Bone physiology and endocrine functions

GOOD MORNING
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BONE PHYSIOLOGYBONE PHYSIOLOGY
AND ENDOCRINEAND ENDOCRINE
FUNCTIONSFUNCTIONS

• Introduction
• Classification of bone
• Calcium metabolism
• Phosphate metabolism
• Bone composition
• Bone morphology
• Bone ossification
• Bone remodeling & repair
• Effects of various hormones on bone function
• Conclusion www.indiandentalacademy.com

INTRODUCTIONINTRODUCTION
 InIn defining the physiologic basis of orthodontics,defining the physiologic basis of orthodontics,
the initial consideration is the bone morphologythe initial consideration is the bone morphology
(osteology) of the craniofacial complex.(osteology) of the craniofacial complex.
 Through systematic study of a personal collectionThrough systematic study of a personal collection
of more than 1000 human skulls, Dr. Spencerof more than 1000 human skulls, Dr. Spencer
Atkinson provided the modern basis of craniofacialAtkinson provided the modern basis of craniofacial
morphology as it relates to the biomechanics ofmorphology as it relates to the biomechanics of
stomatognathic function.stomatognathic function.
*Graber,Vanarsdall- Third Edition

* Graber,Vanarsdall- Third Edition
Two dimensional vectorial
analysis of stress in the
frontal section of human
skull
• Relative to a bilateral biting force of
100 arbitrary units, the load is
distributed to the midface as
compressive (negative) stress.
• The horizontal structural
components are loaded in tension.
• In a nongrowing individual the stress
across the midpalatal suture is zero.
• When masticating, loads increase &
the mid palatal suture is subjected to a
tension load, resulting in an increase
in maxillary width.

Classification of Bone TissueClassification of Bone Tissue
1)1) Woven boneWoven bone
2)2) Lamellar boneLamellar bone
3)3) Composite boneComposite bone
4)4) Bundle boneBundle bone
* Graber,Vanarsdall- Third Editionwww.indiandentalacademy.com

Woven boneWoven bone
 Relatively weak, disorganised, and poorly mineralized.Relatively weak, disorganised, and poorly mineralized.
 Serves a crucial role in wound healing by (1) rapidlyServes a crucial role in wound healing by (1) rapidly
filling osseous defects, (2) Providing initial continuity forfilling osseous defects, (2) Providing initial continuity for
fractures and osteotomy segments, and (3)fractures and osteotomy segments, and (3)
Strengthening a bone weakened by surgery or trauma.Strengthening a bone weakened by surgery or trauma.
 First bone to be formed in response to orthodonticFirst bone to be formed in response to orthodontic
loading is the woven bone type.loading is the woven bone type.
 Functional limitation of woven bone are an importantFunctional limitation of woven bone are an important
aspect both of orthodontic retention and of healingaspect both of orthodontic retention and of healing
period following orthognathic surgery.period following orthognathic surgery.
* Graber,Vanarsdall- Third Editionwww.indiandentalacademy.com

Lamellar boneLamellar bone
 Strong, highly organized, well- mineralized tissue.Strong, highly organized, well- mineralized tissue.
 Makes up more than 99% of the adult humanMakes up more than 99% of the adult human
skeleton.skeleton.
 Full strenght of lamellar bone that supports anFull strenght of lamellar bone that supports an
orthodontically moved tooth is not achieved untilorthodontically moved tooth is not achieved until
approx 1 year after completion of active treatment.approx 1 year after completion of active treatment.
* Graber,Vanarsdall- Third Edition www.indiandentalacademy.com

Composite boneComposite bone
 Osseous tissue formed by the deposition ofOsseous tissue formed by the deposition of
lamellar bone within a woven bone lattice, alamellar bone within a woven bone lattice, a
process calledprocess called CANCELLOUS COMPACTION.CANCELLOUS COMPACTION.
 Quickest means of producing relatively strongQuickest means of producing relatively strong
bone.bone.
 When the bone is formed in the fine compactionWhen the bone is formed in the fine compaction
configuration, the resulting composite of wovenconfiguration, the resulting composite of woven
and lamellar bone form structures known asand lamellar bone form structures known as
primary osteons.primary osteons.

