid PTH Resistance
Postoperative Vitamin D deficiency Pseudo-
hypoparathyroidism
Idiopathic Malabsorption
Post radiation Liver disease
Kidney disease
Vitamin D resistance

CAUSES OF HYPERCALCEMIA
Common Uncommon
Malignant disease, e.g.
some lung cancers
Renal failure
Hyperparathyroidism Sarcoidosis
Vitamin D toxicity
(excessive intake)
Multiple myeloma

SIGNS AND SYMPTOMS OF
HYPERCALCEMIA
• Neurologic
• Lethargy, drowsiness, depression, confusion
• Can lead to coma and death
• Neuromuscular
• Muscle weakness, hyptonia, decreased reflexes
• Cardiac
• Arrhythmias
• Bone
• Ache, pain, fracture

OSTEOPOROSIS
• Osteoporosis is characterized by a significant reduction in bone
mineral density compared with age- and sex-matched norms
• There is a decrease in both bone mineral and bone matrix
• Osteoporosis is the most common metabolic bone disease
• Women lose 50% of their trabecular bone and 30 % of their cortical
bone
• 30% of all postmenapausal women will sustain an osteoporotic
fracture as will 1/6th
of all men

NORMAL AND OSTEOPOROTIC BONE

SEQUELAE OF
OSTEOPOROSIS

OSTEO-
POROSIS

MEDICAL PITFALLS:
• Intravenous infusion with calcium-containing solutions
can cause severe tissue necrosis.
• Failure to distinguish calcium receptor defects from
• Failure to consider an associated cardiac lesion in an
infant with hypocalcaemia.
• Failure to monitor serum calcium concentrations for
at least 24 hours after intravenous calcium
withdrawal (Rebound hypocalcaemia can occur when
intravenous calcium is withdrawn, even on adequate
amounts of oral calcium.)

REFERENCES
• Burket’s textbook of oral medicine, eleventh edition
• Essentials of medical physiology, Sembulingam
• Differential diagnosis of Oral and Maxillofacial lesions, Wood
& Goaz, fifth edition
• White & Pharon, Textbook of Oral Radiology, fifth edition
• WEB

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