Bone /orthodontic courses by Indian dental academy

BONE
www.indiandentalacademy.com

B.D Chaurasia-Anatomy
Ten Cate’s ,Oral Histology 7th edition
Orban’s Oral Histology & Embryology 13th edition
Inderbir singh-histology
HAMS -histology

At the end of the lecture the student should be able to
understand the
 Functions of bone
 Composition of bone
 Classification of bones
 Bone histology
 Bone cells
 Classification of bones
 Bone formation

 Introduction
 Functions
 Composition
 Bone cells in detail
 Classification
 Bone ossification
CONTENTS

 Bone is a mineralised connective tissue with a relatively
flexible character and compressive strength.
 It is a living tisssue which makes up the body skeleton.
 It is one of the hardest structures of the body.
 It provides shape and support for the body.

Mechanical
 The bones of the legs, pelvic girdle, and
vertebral column support the weight of
the erect body.
 The mandible (jawbone) supports the teeth.
 Other bones support various organs and tissues.

 The bones of the skull protect the brain.
 Ribs and sternum protect the lungs and heart.
 Vertebrae protect the spinal cord.

It also provides site of attachment for tendons and muscles,
which are essential for locomotion.
Skeletal muscles use the bones as levers to move the body.

Metabolic
 Mineral storage —bones act as reserves of minerals important
for the body, most notably calcium and phosphorus.
 Growth factor storage —mineralized bone matrix stores
important growth factors such as insulin‐like growth factors,
transforming growth factor, bone morphogenetic proteins and
others.
 Fat storage — the yellow bone marrow acts as a storage
reserve of fatty acids.
 Acid‐base balance —bone buffers the blood against excessive
pH changes by absorbing or releasing alkaline salts.

 Detoxification —bone tissues can also store heavy metals and
other foreign elements, removing them from the blood and
reducing their effects on other tissues.
These can later be gradually released for excretion.
Bone controls phosphate metabolism by releasing fibroblast
growth factor – 23 (FGF‐23), which acts on kidneys to reduce
phosphate reabsorption.
 Synthetic
 Blood cell formation: hematopoiesis occurs within the marrow
cavities of the bone.

 Bone cells also release a hormone called osteocalcin,
which contributes to the regulation of blood sugar
(glucose) and fat deposition.
 Osteocalcin increases both the insulin secretion and
sensitivity, in addition to boosting the number of
insulin‐producing cells and reducing stores of fat.

 Inorganic part of bone is made of bone minerals.
 Hydroxyapetite crystals,
 Carbonate content
 Calcium phosphate
 Bone crystals in the form of thin plates or leaf like
structures.
 Ions-calcium phosphate, hydroxyl and carbonate.
 Citrate, Mg,Na,K,F,Fe,Zn,Cu,Al,Pb,Sr,Si,B are present
in small quantities.

 The organic matrix is known as osteoid and is
made up of collagen and the noncollagenous
proteins.
 Collagen-TypeI,III,V,XII.
 TypeI(>95%)collagen is the principal collagen in
mineralised bone together with typeV
collagen(<5%).
 Sharpey’s fibres contain typeIII collagen with
typeI collagen.

 Types I,V,XII collagens are expressed by osteoblasts.
 The pink to red color of bone matrix seen in H&E sections is
due to the substantial collagen content.
 Non collagenous proteins: Osteocalcin,Osteopontin,Bone
sialoprotein and Osteonectin.
 The matrix also contains proteases and a variety of cytokines.

 Non collagenous proteins
 Comprise the remaining 5% of the total organic content of
bone matrix.
 Most are endogenous proteins produced by bone cells.
 Albumin derived from other sources such as blood and become
incorporated into bone matrix during osteosynthesis.

 First noncollagenous protein recognised –Osteocalcin
 Also known as bone Gla protein as it contains the amino acid
gamma-carboxyl glutamic acid.
 Gla protein has been demonstrated in alveolar bone IHC.