Bundle boneBundle bone
 It is a functional adaptation of lamellar structure toIt is a functional adaptation of lamellar structure to
allow attachment of tendons and ligaments.allow attachment of tendons and ligaments.
 Perpendicular straitions, calledPerpendicular straitions, called Sharpey’sSharpey’s
fibers,fibers, are the major distinguishingare the major distinguishing
characteristics of bundle bone.characteristics of bundle bone.
 Distinct layers of bundle bone usually are seenDistinct layers of bundle bone usually are seen
adjacent to the PDL along physiologic bone-adjacent to the PDL along physiologic bone-
forming surfaces.forming surfaces.

Bone can also be classified asBone can also be classified as
 Compact BoneCompact Bone
 Solid bone, no spacesSolid bone, no spaces
 except for thoseexcept for those
accommodating cells,accommodating cells,
processes and bloodprocesses and blood
vesselsvessels
 Arms and legsArms and legs
 Spongy boneSpongy bone
 Usually interior ofUsually interior of
bonebone
 many spaces betweenmany spaces between
spicules (or trabeculae)spicules (or trabeculae)
of boneof bone
 Marrow found withinMarrow found within
the spacesthe spaces
 Spine, ribs, jaw, wristSpine, ribs, jaw, wrist
 Hips 50-50Hips 50-50

*Grays Anatomy – 39th edition www.indiandentalacademy.com

Calcium metabolismCalcium metabolism
 What is the recommended daily intake?What is the recommended daily intake?
 1000mg1000mg
 What is the plasma concentration?What is the plasma concentration?
 2.2-2.6mmol/L2.2-2.6mmol/L
 How is calcium excreted?How is calcium excreted?
 Kidneys - 2.5-10mmol/24 hrsKidneys - 2.5-10mmol/24 hrs
 How are calcium levels regulated?How are calcium levels regulated?
 PTH and vitamin D (+others)PTH and vitamin D (+others)
* Physiology- Robert M. Berne Fifth Editionwww.indiandentalacademy.com

Phosphate metabolismPhosphate metabolism
 Normal plasma concentration?Normal plasma concentration?
 0.9-1.3 mmol/L0.9-1.3 mmol/L
 Absorption and excretion?Absorption and excretion?
 Gut and kidneysGut and kidneys
 Regulation?Regulation?
 Not as closely regulated as calcium but PTHNot as closely regulated as calcium but PTH
most importantmost important

BONEBONE
 Organic FrameworkOrganic Framework
 Osteoblasts, osteocytes, osteoclastsOsteoblasts, osteocytes, osteoclasts
 CollagenCollagen
 Other organic moleculesOther organic molecules
 Inorganic SaltsInorganic Salts
 calcium and phosphorus keep bone rigidcalcium and phosphorus keep bone rigid
 Bone stores minerals and ions for body functionsBone stores minerals and ions for body functions
*Grays Anatomy – 39th
edition

Non – collagenous organic componentsNon – collagenous organic components
 Osteonectin – Phophorylated glycoprotein secreted byOsteonectin – Phophorylated glycoprotein secreted by
osteoblasts, binds to collagen & hydroxyappatite, play aosteoblasts, binds to collagen & hydroxyappatite, play a
role in hydroxy appatite crystallization.role in hydroxy appatite crystallization.
 Osteocalcin – Glycoprotein synthesized by osteoblasts,Osteocalcin – Glycoprotein synthesized by osteoblasts,
binds hydroxyappatite & Ca, used as a marker of newbinds hydroxyappatite & Ca, used as a marker of new
bone formation.bone formation.
 Bone proteoglycans biglycan & decorin may bindBone proteoglycans biglycan & decorin may bind
transforming growth factor–β (TGF-β).transforming growth factor–β (TGF-β).
 Bone sialoproteins, osteopontin & thrombospondinBone sialoproteins, osteopontin & thrombospondin
mediate osteoclast adhesion to bone surfaces viamediate osteoclast adhesion to bone surfaces via
binding to osteoclast integrins.binding to osteoclast integrins.

 Bone matrix also contains many growth factors,
proteases & protease inhibitors which are secreted by
osteoblasts, often in a latent form.
 Transforming growth factor-β (TGF-β), secreted by
osteoclasts as well as osteoblasts, is activated in the acid
conditions of the ruffled border zone of the osteoblast, &
may be a coupling factor for new bone formation at
resorption site.

