Ca metabolism/ dental crown & bridge courses

Calcium Metabolism
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

Introduction
• Calcium (Ca) is the chemical element with
atomic number 20.
• 5th
most abundant element by mass in the
Earth's crust.
• Ca is essential for living organisms - cell
physiology, functions as a signal for many
cellular processes.

• Ca metabolism or homeostasis is the
mechanism by which the body maintains
adequate Ca levels.
• The average adult human body contains
1000g of Ca,99% is in the bones, 4 - 5g in
the soft tissues (muscles) &1g in the ECF.

• Adult human daily intake - 0.8 to 1g of
which 350mg is absorbed in the intestine.
• 250mg secreted by intestinal juices &
sloughed mucosal cells.
• 900mg/day – excreted in feces.
• 99% of filtered Ca is reabsorbed in
kidneys, 100mg/day – excreted in urine.
• Normal blood Ca level – 9.4mg/dl.

• Forms of Ca in the body –
1. Protein bound Ca
2. Complexed Ca
3. Ionized Ca
• Protein bound Ca – loosely bound almost
entirely to plasma proteins, comprises
40% of total plasma Ca and is inactive.

• Complexed Ca – combined with citrate,
phosphate, or other anions, amounts to
about 10% of total plasma Ca, diffusible,
non-ionized, inactive.
• Ionized Ca – diffusible and physiologically
active, comprises about 50% of the total
plasma Ca.

Absorption & Excretion
• Vit D is required for intestinal absorption –
regulating Ca homeostasis.
• Calbindin (Ca binding protein), essential
for Ca absorption – synthesis induced by
Vit D.
• Ca is absorbed throughout the length of
the small intestine, greater in the
duodenum and proximal jejunum.

• The rate and extent of Ca absorption
depends on – age, body requirements,
availability in the gut.
• Intestinal absorption is increased in late
pregnancy and during lactation – high
requirement.
• Absorption diminishes with age.

• Acidic pH , , alkaline pH absorption.
• Presence of P is essential for optimal
absorption of Ca.
• Bile influences Ca absorption –
1. Bile promotes digestion and absorption of
fat – reduced bile leads to increased
amounts of lipids which inhibit Ca
absorption by forming insoluble
complexes.

2. Bile salts increase the solubility of Ca.
3. Bile is necessary for optimal absorption of
Vit D.
• Ca absorption is inhibited by phytic acid
present in cereals.
• Oxalates form insoluble Calcium oxalate
preventing Ca absorption.

Ca Physiology
• The importance of Ca in physiology was
first revealed by Sydney Ringer in 1883.
• Clotting factor IV.
• Exocytosis, neurotransmitter release, &
muscle contraction.
• Mechanical stability to bones, teeth.
• Electrical conduction system of heart, Ca
depolarizes the cell, proliferating the
action potential – sliding of actin & myosin
- contraction of heart muscle.www.indiandentalacademy.com

Bone Calcification –
1.Secretion of collagen molecules, & ground
substance(proteoglycans) by osteoblasts.
2.Collagen monomers polymerise –
collagen fibers – Osteoid.
3.Ca salts precipitate on collagen fibers –
Hydroxyapetite crystals.

• Plasma Ca conc is principally maintained
by Vit D.
• Calcitriol (1,25 – dihydroxyvitamin D)
achieves this in 3 ways –
1.Increases intestinal absorption of Ca
2.Reduces excretion of Ca
3.Mobilizes bone mineral

• Parathyroid hormone is the most
important hormone involved in Ca
homeostasis.
• Other hormones – 1,25 DHCC, Calcitonin,
Thyroxine, Adrenal glucocorticoids,
Gonadal hormones and Growth hormone.

Parathyroid Hormone –
• Secreted by parathyroid glands.
• Secretion is controlled by Ca ion conc in
blood.
• Half life in circulation – 20min.
• Mainly acts on bone and kidney.