 Osteocalcin is a glycoprotein.
 Involved in bone calcification
 Calcium binding protein
 It is used as a marker of new bone formation

 Secreted by osteoblasts
 Regulated by vitD3 & Parathyroid hormone
 The carboxyl terminal segment acts as a chemoattractant to
osteoclast precursors.
 Suggesting a role in bone resorption

 Osteopontin & bone sialoprotein
Previously
termed
bone sialoprotein I bone sialoprotein II
Demonstrated in alveolar bone IHC
Both proteins are heavily glycosylated and phosphorylated with high levels of
acidic aminoacids
Expression of both proteins stimulated by TGFb & glucocorticoids
Stimulate bone formation

 Osteopontin is aspartate predominant.
 Strongly upregulated by vit D3
 Bone sialoprotein is glutamic acid predominant.
 Bone sialoprotein transcription is supressed by Vit D3.
 Osteopontin, Vitronectin, Fibronectin are termed (RGD)
containing proteins as they have a specific amino acid sequence
(Arg-Gly-Asp).

 Osteonectin
 Noncollagenous protein.
 Bound to collagen &hydroxyapetite crystals.
 It is a secreted calcium binding glycoprotein,that interacts
with extracellular matrix molecules.
 Play a role in 1.regulation of cell adhesion
2.proliferation &modulation of cytokine
activity
3.in initiating hydroxyapetite crystal
formation

 Proteoglycans also present in the bone matrix.
 Bone matrix also contains proteases, protease
inhibitors and a variety of cytokines secreted by
osteoblasts, that regulate cell membrane.
 A large chondroitin sulphate proteoglycan – from non
mineralised bone matrix
 Two small proteoglycans such as biglycan and decorin
–found in EDTA extracts of bone.

 % of decorin and biglycan decreases with maturation
of bone.
 Third small proteoglycan has been found entirely
associated with mineral crystals.

 Biglycan is more prominent in developing bone and has
been mineralised to pericellular areas.
 Function of biglycan & decorin
 It binds TGF-b and extracellular matrix macromolecules
including collagen and thereby regulate-fibrillogenesis.
 Decorin as the name suggests ,binds mainly within the
gap region of collagen fibrils and decorates the fibril
surface.

 The primary calcification in bone follows the removal
of decorin and fusion of collagen fibrils.
 Lysyl oxidase and tyrosine rich acidic matrix proteins
(TRAMP) are components of demineralised bone and
dentin matrix.
 Lysyl oxidase is an enzyme for collagen cross linking.
 (TRAMP),also known as dermatopontin binds decorin
and TGF-b and these proteins regulate the cellular
response to TGF-b.

 Procollagen, peptides, thrombospondin, fibronectin,
vitronectin and alkaline phosphatase are the other
proteins found in the bone.

 Cells of bone
 1.Osteoprogenitor cells
 2.Osteoblasts
 3.Osteocytes
 4.Osteoclasts

 Osteoprogenitor cells
 Stem cells of mesenchymal origin.
 Can proliferate &convert themselves into osteoblasts.
 In fetus, cells are numerous at sites where bone formation is to
take place.
 In adults, cells present over bone surfaces(on both the
periosteal and endosteal aspects).

 Osteoblasts
 Bone forming cells derived from osteoprogenitor cells.
 These are mononucleated cells responsible for the
synthesis and secretion of the constituents of the bone
matrix.
 Periosteum serves as an important reservoir of osteoblats,
particularly during childhood growth, after skeletal
fractures or with bone forming tumors.

 Morphology
 Osteoblasts are basophilic,plump cuboidal or slightly
flattened cells.
 The cells are found on the forming surfaces of growing
or remodelling bone.
 They form a protein mixture known as osteoid, which
mineralizes to become bone.
 Osteoid is primarily composed of Type I collagen.

 Osteoblasts exhibit abundant and well developed
protein synthetic organelles.
 The intense cytoplasmic basophilia is due to an
abundance of RER.
 Nucleus is situated eccentrically in the part of the cell
that is farthest away from the adjacent bone surface.
 The cells contact one another by adherens and gap
junctions.