Osteoprogenitor or Osteogenic cellsOsteoprogenitor or Osteogenic cells
 AppearanceAppearance
 pale staining,pale staining,
 small, spindle shapedsmall, spindle shaped
 LocationLocation
 present on all non-present on all non-
resorbing surfacesresorbing surfaces
 periosteumperiosteum andand
endosteumendosteum
 FunctionFunction
 give rise to osteoblastsgive rise to osteoblasts
in vascularized regionsin vascularized regions
 chondroblasts inchondroblasts in
avascular regionsavascular regions

OsteoblastsOsteoblasts
 large, nondividinglarge, nondividing
cells,cells,
 eccentric nucleus,eccentric nucleus,
 basophilic cytoplasm,basophilic cytoplasm,
 negative Golgi image,negative Golgi image,
 cytoplasmic processescytoplasmic processes
 synthesize andsynthesize and
secrete organicsecrete organic
constituents of boneconstituents of bone
matrix (matrix (osteoidosteoid))
 aid in calcificationaid in calcification

osteoblastsosteoblasts

OsteocyteOsteocyte
 smaller and lesssmaller and less
basophilic thanbasophilic than
osteoblast,osteoblast,
 have interconnectinghave interconnecting
processesprocesses
 keeps bone matrix inkeeps bone matrix in
good repairgood repair
 release calcium ionsrelease calcium ions
from bone matrixfrom bone matrix
when calciumwhen calcium
demands increasedemands increase

OsteoclastsOsteoclasts
 multinucleated,multinucleated,
 non-dividing cells,non-dividing cells,
 very acidophilic.very acidophilic.
 Have aHave a ruffledruffled
borderborder and aand a clearclear
zonezone..
 OriginOrigin
 From bloodFrom blood
monocytes/monocytes/
macrophagesmacrophages
 move around on bonemove around on bone
surfaces,surfaces,
 resorbs bone matrixresorbs bone matrix
 Focal decalcificationFocal decalcification
and extracellularand extracellular
digestion by aciddigestion by acid
hydrolases and uptakehydrolases and uptake
of digested materialof digested material
*Grays Anatomy – 39th edition

osteoclastosteoclast
*Grays Anatomy – 39th editionwww.indiandentalacademy.com

Osteoclast in Howship’s lacuna

PeriosteumPeriosteum
 A thin connective tissue layer surroundingA thin connective tissue layer surrounding
bonebone
 Contains the cells that are the source of boneContains the cells that are the source of bone
 Osteoprogenitor cellsOsteoprogenitor cells
 Must be preserved during surgeryMust be preserved during surgery

Relationships between bone cells & bone surfaces
• The canaliculi provide a
huge interface between
the interior surfaces of
mineralized bone &
intercellular fluid.
• This permits efficient
osteolysis with transfer of
calcium & phosphate to
the exterior via syncytial
processes connecting
interior osteocytes &
surface lining cells.

Bone schematicBone schematic
Osteoprogenitor cells
Periosteum
Osteocytes
Osteoclasts
Howship’s
lacunae
Osteoblasts

Cancellous boneCancellous boneCompact boneCompact bone
Not at same magnification

Compact bone morphologyCompact bone morphology
 LacunaLacuna
 osteocyte homeosteocyte home
 Haversian canalHaversian canal
 Central canal for bloodCentral canal for blood
vessels, etcvessels, etc
 CanaliculiCanaliculi
 Osteocyte processesOsteocyte processes
 LamellaeLamellae
 Concentric circlesConcentric circles
representingrepresenting
appositional boneappositional bone
depositiondeposition

Cancellous boneCancellous bone
trabeculaetrabeculae
marrowmarrow

Bone OssificationBone Ossification
 Involves both production of organic boneInvolves both production of organic bone
matrix and calcificationmatrix and calcification
 This isThis is NOTNOT bone GROWTH!!!bone GROWTH!!!
 Bone growsBone grows appositionallyappositionally (see cartilage)(see cartilage)
 Two types of ossification:Two types of ossification:
 IntramembranousIntramembranous
 EndochondralEndochondral
*Grays Anatomy – 39th editionwww.indiandentalacademy.com

Intramembranous ossificationIntramembranous ossification
 From undifferentiatedFrom undifferentiated
connective tissue cellsconnective tissue cells
 Mesenchymal cellsMesenchymal cells
 Vascularized areas of theVascularized areas of the
skull and facial bonesskull and facial bones
 Differentiate intoDifferentiate into
osteoblasts->osteocytesosteoblasts->osteocytes

