Calcium & phosphorus metabolism and its applied aspects
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Transcript of Calcium & phosphorus metabolism and its applied aspects
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CALCIUM & PHOSPHORUS METABOLISM
DEPARTMENT OF ORAL PATHOLOGY AND
MICROBIOLOGY
2
PRESENTED BY
Dr G SHYAM RAJ
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CONTENTS• INTRODUCTION
• CALCIUM METABOLISM
FUNCTIONS
NORMAL VALUES AND TYPES
SOURCES AND REQUIREMENTS
ABSORPTION AND EXCRETION
REGULATION
• PHOSPHORUS METABOLISM
FUNCTIONS
NORMAL VALUES AND SOURCES
ABSORPTION AND EXCRETION
REGULATION
• APPLIED ASPECTS
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INTRODUCTION
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TOTAL BODY CALCIUM-
1100-1200gms
Skeleton(99%)
Intracellular(1%)
Extracellular(0.1%)
Ca10(PO4)6(OH)2
PLASMA : 2.5mmol/L
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TYPES OF CALCIUM
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CALCIUM IN BONES
• RAPIDLY EXCHANGEABLE CALCIUM : Small quantity
Exchangeable Ca
Maintain plasma Ca level
• SLOWLY EXCHANGEABLE CALCIUM : Large quantity
Stable calcium
Bone remodelling
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DAILY REQUIREMENTS OF CALCIUM
• 1-3 years :- 500 mg
• 4-8 years :– 800 mg
• 9-18 years :- 1300 mg
• 19-50 years :- 1000 mg
• 51 years and above :- 1200 mg
• Pregnant ladies and lactating mothers :- 1200 mg8
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SOURCES
• Whole milk : 10%
• Low fat milk : 18%
• Cheese : 27%
• Other diary products : 17%
• Vegetables : 7%
• Others ( meat, egg, grains, sugar, coffee, tea, chocolate etc) : 21%
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FUNCTIONS OF CALCIUM
• Contributes to hardness of bone
• Maintenance of excitability of nerve and muscle
• Normal skeletal and cardiac muscle contraction
• Hormone response coupling
• Cell division and growth
• Blood coagulation
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CALCIUM METABOLISM
• A complex regulatory system maintains the normal amounts of Ca,
phosphate in the body.
• Key hormone to regulate the amounts of Ca & phosphate are
1. Parathormone,
2. 1,25 – dihydroxycholecalciferol(calcitriol),
3. calcitonin
These hormones act on 3 organ system
Intestinal tract
The bone
Kidney 11
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ABSORPTION & EXCRETION OF CALCIUM
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PARACELLULAR PATHWAY
• Passive• Nonsaturable• Altering structure of intercellular
tight junctions
TRANSCELLULAR ROUTE
• Active• Saturable• 1,25-dihydroxy vitamin D3
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FACTORS INFUENCING CALCIUM & PHOSPHORUS IN GUT
• Vitamin D
• PTH
• Calcitonin
• Steroid hormones
• Fats
• Bile salts
• Protein diet
• Phosphorus
• pH
• Estrogen & androgen
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VITAMIN D IN CALCIUM ABSORPTION
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PARATHYROID HORMONE
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Normal plasma level : 1.5-5.5 ng/dL60-70% - degraded by kupffer cells of liver by proteolysis20-30% - occurs in kidneys
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FUNCTIONS
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Regulating intestinal absorption
Renal excretion
Exchange between extracellular fluid and bone
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EFFECT OF PTH ON CALCIUM AND PHOSPHATE CONCENTRATIONS
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CONTROL OF PARATHYROID SECRETION BY CALCIUM ION CONCENTRATION
• Decrease in Ca ion conc. in ECF causes the PTH gland to increase the
rate of secretions within minutes.