 Osteoblasts also contain prominent bundles of actin,
myosin and cytoskeletal proteins which are associated
with maintenance of cell shape, attachment and
motility.
 Formation of osteoblasts
 They are derived from undifferentiated pluripotent
stem cells.
 Osteoprogenitor cells are divided into two types
 1.determined osteogenic precursor cells
 2.inducible osteogenic precursor cells

 The osteoprogenitor cells express transcriptional
factors cbfa-1/Runx-2 and osterix (Zinc finger
containing) which are essential for osteoblast
differentiation.
 The activity of osteoblasts is regulated by
hormones like PTH, vitD3, growth hormone and
insulin.
 The other factors are BMPs, IGF-1 and 2, FGF,
TGF-b and PDGF.

 They robustly produce alkaline phosphatase, an
enzyme that has a role in the mineralization of bone, as
well as many matrix proteins.
 Osteoblasts are the immature bone cells, and
eventually become entrapped in the bone matrix to
become osteocytes, which are the mature bone cells.
 All bone lining cells are osteoblasts.

 Functions
 Formation of new bone via synthesis of various
proteins and polysaccharides.
 Regulation of bone remodelling and mineral
metabolism.
 It plays a significant role in the mineralisation of
osteoid.
 They secrete typeI collagen which is widely distributed
and not unique to osteoblasts whereas ,osteocalcin and
cbfa-1 are specific to cells of osteoblast lineage.

 These provide useful markers of osteoblast phenotype.
 Osteoblasts also secrete small amounts of typeVcollagen ,
osteonectin, osteopontin, RANKL, osteoprotegerin,
proteoglycans, proteases, growth factors etc
 They exhibit high levels of alkaline phosphatase on outer
surface of plasma membrane –used as a cytochemical
marker to distinguish preosteoblasts from fibroblasts.
 Total alkaline phosphatase activity has been recognised as
a reliable indicator of osteoblast function.

• Osteoblasts express receptors for various hormones
including PTH, vitD3, estrogen and glucocorticoids,
involved in the regulation of osteoblasts differentiation.
• Osteoblast recognise the resorptive signal and transmit it
to the osteoclast.
• RANKL is a membrane bound TNF related factor that is
expressed by osteoblast/stromal cells.
• The presence of RANKL is vital in osteoclast
differentiation.

 (b) Three key intrinsic factors regulate osteoblast
maturation and bone formation: the Runx2 platform for
hormone and cytokine action (receptors not shown), with its
assortment of cytosolic and nuclear co-activators (blue) and
co-repressors (red); osterix, through its interaction with
NFAT2; and the Wnt–-catenin signals and their inhibitors
(red). AR, androgen receptor; ATF-4, activating
transcription factor-4; C/EBP, CCAAT/enhancer binding
protein; CBP, CREB binding protein; DCX, double cortin;
Dlx-5, distalless homeobox-5; FIAT, factor inhibiting
activating transcription factor-4; GR, glucocorticoid
receptor; HDAC, histone deacetylase; MORF, mortality
factor; Oct-1; octamer binding protein-1; PLC,
phospholipase C; PPAR, peroxisome proliferator-activated
receptor; RSK, 90-kDa ribosomal S6 kinase; YAP, yes-
associated protein.

 Regulation of osteoblast activity
 The overall integrity of bone is controlled by
1.hormones
2.proteins secreted by hematopoietic bone marrow cells
and bone cells.

Role of parathyroid hormone
• In response to hypocalcemia, the hormone activates a
mechanism for the release of calcium from bone.
• PTH does so by an indirect effect mediated by PTH
receptors on bone stromal cells including osteoblasts,
as osteoclasts are devoid of PTH receptors.
• PTH regulates serum calcium levels by stimulation of
bone resorption and can also have anabolic effects in
vivo that appear to be mediated through TGF-b and
IGF-I.

 These opposing effects of PTH are consistent with the
apparent coupling of bone formation and remodelling.

 Role of vit D3
 Vit D3 stimulates bone resorption .
 Also essential for normal bone growth and mineralisation.
 It also promotes calcium absorption from intestine.
 It stimulates synthesis of osteocalcin,osteopontin by osteoblasts
and supresses collagen production.