Endochondral ossificationEndochondral ossification
 All long bones thatAll long bones that
begin as cartilagebegin as cartilage
 Chondrocytes andChondrocytes and
chrondroblasts tochrondroblasts to
differentiate todifferentiate to
 Needs vascularizationNeeds vascularization

WOLFF’S LAW OF BONE
A. Bone trabeculae in the head of femur follow the calculated stress
lines
B. Frontal section through the head of mandibular condyle
C. Saggital section through the head of mandibular condyle.
Note the arrangement of bony trabeculae, indicating similar arrangement
for resistance to stress as seen in the head of femur.
*William R. Proffit – 3rd
Edition www.indiandentalacademy.com

•During the power stroke, the mandibular
corpus on the balancing side is bent
primarily in the saggital plane, resulting in
residual stress along the alveolar bone and
compression stress along the lower border
of mandible.
• On the working side the corpus is twisted
primarily about its long axis. The muscle
force on this side tends to evert the lower
border of the mandible and invert the
alveolar process.
• The twisting movement associated with
the bite force has the opposite effect.
• The portion of the corpus between these
two twisting movements experiences
maximal twisting stress.
*Graber,Vanarsdall- Third Edition

Bone Remodeling and RepairBone Remodeling and Repair
 Occurs throughoutOccurs throughout
lifetime, involveslifetime, involves
osteoclasts andosteoclasts and
*BJO- 1998; 25: 101-107 www.indiandentalacademy.com

The cross-section through a bone
shows the
physiological relationship of bone
modeling and remodeling.
Modeling (M) changes the size or
shape of
a bone by forming or resorbing
bone along periosteal
and endosteal surfaces.
Remodeling (R) is internal
bone turnover to form new
secondary osteons. Osteo
clasts open resorption cavities
and osteoblasts fill
them with new bone.
*Seminars in Orthodontics Vol 6, No. 3
Modeling & Remodeling

Bone remodelling cycle

Growth factors that regulate bone remodellingGrowth factors that regulate bone remodelling
1.1. Insulin – like growth factors (IGF) I & IIInsulin – like growth factors (IGF) I & II
2.2. Transforming growth factor –b (TGF – b)Transforming growth factor –b (TGF – b)
superfamily, including the bone morphogeneticsuperfamily, including the bone morphogenetic
proteins (BMPs)proteins (BMPs)
3.3. Fibroblast growth factors (FGF)Fibroblast growth factors (FGF)
4.4. Selected cytokines of the interleukin (IL), tumourSelected cytokines of the interleukin (IL), tumour
necrosis factor (TNF), & colony – stimulating factornecrosis factor (TNF), & colony – stimulating factor
(CSF) families(CSF) families

Light Micrograph of trabecullar bone
• Multinucleate osteoclasts
(large arrows) are resorbing
calcified bone in a Howship’s
resorption lacuna, while
osteoblasts (small arrows) are
laying down matrix on the
surface of osteoid.
• Osteocytes (arrowheads)
are found within the
mineralized matrix.
• (Haematoxylin and Eosin,
x80, enlarged to 250%on
reproduction).
*BJO- 1998; 25: 101-107

BONE REMODELLING (COUPLING)
• The initial event involves the
synthesis and release of matrix
metalloproteinases (MMPs) by
osteoblasts which are responsible for
degrading the osteoid, exposing the
mineralized matrix which maybe
chemotactic to the osteoblast.
• The osteoblast also directly
stimulates osteoclast activity.
• During the resorption process
growth factors are released from the
matrix which then activate
osteoprogenitor cells.
• The osteoprogenitor cells mature into osteoblasts and ultimately replace the resorbed
bone.
• The mechanism by which osteoblasts are directed to form bone only in the resorption
lacunae may be due to the presence of molecules such as TGF- and BMPs which are leftβ
behind during osteoclastic activity.
*BJO- 1998; 25: 101-107www.indiandentalacademy.com

PROCESS OF BONE REMODELING
Signals carried by canalicular and syncytial routes from interior osteocytes, and endocrine
signals to resting osteoblasts and lining cells generate local paracrine signals. The
osteoclasts resorb an area of mineralized bone, and local macrophages complete the clean
up of dissolved elements. The process then reverses to formation as osteoblast precursors
are recruited to the site and differentiate into active osteoblasts. These lay down new
organic matrix and mineralize it. Thus, new bone replaces previously resorbed mature bone.
* Physiology- Robert M. Berne Fifth Edition