Actions of PTH –
1.Hypercalcemia & Hypophosphatemia.
2.Hyperphosphaturia & Hypocalcuria.
3.Increased bone resorption.
4.Conversion of 25-HCC to 1, 25-DHCC in
kidneys.

Calcitonin –
• A peptide hormone secreted by
parafollicular cells of thyroid gland, tends
to decrease plasma Ca conc – opp in
action to PTH.
• Secreted by increased Ca conc.
• Stops bone resorption by inhibiting
osteoclasts activity and their production.

Disorders of Ca Metabolism
Hypocalcemia –
• Ca levels <9.4mg/dl.
• Hyperexcitability of nervous system –
increased neural permeability to Na –
repeated initiation of action potentials.
• Seizures – increased excitability in brain.
• At 6.4mg/dl – Tetany – carpopedal spasm.
• At 4mg/dl – lethal.

Hypercalcemia –
• Ca levels >12mg/dl.
• Depression of nervous system.
• Lack of appetite, constipation – depressed
contractility of GIT.
• At 17mg/dl, calcium phosphate crystals
are precipitated throughout the body.

Hypoparathyroidism –
• Decreased secretion of PTH.
• Accidental removal of parathyroids during
thyroidectomy.
• DiGeorge syndrome – congenital absence
of parathyroids.
• Decreased osteoclastic reabsorption of Ca
from the bones – decreased Ca levels.

• Increased neuromuscular excitability –
muscle spasm, stiffness – hands, feet,
face, tongue, larynx.
• Tetany – Ca conc 0f 6-7mg/dl.
• Tetanic spasm of laryngeal muscles
obstructs respiration – death.

• Prone to memory loss.
• Seizures.
• Scaly skin.
• Increased bone density.
Two clinical signs important in the diagnosis
of hypoparathyroidism –
• Chvostek’s sign
• Trousseau’s sign

• Chvostek’s sign – spasm of facial muscles
especially lips and ala of nose produced
by tapping the facial nerve at its point of
origin anterior to the tragus of ear.
• Trousseau’s sign – spasm of the hand
after inflating the cuff of
sphygmomanometer because of
temporary occlusion of blood supply to the
arm.

O/M –
• Altered tooth eruption.
• Short, blunted roots.
• Enamel hypoplasia.
• Dentin dysplasia.
• Circumoral paresthesia – first symptoms.
• Predisposition to Oral Candidiasis.

Management –
• Calcium gluconate.
• PTH.
• Vit D or 1,25-dihydroxycholecalciferol.

Pseudohypoparathyroidism –
• X – linked dominant disorder
characterized by low Ca & elevated P.
• Insensitivity of bone and kidney to PTH.

Primary Hyperparathyroidism –
• Abnormality of parathyroid glands
resulting in excess secretion of PTH.
• Tumors of parathyroid gland, pregnancy
and lactation.
• Increased osteoblastic & osteoclastic
activity(outnumber) – bone resorption.
• Osteoblasts secretes alkaline
phosphatase – high levels aid in the
diagnosis.

C/F –
• Musculoskeletal system - weakness &
pain.
• Genitourinary system – polyuria,
polydipsia, renal stones.
• CVS – arrhythmias.
• GI – abdominal pain, anorexia,
constipation, peptic ulcers.

• Neuropsychiatric – mental confusion,
lethargy, drowsiness.
• Eye – band keratopathy – Ca deposition in
cornea.
• Vague bone pain is common.
• Bones, (psychic) moans, (abdominal)
groans & (renal)stones.
• Calcium phosphate crystals deposition in
alveoli of lungs, kidneys, thyroid, stomach
mucosa, arteries throughout the body.

R/F –
• Extensive decalcification and large
punched out cystic areas – osteitis fibrosa
cystica – classic osseous change.
• Multiple fractures of weakened bones on
slight trauma & osteopenia.
• CGCG – Brown tumor.