• Hypertrophy – rickets, pregnancy, lactation
• Decrease in PTH secretions
Excess quantity of Ca in diet
Increased Vitamin D in diet
Bone absorption caused by factors other than PTH
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PTH INCREASES CA ABSORPTION
Late distal tubules
Collecting tubules
Early collecting ducts
Ascending loop of Henle (lesser extent)
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CALCITONIN
• Parafollicular cells or clear cells ( C cells ) – follicles in thyroid
• In lower animals – parafollicular cells ultimobranchial glands
pharyngeal pouches
• Polypeptide chain- 32 aminoacids
• Plasma level : 1-2ng/dL
• Half life : 5-10 mins
• Degraded and excreted by liver and kidney
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• Decreases blood calcium levels by acting on bones, kidneys and
intestine
• Facilitates deposition of calcium on bones
• Increases excretion of calcium through urine
• Prevents absorption of calcium from intestine
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MECHANISM OF BONE CALCIFICATION
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Osteoblasts secrete collagen & ground substance
Polymerization
Osteoid (collagen)
Osteoblasts entrapped –osteoids
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Ca salt ppt. on the surface
Amorphous compounds (non-crystalline)
Reabsorption & reprecipitation
Hydroxyapatite crystals
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MECHANISM OF CA SALTS TO BE DEPOSITED IN OSTEOIDS
• Collagen fibers causes precipitation of Ca salts
• Osteoblasts secrete a substance into osteoids that neutralizes the
inhibitor(pyrophosphate)
• Natural affinity of collagen fibers for Ca salts causes precipitations
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BONE & EXTRACELLULAR FLUID
• Bone contains a type of exchangeable Ca that is always in
equilibrium with Ca ions in the extra-cellular fluids.
• Accounts for 0.4 – 1% of total bone Ca.
• Provides a rapid buffering mechanism to keep Ca ion conc. in
extracellular fluid.
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PTH increases Ca & P absorption from bone
Rapid phase
Slow phase
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RAPID PHASE
Removal of bone
Bone matrix in vicinity of osteocytes
Vicinity of osteoblasts along bone surface
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RAPID PHASE
• Osteocytes and osteoblasts form a system of interconnected cells.
• Osteocytic membrane system( separates the bone from ECF)
• Osteocytic membrane pumps Ca ions from the bone fluid into
extracellular fluid, creating Ca ion conc. 1/3rd that of extracellular
fluid.
• Osteolysis – Osteocytic pump becomes excessive activated.
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SLOW PHASE
Activation of slow phase
Already formed osteoclasts
New osteoclasts
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SLOW PHASE
• Osteoblasts & osteocytes send a secondary signal to osteoclasts.
• Osteoclastic resorption of bone lead to weakened bones &
secondary stimulation of osteoblasts.
• Prolonged administration or secretion of PTH over a period of
months to years results in evident resorption in all bones & even
development of large cavities filled with large multinucleated
osteoclasts.
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PHOSPHORUS
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• Essential mineral
• Diet : peas, dried beans, nuts, milk, cheese and butter
• Inorganic form – phosphate(PO4)
• Most abundant intracellular anion.
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FUNCTIONS
• Important component – ATP, DNA, RNA and many intermediates of
metabolic pathways
• Important constituent – bones and teeth
• Buffer – acid base balance
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NORMAL VALUES
• Total amount in body :– 500-800 gms
• 80% - bones and teeth
• 10.9% - Viscera
• 9% - skeletal muscle
• 0.1% - extracellular
• Normal plasma level : 0.84 – 1.44mmol/L (2.8-4.5 mg/dL)
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PHOSPHORUS METABOLISM
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FUNCTIONS
• Formation of bone & teeth
• Important constituent of high energy phosphate compounds.
• Helps in regulation of glycolysis
• Phosphorylation of lipids & sugar
• Urinary buffer, which regulates urinary pH.
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DEPLETION OF PHOSPHATE
• Skeletal muscle weakness
• Cardiac & respiratory muscle dysfunction
• Loss of red blood cell membrane integrity
• Abnormal formation of bone
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HYPOCALCEMIA
• Neuromuscular irritability
• Numbness and tingling sensation
• Tetanic muscle contraction in hands & feet
• Spasm of muscles of larynx & consequent airway obstruction.
• CNS causes seizures
• Marked dilatation of heart
• Changes in cellular enzyme activity
• Increased in membrane permeability in some cells
• Impaired blood clotting44
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CHVOSTEK’S SIGN
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TROUSSEAU’S SIGN
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ERBS SIGN
• Hyperexcitability of muscles to electrical stimulation
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ACCOUCHER’S HAND
• Muscular spasm leading to uncontrolled prolonged flexion of
metacarpophalangeal joints while the fingers remain extended.
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HYPERCALCEMIA
• Level above 12mg/dl & become marked at 15mg/dl
• Depresses nervous system & muscle activity
• Decreases the QT interval of heart causes constipation & lack of
appetite.
• Polyuria, nausea, tiredness
• Impaired mentation
• Coma
• Parathyroid poisoning (>17mg/dl)
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HYPOPARATHYROIDISM
• PTH glands are suddenly removed, Ca level 6 – 7 mg/dl within 2-3
days.