 The action of parathormone and vitD3 is that they
enhance bone resorption at high concentrations
(pharmacological).
 Support bone formation at low (physiologic)
concentrations.

 Growth hormone
 Required for attaining normal bone mass which is
mediated by the local production of IGF-I.
 It binds to membrane bound growth hormone receptors
on activated osteoblasts.
 Insulin targets osteoblasts directly and stimulates bone
matrix formation and mineralisation.
 It indirectly affects bone formation through stimulation
of IGF-I produced in the liver.

 Bone morphogenic proteins
These are the only factors that can initiate osteoblastogenesis
from uncommitted progenitor cells.
These proteins are expressed during embryonic development
as well as in adulthood.
BMPs 2,4,6 direct the pluripotent cells to commit to an
osteoblastic pathway.
BMPs can regulate cbfa-1 under certain conditions during
osteoblast differentiation.

 Cbfa-1 inturn activates osteoblast-specific genes such
as osteopontin,bone sialoprotein,type-I collagen and
osteocalcin.

 During early stages of bone formation
TGF-b
recruit and stimulate osteoprogenitor cells
proliferate
providing a pool of early osteoblasts
During later stages of osteoblast differentiation
TGF-b
blocks differentiation and mineralisation

 These effects appear to be highly dependant on bone
cell source,dose applied and local environment,which
may be a result of inhibition of DNA synthesis at high
TGF-b concentration.

 IGF-I and II increase proliferation and play a role in
stimulating mature osteoblast function.
 It upregulates osterix but not cbfa-1.
 FGF exert their effect on bone formation, primarily
through increased proliferation of osteoprogenitor cells
and promotion of osteogenic differentiation.
 FGF-2 is expressed by osteoblasts and is more potent
than FGF-1.

 Glucocorticoids promote differentiation of osteoblasts
and stimulate bone matrix formation in vitro.
 Prolonged treatment with glucocorticoids in vivo,
results in bone loss, which can be attributed to
increased PTH production in response to inhibitory
effects of glucocorticoids on ca absorption and
depletion of osteogenic precursor cells.

 PDGF have a strong chemotactic effect on osteoblasts and
other connective tissue cells.
 It may act to recruit mesenchymal cells during bone
development and remodelling.
 It acts as a potent mitogen for all cells of mesenchymal
origin.
 It may have a direct and indirect effects on bone resorption
by the upregulation of collagenase transcription and
increase in IL-6 expression in osteoblasts.

 VEGF acts directly on osteoblasts to promote
osteoblasts migration ,proliferation and differentiation.
 It is also a mediator of osteoinductive factors like TGF-
b,IGF-1,FGF-2,which upregulate VEGF expression in
osteoblasts.
 It stimulates the production of bone forming factors for
osteoblasts by endothelial cells.

 Bone lining cells
 Once osteoblasts have completed their function,they
are either entrapped in the bone matrix and become
osteocytes or remain on the surface as lining cells.
 Osteoblasts flatten, when bone is not forming and
extend along the bone surface .
 Missing osteoblasts die by apoptosis.
 Growth factors and cytokines produced in the bone
microenvironment influence this process.
 TGF-b and IL-6 have anti-apoptotic effects.
 Glucocorticoids and estrogen withdrawal promote
apoptosis in osteoblasts and osteocytes.

 Osteocytes
 Cells of mature bone.
 Lie in the lacunae of bone.
 Represent osteoblasts imprisoned in the matrix during bone
formation.
 Their functions include formation of bone, maintenance of
matrix and homeostasis of Calcium.

 The no.of osteoblasts that become osteocytes depends
on the rapidity of bone formation.
 Embryonic(woven)bone and repair bone show more
osteocytes than lamellar bone,as they are formed
rapidly.
 The avg half life of human osteocytes is approx 25yrs.
 The life span of osteocytes exceeds that of active
osteoblasts, which is estimated to be only three months
in human bones.

 During the preparation of ground substance the
osteocytes are lost, but the spaces are filled with debris
and appears black, when viewed under microscope.
 Within the bone matrix,the osteocyte reduces in size,
creating a space around it called the osteocytic lacuna.
 Under EM, it has been observed that a thin layer of
uncalcified tissue lines the lacuna.