O/M –
• Vague jaw bone pain.
• Tooth mobility, pain – mastication,
percussion.
• Pulp stones, root resorption.
• Soft tissue calcifications of salivary glands.
• Fasciculations of tongue.
• Generalized loss of lamina dura.

• Loss of medullary trabeculations - ground
glass appearance of bone.
• Loss of cortication of inferior border of
mandible and mandibular canal.
• Solitary or multiple intraosseous
radiolucent lesions – brown tumor of
hyperparathyroidism – resembling CGCG
histologically.

Secondary Hyperparathyroidism –
• Elevated PTH - compensation to
hypocalcemia.
• Caused by Ca malabsorptive disease of
GIT, Vit D deficiency, CRF.
• Ca levels may be normal or decreased.

R/F – Teeth & Jaw Bones -
• Pulp calcifications.
• Widening of PDL space.
• Total or partial loss of lamina dura.
• Bone demineralisation.
• Ground glass appearance.
• Metastatic soft tissue calcifications.
• Brown tumor.
• Abnormal bone healing post extraction.

Tertiary Hyperparathyroidism –
• Due to long standing secondary
hyperparathyroidism.
• Seen in CRF patients.
• Hypercalcemia and 5 times elevation of
alkaline phosphatase levels.

Pseudohyperparathyroidism –
• Excessive PTH production by tissues
other than parathyroid glands.
• Carcinoma – breast, lung, liver, pancreas
and kidney – hypercalcemia.

Rickets –
• Occurs mainly in children.
• Vit D deficiency – Ca & P deficiency.
• Bone resorption – compensatory
increased secretion of PTH.
• Excess Ca depletion – Tetany.
• Treatment – Vit D, Ca & P.

Osteomalacia –
• Ault Rickets.
• Ca def disorder caused by defective
deposition of Ca & P in developing bone
matrix of the adult.
• Dietary deficiency of Vit D and Ca.
• CRF.

• Hypocalcemia, hypophosphatemia & Vit D
deficiency - impaired mineralization of
bone matrix – Osteomalacia.
• Bowing of weight bearing extremities –
abnormal remodelling.
• Prone for bone fracture.
• Growth and development of condyle may
be slow.

R/F –
• Decreased bone density
• Thinning of cortices.
• Rarified zones called Milk man’s lines or
Looser’s zones.
• Vit D 2000 to 4000IU/day for 6 to 12
weeks followed by 200 to 400IU/day.

Osteoporosis –
• Most common of all bone diseases in
adults, especially in old age.
• Diminished organic bone matrix rather
than from poor bone calcification.
• C/F – pain, fracture, bone deformity.

Causes of Osteoporosis –
• Lack of physical activity.
• Malnutrition – lack of protein matrix
formation.
• Lack of Vit C – def osteoid formation by
osteoblasts.
• Post menopausal def of estrogen.
• Cushing’s syndrome – excess
glucocorticoids – decreased deposition,
increased catabolism of protein,
depressed osteoblastic activity.www.indiandentalacademy.com

R/F –
• Increased bone translucency.
• Thinning of trabeculae and cortex.
• Edge deformities of vertebrae – fish
shaped vertebrae.
• Axial bones first involved followed by skull
and jaw bones.

References
• Text Book of Medical Physiology, Guyton,
11th
Edition.
• Samson Wright – Applied Physiology, 13th
Edition.
• Harpers Illustrated Biochemistry, 27th
Edition.
• Merck Manual of Geriatric Medicine, 3rd
Edition.

• Burket’s – Oral Medicine – 11th
Edition.
• Harrison’s Principles of Internal Medicine,
16th
Edition.
• Oral Diagnosis, Oral Medicine, and
Treatment Planning – Bricker – 2nd
Edition.
• Chang et.al. Unique Imaging Findings in
the Facial Bones of Renal
Osteodystrophy. Am J Neuroradiol
28:608–09 Apr 2007.

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