• Blood phosphate conc. Doubles
• Signs of tetany develop.
• Osteocytic reabsorption of exchangeable Ca decreases & the
osteoclasts become totally inactive
• Ca reabsorption is depressed
• Bone is usually strong
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PSEUDOHYPOPARATHROIDISM
• Deficiency of receptors for PTH in the target cells
• EVENTHOUGH – PTH secretion is increased – cannot act on target cells
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TREATMENT
• Parathyroid hormone
• Vitamin D (1,00,000 units)
• 1-2 gram intake of Calcium
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HYPERPARATHYROIDISM
• Primary hyperparathyroidism
• Secondary hyperparathyroidism
• Tertiary hyperparathyroidism
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PRIMARY HYPERPARATHYROIDISM
• Tumor of one of PTH gland.
• Mostly seen in women than men & children
• Extreme osteoclastic activity in bones
• Elevates Ca ion conc. in ECF which depresses phosphate ions.
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BROWN TUMOR
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Hyperparathyroidism results in disorders of bone and mineral metabolism.
Diffuse and focal lesions may arise in multiple bones.
On occasion, a patient with undiagnosed hyperparathyroidism presents with a lytic lesion that may be mistaken for a tumor.
These lesions are termed "Brown Tumors" due to the presence of old hemorrhage in the lesion.
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BONE DISEASE IN HYPERPARATHYROIDISM
• In mild disease new bone is deposited along with osteoclastic effect.
• In severe form osteoclastic absorption soon far outstrips
osteoblastic activity.
• Osteitis fibrosa cystica
• Slight trauma cause fracture.
• Alkaline phosphatase is increased
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• Jaw bone
Normal trabecular pattern is lost & replaced by granular or
ground glass appearance.
Moth-eaten like appearance.
Teeth are mobile and migrate.
Lamina dura diminished or completely absent in 10% of cases.
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PARATHYROID POISONING
• Ca level must rise above 17 mg/dl
• CaHPO4 crystals deposit
Alveoli of lungs
Tubules of kidney
Thyroid gland
Wall of arteries throughout the body
• Death occurs in few days
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KIDNEY STONES IN HYPERPARATHYROIDISM
• CaPO4 crystals tend to ppt. in kidneys, forming CaPO4.
• More in alkaline urine than acidic urine
• Acidotic diets and acidic drugs are used for treating renal calculi.
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SECONDARY HYPERPARATHYROIDISM
• Vitamin D deficiency
• Chronic renal disease
• Hypocalcemia, hyperphosphatemia & increased serum alkaline
phosphatase
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TERTIARY HYPERPARATHYROIDISM
• Parathyroid tumor develop from long standing secondary
hyperparathyroidism.
• Serum calcium is increased
• Phosphorus is normal to increased
• Alkaline phosphatase is increased
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MANAGEMENT
• Primary and tertiary require excision of parathyroid tumor.
• Secondary type - Subtotal parathyroidectomy is beneficial
• Renal osteodystrophy – high Ca diet, Vit.D supplementation and
reduction in dietary phosphate.
• Recent studies – use of calcitriol an inhibitor of PTH synthesis &
secretion.