 The lacunae can appear ovoid or flattened.
 Narrow extensions of these lacunae form channels
called canaliculi.
 The canaliculi do not extend through and beyond the
reversal line surrounding an osteon,and so do not
communicate with neighbouring systems.

 Osteocytic processes are present within these
canaliculi.
 These processes contain bundles of microfilaments and
some smooth ER.
 At the distal end, these processes contact the processes
of adjacent cells,i.e other osteocytes through gap
junctions.
 They also maintain contact with osteoblasts and bone
lining cells on the surface.

 The canaliculi penetrate the bone matrix and permit
diffusion of nutrients, gases and waste products
between osteocytes and blood vessels.
 Osteocytes also sense the changes in the environment
and send signals that affect response of other cells
involved in bone remodelling.
 This interconnecting system maintains the bone
integrity and bone vitality.

 Failure of the interconnecting system between
osteocytes and osteoblasts leads to sclerosis and death
of bone.
 Old osteocytes retract their processes from the
canaliculi, and when dead,t heir lacunae and canliculi
may get plugged with debris.
 The death of the osteocytes leads to resorption of the
matrix by osteoclasts.

 Two different mechanisms of transformation have been
proposed
 1.stationary osteoblasts transform into osteocytes by
self burial
 2.Dynamic osteoblasts are selected to transform into
osteocytes by secretory activity of neighbouring
osteoblasts.

 Osteocytes –eosinophilic or lightly basophilic cytoplasm.
 Indicates negligible secretory activity.
 Small amount of RER.
 Osteoblasts –basophilic cytoplasm
 Indicates synthetic activity well developed.
 Large amount of RER.

 Osteocytes –greatest no’s in young bone & decreases with
age.
 Functions:
 1.maintain the integrity of the lacunae &canaliculi.
 2.keep open the channels for diffusion of nutrition through
bone.
 3.Play a role in removal or deposition of matrix and of
calcium when required.

 Osteoclasts
 Bone resorbing cells derived from the hemopoietic cells of
monocytes-macrophage lineage
 They appear as multinucleated giant cells.
 Bone removal essential for maintaining the proper shape of
growing bone.
 Found in relation to surfaces where bone removal is taking
place.

 Osteoclast is a much larger cell and because of its size ,
they can be identified easily under light microscope,often
seen in clusters.
 The osteoclasts is characterised cytochemically by
possessing tartarate resistant acid phosphatase within its
cytoplasmic vesicles and vacuoles.
 Osteoclasts are found against the bone surface occupying
hollowed-out depressions called Howship’s lacunae that
they have created.

 At sites of bone resorption,the surface of an osteoclast show
many folds described as –ruffled border.
 At the periphery of this border, the plasma membrane is apposed
closely to the bone surface and the adjacent cytoplasm devoid of
cell organelles.
 It is enriched with actin, vinculin, talin proteins associated with
integrin mediated cell adhesion.
 This clear or sealing zone not only attaches to the mineralised
surface but also isolates a micro environment between them and the
bone surface.

 Another feature of osteoclasts is a proton pump
associated with ruffled border that pumps hydrogen
ions into the sealed compartment.
 Sequence of resorptive events:
 1.Attachment of osteoclasts to the mineralised surface
of bone
 2.Creation of sealed acidic microenvironment through
action of the proton pump, demineralising bone and
exposing the organic matrix.

 3.Degradation of the exposed matrix by the action of
released enzymes such as acid phosphatase and
cathepsin B.
 4.Endocytosis at the ruffled border of organic
degradation products.
 5.Translocation of degradation products in transport
vesicles and extracellular release along the membrane
opposite the ruffled border.

Classification of Bones
 According to their location
 According to their shape
 According to the mode of development
 According to their histologic appearance

 Classification based on their location:
 The human skeleton may be divided into :
a)the axial skeleton consisting of the bones of the
head, neck, and trunk;
b)the appendicular skeleton consisting of the bones of
the limbs

 The skeleton of the head is called the skull.
 The skull contains a large cranial cavity in which the brain is
lodged.
 The skull is made up of a large number of bones that are
firmly joined together.