Parathyroid hormoneParathyroid hormone
 4 parathyroid glands located immediately behind the4 parathyroid glands located immediately behind the
thyroid gland – one behind each of the upper & each ofthyroid gland – one behind each of the upper & each of
the lower poles of the thyroid.the lower poles of the thyroid.
 Each gland is 6mm long, 3mm wide, & 2mm thick.Each gland is 6mm long, 3mm wide, & 2mm thick.
 Contains mainly chief cells & moderate no. of oxyphilContains mainly chief cells & moderate no. of oxyphil
cells.cells.
 Chief cells secrete PTH & oxyphil cells are believed to beChief cells secrete PTH & oxyphil cells are believed to be
modified or depleted chief cells that no longer secretemodified or depleted chief cells that no longer secrete
hormone.hormone.
 PTH is first synthesized on the ribosomes in the form of aPTH is first synthesized on the ribosomes in the form of a
preprohormone, a polypeptide chain of 110 amino acids.preprohormone, a polypeptide chain of 110 amino acids.

• This is cleaved first to a prohormone with 90 amino acids,
then to the hormone itself with 84 amino acids by the
endoplasmic reticulum & golgi apparatus, & finally is packed in
secretory granules in the cytoplasm of the cells.
Actions of Parathyroid hormone
1. The overall effect of PTH is to increase the plasma calcium
concentration & decrease the plasma phosphate concentration
by acting on 3 major target organs; directly on bone & kidney,
& indirectly on the gastrointestinal tract.

Effect on BoneEffect on Bone
 PTH accelerates removal of calcium from bone by 2PTH accelerates removal of calcium from bone by 2
processes.processes.
 Its initial effect is to stimulate osteolysis.Its initial effect is to stimulate osteolysis.
 A 2A 2ndnd
more slowly developing effect of constantmore slowly developing effect of constant
exposure to PTH is to stimulate the osteoclasts toexposure to PTH is to stimulate the osteoclasts to
resorb completely mineralized mature bone.resorb completely mineralized mature bone.
 Although PTH receptors are present on osteoclasts, theAlthough PTH receptors are present on osteoclasts, the
resorptive effects of PTH cannot be demonstrated inresorptive effects of PTH cannot be demonstrated in
vitro unless osteoblasts are also present as intermediaryvitro unless osteoblasts are also present as intermediary
cells.cells.
 PTH also has anabolic actions on bone.PTH also has anabolic actions on bone.

Effect of Estrogen on BoneEffect of Estrogen on Bone
 Estrogen defend against PTH- mediated resorption ofEstrogen defend against PTH- mediated resorption of
bone.bone.
 In estrogen- deficient conditions, such as that afterIn estrogen- deficient conditions, such as that after
menopause, the unabated effect of PTH on bonemenopause, the unabated effect of PTH on bone
contributes to the development of osteoporosis.contributes to the development of osteoporosis.
 Estrogen replacement therapy, which should beEstrogen replacement therapy, which should be
accompanied by progesterone, is useful for women ataccompanied by progesterone, is useful for women at
high risk for developing osteoporosis.high risk for developing osteoporosis.

Vitamin DVitamin D
 Source :-Source :-
1.1. Produced in the skin by ultravoilet radiation (D³)Produced in the skin by ultravoilet radiation (D³)
2.2. Ingested in the diet (D² & D³)Ingested in the diet (D² & D³)
 Not a classic hormoneNot a classic hormone
 Minimum daily requirement is approximatelyMinimum daily requirement is approximately
2.5μg, & the recommended daily intake is 10μg2.5μg, & the recommended daily intake is 10μg
(400 units)(400 units)
 Most important diet source areMost important diet source are fish, liver &fish, liver &
irradiated milk.irradiated milk.

Vitamin D ActionsVitamin D Actions
 The major action of 1, 25,-(OH)²- D is to stimulateThe major action of 1, 25,-(OH)²- D is to stimulate
absorption of calcium from the intestinal lumenabsorption of calcium from the intestinal lumen
against the concentration gradient.against the concentration gradient.
 In addition to calcium absorption, it stimulates theIn addition to calcium absorption, it stimulates the
active absorption of phosphate & magnesium acrossactive absorption of phosphate & magnesium across
the intestinal cell membrane.the intestinal cell membrane.
 Effects on bone –Effects on bone –
1.1. Stimulates bone resorption.Stimulates bone resorption.
2.2. Also plays a key role in bone formation.Also plays a key role in bone formation.
 Stimulates renal calcium reabsorption by increasingStimulates renal calcium reabsorption by increasing
the number of calcium pumps.the number of calcium pumps.