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OSTEOPOROSIS
• Primary deficit of bone matrix with a secondary deficit of minerals
• Develop in 3 ways
Slight increase in bone resorption with slight decrease in
formation
Severe increase in bone resorption with normal rate of
formation
Normal resorption with severe decrease in formation
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ETIOLOGY
• Ageing
• Hereditary
• Nutrition & lifestyle
• Medications & other illness
• Decrease in muscle activity
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RADIOGRAPHIC FEATURES
• Decrease in density of bone
• Loss of normal trabecular pattern
• Thinning of matrix
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Types of osteoporosis
PostmenopausalSenile
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RICKETS
• THE PRIMARY DEFECTS :
1. MINERALISATION INTERFRENCE
2.DERANGED BONE GROWTH
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OSTEOMALACIA
• Accumulation of osteoid in place of mineralized bone
• Etiology
Vitamin D deficiency
Calcium mal-absorption
Liver & renal disorders
Prolonged anticonvulsive drugs
Hypophosphatemic rickets
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CLINICAL FEATURES
• Weakness & generalized bone pain
• Pseudofracture
• Partial or complete fracture without displacement
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RADIOGRAPHIC FEATURES
• Generalized rarefaction
• Cortical thinning
• Homogenous granular appearance throughout the maxilla &
mandible
• Lamina dura absent or less prominent
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OSTEITIS DEFORMANS
• Early
• Intermediate
• Late
• Etiology
Genetic link
Viral infection
Inflammatory
Vascular disorders
Autoimmune connective tissue
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CLINICAL FEATURES
• Non specific headaches
• Impaired hearing
• Involved bone become warm to touch
• Maxilla involved more
Alveolar ridge becomes widened & the palate is flattened
Teeth become loose & migrate, producing spacing
Mouth may remain open, exposing the teeth (lips are too small)
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LABORATORY FINDINGS
• Serum Ca & Phosphatase level – normal limits
• Serum alkaline phosphatase – elevated
• Urine hydroxyproline - elevated
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HYPOPHOSPHATEMIA
• Serum phosphate < 0.80 mmol/L
• MODERATE : - 0.32-0.65 mmol/L
• SEVERE :- <0.32 mmol/L
• Results from
1. Internal redistribution of phosphorus
2. Increased urinary excretion
3. Decreased intestinal absorption
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• CLINICAL FEATURES:-
• MUSCLE DISORDERS: Proximal myopathy, dysphagia and ileus
• Myocardial dysfunction
• Respiratory failure and failed weaning from ventilators
• Hemolysis, thrombocytopenia
• Metabolic acidosis and metabolic encephalopathy
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HYPERPHOSPHATEMIA
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• Occurs due to
1. Increased phosphate load due to endogenous and exogenous
sources – exceeds – renal excretory ability
2. Decreased urinary excretion
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CLINICAL MANIFESTATIONS
• Tetany and seizures due to hypocalcemia
• Elevation of calcium x phosphate product – soft tissue calcification
• Nephrocalcinosis, cardiac and pulmonary calcification
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DENTAL
CONSIDERATIONS
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DENTINAL SCLEROSIS
Sclerosis of primary dentin is a regressive alteration in tooth
substance that is characterised by calcification of the dentinal tubules
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DEAD TRACTS
• dead tracts in dentin are seen in ground sections of teeth and are
manifested as a black zone by transmitted light
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SECONDARY DENTIN
• secondary dentin , which is formed after deposition of the primary
dentin has been completed , is characterised by its irregular
morphological pattern
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HETEROTOPIC CALCIFICATION
• it is defined as deposition of calcium salts in tissue other than
osteoid or enamel
• it is of 2 types
1.METASTATIC CALCIFICATION :
calcium salts are precipitated in undamaged tissue
it is commonly seen in kidney
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• CAUSES OF METASTATIC CALCIFICATION :
hyperparathyroidism
hypervitaminosis D
excessive absorption of calcium
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• DYSTROPHIC CALCIFICATION
• it is deposition of calcium salts in dead or degenerating tissues
• Pathogenesis : related to change in local condition of the tissues
• Clinical features :
it is found intraorally in gingiva , tongue , pulp of the teeth.
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PULP CALCIFICATION
• 1.PULP STONES
• 2.DIFFUSE CALCIFICATION
PULP STONES CLASSIFIED AS
TRUE
FALSE
TRUE DENTICLE : localized masses of calcified tissue resembling tubular structure
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• FALSE DENTICLES : do not exhibits dentinal tubules
• FREE & ATTACHED DENTICLES
FREE DENTICLES : lying entirely within pulp tissue
ATTACHED DENTICLES : continuous with dentinal walls
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DIFFUSE CALCIFICATION
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• Most common – root canals
• Resembles calcifications seen in other tissues following degeneration
• Calcific degeneration
• Amorphous unorganized linear strands paralleling blood vessels and nerves
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HYPERCEMENTOSIS
• It may be regarded as a regressive change of teeth characterised by
the deposition of excessive amounts of secondary cementum on
root surface
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REFERENCES
• Textbook of Medical physiology – Guyton & Hall (10th edition)
• Anthony’s textbook of anatomy & physiology – Gary.A.Thibodeau (14th
edition)
• Textbook of physiology – Robert.M.Beene
• Differential diagnosis of Oral & Maxillofacial lesions – Woods & Goaz.
• Applied Oral physiology ( 2nd edition) – Christopher L.B Lavelle
• JAPI - Vol 56 – Aug 2008 - Disorders of Calcium, Phosphorus and
Magnesium Metabolism – Amit K Ghosh , Shashank R Joshi
• ATLAS OF DISEASES OF KIDNEY - Robert W. Schrier VOL 1
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