 Below the skull,the central axis of the body is formed by the
backbone or vertebral column.
 The vertebral column is made up of a large number of bones of
irregular shape called vertebrae.
 Taking the sacrum and coccyx
as single bones the vertebral
column has twenty six bones.

 Classification based on shape
 Long bones-
 includes bones of the arm, leg, fingers
and toes, palms of hands and soles of feet.

 Short bones
 They are usually cube shaped of equal length and width.
 Consist of spongy bone covered by a thin layer of compact
bone.
 They contain bone marrow, but no marrow cavity.
 These bones include bones of wrist-carpals and ankle-tarsals.

Flat bones
 These bones are thin, flat, curved with no marrow cavity.
 spongy bone is present between upper and lower layers of
compact bone.
 Flat bones include-bones of sternum,ribs,scapula,clavicle,and
bones that form roof of the skull-parietal,frontal,temporal and
occipital.

 Irregular bones
 These bones have complex shapes.
 Primarily made of spongy bone which is covered with a thin
layer of compact bone,with bone marrow but no marrow cavity.
 Include bones of vertebrae,facial bones(ethmoid,sphenoid)
Pelvic bones(ischium and pubis),calcareous(heel bone) and
mandible.

 Sesamoid bones
 These bones develop in tendons,where there is considerable
pressure,tension or friction.
 Patella(knee-cap)

 Classification based on development
 Endochondral bones
 Intramembranous bones

 Intramembranous ossification
 Intramembranous ossification mainly occurs during
formation of the flat bones of the skull but also the
mandible, maxilla, and clavicles; the bone is formed
from connective tissue such as mesenchyme tissue
rather than from cartilage.
 The steps in intramembranous ossification are:
 Development of ossification center
 Calcification
 Formation of trabeculae
 Development of periosteum

 Endochondral ossification
 Endochondral ossification, on the other hand, occurs in long
bones and most of the rest of the bones in the body; it involves an
initial hyaline cartilage that continues to grow.
 The steps in endochondral ossification are:
 Development of cartilage model
 Growth of cartilage model
 Development of the primary ossification center
 Development of the secondary ossification center
 Formation of articular cartilage and epiphyseal plate

Classification based on microscopic structure
Histologically,bones are classified as
Mature bone
Immature bone

Immature bone
(Woven bone)
Mature bone
(Lamellar bone)
Intertwined collagen fibres oriented in
many directions.
Distinctive,orderly arrangement is seen.
Great amount of interfibrillar space Interfibrillar space is less
Matrix of woven bone in h&e sections is
tinged blue.
Acidophilic staining of the matrix
Rates of deposition and mineralisation is
faster.
Comparitively slower
Woven bone shows higher proportions of
osteocytes.
Lesser protions of osteocytes.
Osteocytes are isodiametric Osteocytes are flattened and oblate
Enriched in BAG-75 &BSP
(Bone acidic glycoprotien)
Enriched in Osteocalcin
Mineral density is lower Mineral density is higher
More ground substance Less comparitively

Immature bone Mature bone
Water content is higher water content is less
woven bone can be entirely
removed by osteoclasts.
Only a portion of lamellar matrix
resorbed at one time.
Matrix vesicles participate in
initiation of woven bone.
Collagen mediated mechanism is
operative in calcification of lamellar
bone.

 Bone histology
 Osteoid-unmineralised bone matrix on the
surface,where active bone formation is taking place.
 It is approx 5-10um before commencement of
mineralisation.
 Contains typeI collagen fibres, parellel to the bone
surface.

 All mature bones dense outer sheet of compact
bone
central medullary cavity
(red or yellow bone marrow)
This shows a network of bone trabeculae.
Trabecular,spongy or cancellous bone are the terms used
to describe this network.

compact bone
outer aspect inner aspect
periosteum endosteum
(fibro collagenous layer) (thin cellular layer)
Outer layer inner layer In the resting adult bone,quiescent
osteoblasts&osteoprogenitor cells are
present on the endosteal surfaces.
Dense osteogenic layer
Irregular ct consisting of bone cells,
Fibrous layer their precursors,
rich vascular supply.