• In the absence of vitamin D, the effect of PTH in
causing bone absorption is greatly reduced
or even prevented.
• The mechanisum of this action of vitamin D is not
known, but it is believed to result from the effect of
1,25 –dihydroxycholecalciferol to increase calcium
transport throughcellular membranes.
• Vitamin D in smaller quantites promotes bone
calcification, by increasing calcium & phosphate
absorption from the intestines.
*Guyton

CalcitoninCalcitonin
 A peptideA peptide hormone secreted by thyroid gland.hormone secreted by thyroid gland.
 Tends to decrease plasma calcium concentrationTends to decrease plasma calcium concentration
&, in general, has effects opposite to those of PTH.&, in general, has effects opposite to those of PTH.
 Quantitative role of calcitonin is far less than thatQuantitative role of calcitonin is far less than that
of PTH in regulating calcium ion concentration.of PTH in regulating calcium ion concentration.
 Synthesis & secretion of calcitonin occur in theSynthesis & secretion of calcitonin occur in the
parafollicular cells, or C cells, lying in the interstitialparafollicular cells, or C cells, lying in the interstitial
fluid of the thyroid gland.fluid of the thyroid gland.

Calcitonin ActionsCalcitonin Actions
 The major effects of calcitonin administration is a rapidThe major effects of calcitonin administration is a rapid
fall in the plasma calcium concentration, caused byfall in the plasma calcium concentration, caused by
inhibition of bone resorption.inhibition of bone resorption.
 Calcitonin is a physiologic antagonist to PTH wrtCalcitonin is a physiologic antagonist to PTH wrt
calcium. However, with respect to phosphate, it has thecalcium. However, with respect to phosphate, it has the
same net effect as PTH ; that is, it decreases the plasmasame net effect as PTH ; that is, it decreases the plasma
phosphate level.phosphate level.
 Calcitonin also inhibits renal tubular calciumCalcitonin also inhibits renal tubular calcium
reabsorption, & thereby increases calcium excretion inreabsorption, & thereby increases calcium excretion in
the urine. This represents another mechanism forthe urine. This represents another mechanism for
preventing or reducing hypercalcemia.preventing or reducing hypercalcemia.

Cytokines & ProstaglandinsCytokines & Prostaglandins
 Cytokines are local biochemical mediators,Cytokines are local biochemical mediators,
secreted by mononuclear cells, that may interactsecreted by mononuclear cells, that may interact
directly or indirectly (by affecting neighboring cells)directly or indirectly (by affecting neighboring cells)
with bone cells.with bone cells.
 Cytokines can evoke the synthesis & secretion ofCytokines can evoke the synthesis & secretion of
numerous substances by their target cells,numerous substances by their target cells,
including prostaglandins, a variety of growthincluding prostaglandins, a variety of growth
factors, or cytokines.factors, or cytokines.
* Mayumi Saito et al – Interleukin 1 & prostaglandin E are involved in the response ofβ
periodontal cells to mechanical stress in vivo & in vitro – AJO 1991:99:226-40www.indiandentalacademy.com

• Interleukin-1 (IL-1) is a cytokine known to mediate a variety of
actions important to host defense mechanisms, inflammations
& autoimmunity.
• There are two molecular forms of IL-1 – IL-1 & IL-1α β
• The biological effects of IL-1 are manifested in nearly every
tissue & organ. IL-1 has potent amplifying effects on the
inflammatory response.
• One of the striking properties is the induction of
eicosanoid production, in particular PGE2, in several
types of cells such as fibroblasts. As PGE2 itself is known
to be a regulator of the inflammatory process, this effect
may be an important one in the acute episodes of PDL
inflammatory response to orthodontic force application.

• Prostaglandin E (PGE) was implicated in vivo as a mediator of
the effect of compression on osteoclasts during orthodontic tooth
movement. Indomethacin, a specific inhibitor of prsotaglandin
synthesis, reduced the rate of orthodontic tooth movement.
• PGE is a potent stimulator of bone resorption, & it produces a
dose-related increase in calcium release from bone, over the
concentration range of 10-9
to 10-5
M.
• Endogenous prostaglandin production has been shown to
mediate the bone-resorptive effects of a number of different
stimuli.
•Serum complement (in the presence of antibodies to cell-surface
antigens) increases PGE production & resorption in fetal rat long
bones.