 At the periosteal and the endosteal surfaces, the lamellae are
arranged in parallel layers surrounding the bony surface and are
called circumferential lamellae.
 Deep to circumferential lamellae, the lamellae are arranged in
concentric layers around a central vascular canal.
 Also called haversian canal (50um in dia).
 Haversian canal+concentric lamellae OSTEON
or
HAVERSIAN SYSTEM

 Adjacent haversian canals are interconncted by VOLKMANS
CANALS.
 These are the channels that contain blood vessels,creating a rich
network throughout the bone.
 Osteocytes are present in the lacunae at the junctions of the
lamellae.
 Small canaliculi radiate from the lacunae to haversian canal to
provide a passage way through
the hard matrix.

 The canaliculi connects all the osteocytes in an osteon together.
 This connecting system permits nutrients &wastes to be
relayed from one osteocyte to the other.
 The adult bones, between the osteons are the interstitial
lamellae.

 A cement line of mineralised matrix delineates the haversian
system.
 This cement line contains little or no collagen & is strongly
basophilic.
 It has high content of proteoglycans and glycoproteins.
 It marks the limit of bone erosion prior to the formation of
osteon, and is known as REVERSAL LINE.

 Reversal lines Resting lines
 irregular lines more regular appearance
 Formed by the scalloped denotes periods of rest during
outline of howships lacunae. the formation of bone.

 Primary osteons &Secondary osteons
 During bone formation first formed osteons do not have a clear
lamellar structure but consists of woven bone-Primary osteons.
 Subsequently primary osteons are replaced by secondary
osteons(typical haversian systems).

Alveolar bone
 Alveolar bone is that part of maxilla and mandible that forms
and supports the tooth socket.
 It is formed when tooth erupts to provide osseous attachment to
forming periodontal ligament.
 It gradually disappears when tooth is lost.

 Functions of alveolar bone
1. Houses roots of teeth.
2. Anchors roots of teeth to alveoli.
3. Helps to move teeth for better occlusion.
4. Helps to absorb & distribute occlusal forces.
5. Supplies vessel to Pdl.
6. Houses & protects developing permanent teeth while
supporting primary teeth.
7. Organises eruption of primary & permanent teeth.

 ALVEOLAR BONE PROPER
 Surrounds the root of tooth
 Consists partly laminated & partly bundle bone.
 Laminated bone - lamellae arranged parallel to adjacent
marrow spaces.

Bundle bone
- anchors principal fibers
- scarcity of fibrils in intercellular substance
- conatins few fibers so appear dark in H&E stain
- formed in area of recent bone apposition.

 Alveolar bone proper – inner wall of socket
 Perforated by many openings hence c/d cribriform
plate
 Bone between teeth – interdental septum
 Interdental & interradicular septa contain perforating
canals of Zuckerkandl & Hirschfeld.

 INTERDENTAL SEPTUM
 Consist of cancellous bone bordered by cribriform plate of
approximating teeth and facial & lingual cortical plates
 If the interdental space is narrow, the septum consist of only
cribriform plate.
 Meiodistal angulation of crest of interdental septum – parellels
line drawn between CEJ & approximating teeth
 Young adults – 0.75 – 1.49mm
 Increase with age – avg 2.81mm



 CORTICAL PLATE
 Compact bone
 Forms outer & inner plate
 Thinner in maxilla
 Maxilla – perforated
 Mandible – dense
 Bone underlying gingiva
 Cribriform plate & cortical plate are compact bone seperated
by spongy bone.

 Trabeculae – less prominent in upper jaw
 Marrow spaces in alveolar process – hemopoietic /fatty
marrow.
 Condylar process, angle of mandible, maxillary
tuberosity- hemopoietic cellular marrow.

 BONE MARROW
 Embryo & newborn – red hematopoietic marrow.
 This undergoes physiologic change – fatty / yellow
inactive(seen in adults).
 Red marrow found – ribs,sternum,vertebrae,skull &
humerus.
 Foci of red marrow seen in jaws accompanied by resorption
of bony trabeculae.

 Bone Growth
 Bone length is dependent upon the activity that occurs in the
epiphyseal plate.
 Bone growth stops when the cartilage of the epiphyseal plate
ceases proliferation and bone development continues to unite
the diaphysis and epiphysis.

 An increase in bone width occurs by a process called
appositional growth.
 Bone is produced by the periosteum (intramembranous
ossification) on the external surface of the bone collar,
and at the same time bone is removed from the internal
surface causing the marrow cavity to increase in size.

 During infancy and childhood the most important stimulus of
epiphyseal plate activity is growth hormone (somatotropin),
which is released from the anterior pituitary gland.
 Normal bone growth is dependent on proper dietary intake of
protein, minerals and vitamins.

 A deficiency of vitamin D prevents calcium absorption
from the GI tract resulting in rickets (children) or
osteomalacia (adults).
 Osteoid is produced but calcium salts are not deposited,
so bones soften and weaken.

 Bone Remodeling
 In a growing person bone deposition exceeds bone resorption.
In adulthood after the closure of the epiphyseal plates, bone
deposition is balanced with bone resorption.
 Osteons are replaced by osteoprogenitor cells and osteoblasts
from the periosteum.

 Trabeculae are replaced by Osteoprogenitor cells and
osteoblasts from the endosteum.
 Bone resorption is accomplished by osteoclasts.
 If bone resorption exceeds bone deposition then
osteoporosis will occur.

 Fracture Repair
The bone matrix is destroyed and the bone cells adjoining the
fracture die.
 The damaged blood vessels form a blood clot.
 The blood clot, damaged bone matrix, and dead cells are
removed by macrophages.
 Granulation tissue forms in the site of the blood clot and
condenses into connective tissue and later into a
fibrocartilagenous callus.

 At the same time, osteoprogenitor cells of the periosteum
are activated and become osteoblasts that begin to deposit
new bone. The new bone, which is a meshwork of
trabeculae of primary bone, forms a bone callus around the
fracture site.
 A similar activation of cells of the endosteum results in
deposition of bone around the fibrocartilagenous callus that
is slowly eroded away and replaced by bone (endochondral
ossification).

 The spongy bone uniting the bones is transformed into
compact bone by osteoblastic deposition of bone
matrix, which gradually obliterates the spaces among
the trabeculae.
 Resorption of excess bone by osteoclasts reestablishes
the marrow cavity and the normal surface contours of
the bone.

Genetic
 1.Osteogenesis imperfecta
 2.Osteopetrosis
 3.Achondroplasia
 4.Cleidocranial dysplasia
 5.Cherubism
 6.Hypophosphatasia
 7.Sickle cell anaemia and Thalassaemia
 8.Hyperparathyroidism-jaw tumor syndrome
 9.Gigantism and Acromegaly
 10.Fluorosis

 Metabolic bone disease
 1.Rickets
 2.Vit-D resistant rickets
 3.Scurvy
 4.Hyperparathyroidism
 Other bone diseases
 Pagets disease of bone

 Fibro-osseous lesions
 1.Fibrous dysplasia
 2.Monostotic fibrous dysplasia
 3.Polyostotic fibrous dysplasia
 4.Albright’s syndrome
 5.Cemento-osseous dysplasias
 6.Solitary bone cyst
 7.Osteoporotic bone marrow defect
 8.Aneurysmal bone cyst

 In older individuals:
 Alveolar sockets appear jagged and uneven.
 The marrow spaces have fatty infiltration.
 The alveolar process in edentulous jaws decrease in
size.

 Loss of maxillary bone is accompanied by increase in
size of the maxillary sinus.
 Internal trabecular arrangement is more open,which
indicates bone loss.
 The distance between the crest of the alveolar bone and
CEJ increases with age-approx by 2.81mm.

• Orthodontic tooth movement
• Adaptation of bone to function
- Increase & decrease in functional forces.
• Periodontal disease - Bone resorption (Horizontal &
Vertical)

Bone /orthodontic courses by Indian dental academy

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