• Bacterial collagenase, phorbol esters, meletin, fibroblasts, &
epidermal- & platelet-derived growth factors have all been found to
stimulate bone resorption in mouse calvaria by a protaglandin-
mediated mechanisum.
• Thus PGE synthesized by fibroblasts may affect the process of
bone remodeling by interacting with neighboring bone cells.
• Kenichi et al studied the clinical application of prostaglandin E1
(PGE1) upon orthodontic tooth movement. They found out that the
rate of tooth movement approximately doubled on the side of
several PGE1 injections compared to the control side.
* Kenichi Yamasaki- Clinical application of prostaglandin E1 (PGE1) upon orthodontic
tooth movement- AJO 1984; 85:508-18www.indiandentalacademy.com

Functionsof Growth HormoneFunctionsof Growth Hormone
It has effects:It has effects:
1)1) On growth of skeleton, skeletal muscleOn growth of skeleton, skeletal muscle
and viscera.and viscera.
2) On metabolism of a) carbohydrate b)2) On metabolism of a) carbohydrate b)
protein c) fat d) electrolytes.protein c) fat d) electrolytes.
3) On milk production - lactogenic effect.3) On milk production - lactogenic effect.
4) On erythropoisis.4) On erythropoisis.

Action On GrowthAction On Growth ::
a)a) G.H. stimulates the growth of skeleton. It hasG.H. stimulates the growth of skeleton. It has
specific action on the epiphysis, cartilages andspecific action on the epiphysis, cartilages and
promote chondrgenesis,promote chondrgenesis, consequentconsequent
mineralization causes linear growth of bones.mineralization causes linear growth of bones.
b) Growth hormone stimulate growth of viscera e.g.b) Growth hormone stimulate growth of viscera e.g.
Liver, Kidney, Thymus and alimentary canal.Liver, Kidney, Thymus and alimentary canal.
c) Growth hormones increase skeletal muscle mass.c) Growth hormones increase skeletal muscle mass.

TThyroid glandhyroid gland
 Regulates metabolism and blood calcium levels.Regulates metabolism and blood calcium levels.
 On skeletal system.On skeletal system. Thyroxine is required for theThyroxine is required for the
growth and maturation of epiphyseal cartilage so that ingrowth and maturation of epiphyseal cartilage so that in
the absence of this hormone, linear skeletal growththe absence of this hormone, linear skeletal growth
does not occur.does not occur.
 Excess thyroxine causesExcess thyroxine causes osteoporosisosteoporosis because ofbecause of
calcium drainage from the bone.calcium drainage from the bone.

Effects of Glucocorticoids on boneEffects of Glucocorticoids on bone
metabolismmetabolism
 ↓↓ Bone formationBone formation
 Most importantMost important
 ↑↑ Bone resorbtionBone resorbtion
 Probably only during 1Probably only during 1stst
6 – 12 months of Rx6 – 12 months of Rx
 ↑↑ OC production & postponed apoptosisOC production & postponed apoptosis
 Longterm,Longterm, ↓↓ bone turnoverbone turnover
 ↓↓ Intestinal absorbtion of calciumIntestinal absorbtion of calcium
 ↑↑ Urinary phosphate & calcium lossUrinary phosphate & calcium loss
 Direct effect on kidneyDirect effect on kidney
 Secondary HyperparathyroidismSecondary Hyperparathyroidism
 ↑↑ Bone lossBone loss
 Early but temporaryEarly but temporary

CONCLUSIONCONCLUSION
 Bone physiologic, metabolic, & cell kinetic conceptsBone physiologic, metabolic, & cell kinetic concepts
have important clinical applications in orthodontics &have important clinical applications in orthodontics &
dentofacial orthopedics. The application ofdentofacial orthopedics. The application of
fundamental concepts is limited only by the knowledgefundamental concepts is limited only by the knowledge
& imagination of the clinician. Modern clinical pratice is& imagination of the clinician. Modern clinical pratice is
characterized by a continual evolution of methodscharacterized by a continual evolution of methods
based on fundamental & applied research.based on fundamental & applied research.
*Graber,Vanarsdall- Third Editionwww.indiandentalacademy.com

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Bone physiology and endocrine functions

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Bone physiology and endocrine functions