ALVEOLAR BONE

Introduction
Development of bone
Alveolar bone
a) Development
b) Structure
Composition
Microstructure
Bone formation
Factors regulating bone Formation
Resorption
Factors affecting bone resorption
Bone remodeling
Blood supply
Clinical consideration
Alveolar bone in disease

Conclusion

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INTRODUCTION & DEVELOPMENT
Bone is a specialized mineralized connective tissue that participates
in various functions such as support, protection, locomotion, homeostasis
and blood cell production. The process of bone formation is called
osteogenesis. It occurs by three mechanisms,
1. Endochondral
2. Intramembranous
3. Sutural

Endochondral/Indirect bone formation:

In this type of osteogenesis, bone formation is preceded by the
formation of a cartilaginous tissue, which is subsequently replaced by
bone. This type of bone formation is seen at the head of the mandible,
ends of all long bones, vertebrae, ribs and base of the skull. Mesenchymal
cells become condensed at the site of bone formation. Some of these
mesenchymal cells differentiate into chondroblasts and lay down hyaline
cartilage. The cartilage is surrounded by a membranous perichondrium,
which is highly vascular and contains osteogenic cells. Intercellular
substance surrounding the cartilage cells become calcified due to the
influence of the enzyme alkaline phosphatase secreted by the cartilage
cells. Thus the nutrition of these cartilage cells is cut off leading to their
death, which results in the formation of empty spaces called primary
areolae.

The blood vessels and osteogenic cells from the perichondrium

invade the calcified cartilaginous matrix, which is now reduced to bars or
walls due to eating away of the calcified matrix. This leaves large empty
spaces between the walls called secondary areolae. The osteogenic cells
from the periochondrium become osteoblasts and arrange themselves along
the surface of these bars of calcified matrix. The osteoblasts lay down
osteoid which later becomes calcified to form a lamella of bone.

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Intramembranous/Direct bone formation:
In this kind of osteogenesis bone formation is not preceded by
formation of cartilage. Bone is directly laid down on a connective tissue
membrane. This kind of formation is seen in the maxilla and body of the
mandible. At the site where a membrane bone is to be formed the
mesenchymal cells become closely packed. Some of the mesenchymal
cells lay down bundles of collagen fibres in the mesenchymal
condensation. Some mesenchymal cells enlarge and acquire a basophilic
cytoplasm and may now be called osteoblasts. They come to lie along the
bundles of collagen fibres. The fibres may also swell up. This mass of
swollen fibres and matrix is called OSTEOID.

Under the influence of the osteoblasts calcium salts are deposited in

the osteoid. As soon as this happens the layer of osteoid becomes a
lamella of bone. Over this lamella another layer of osteoid is laid down by
the osteoblasts. The osteoblasts move away from the lamella to line the
new layer of osteoid. Due to the initial rapid deposition of calcium salts
there is not enough time for some of the osteoblasts to retreat and hence
they get retained as osteocytes. The first formed poorly mineralized, ill
organized, highly cellular bone is called WOVEN BONE.

As bone maturation proceeds the mineral deposition slows down and

mature bone that is well organized into lamellae and is less cellular is
formed. This is called LAMELLAR BONE. These lamellae are laid down
one over the other and together form trabeculae. In this way spongy bone
is formed. All newly formed bones are spongy. The spaces between the
trabeculae of spongy bone are filled with tissue that is vascular and has
osteogenic cells. These osteogenic cells become osteoblasts and come to
line the walls of the space. As they start secreting the matrix which
eventually becomes mineralized the space becomes smaller and smaller

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until it is reduced to a small canal carrying a few blood vessels. Thus this
canal is surrounded by concentrically arranged lamellae. Haversian
systems are thus formed and spongy bone becomes compact.

Sutural bone formation:

This type of bone formation occurs in sutures of the skull to permit
accommodation of growing organs such as the eyes and the brain.

ALVEOLAR BONE DEFINITION:

Alveolar process is defined as the parts of the maxilla and mandible
that form and support the sockets of the teeth.

It develops in conjunction with the development and eruption of the

teeth and is resorbed gradually if the teeth are lost. Together with root
cementum and the PDL it forms the attachment apparatus of the teeth,
which absorb and distribute forces generated by mastication and other
tooth contacts.

DEVELOPMENT AND STRUCTURE

Near the end of the 2 n d month of fetal life, the maxilla as well as
mandible forms a groove that is open towards the surface or the oral
cavity. The tooth germs are contained in this groove, which also includes
the alveolar nerves and vessels. Gradually bony septa develop between the
adjacent tooth germs, and much later the primetime mandibular canal is
separated from the dental crypts by horizontal plate of bone. The alveolar
process in the strict sense of the word develops only during eruption of
the teeth.

The parts of the alveolar bone are,

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1. Alveolar bone proper. {Innermost} thin compact bone.
2. Supporting alveolar bone. It consists of,
I. Cortical plates {outermost}, forms outer and inner plates {buccal and
lingual} of alveoli.
II. Spongiosa {middle portion} fills the area between, the cortical plates
and alveolar bone proper.

Alveolar bone proper

1. The inner socket wall of thin compact bone, surrounding the roots
of the teeth.
2. In radiographs, it appears is an opaque line, and is called as lamina
dura. Because of its increased radio opacity. This is due to the
thick bone without trabeculations, through which, X-rays will not
penetrate.
3. In to this the periodontal ligament fibers attach and extend to
cementum. The periodontal ligament fibers are embedded in this
bone are known as Sharpeys fibers.
4. This is also known as bundle bone, as it provides, attachment for
the periodontal ligament fiber bundles. It is perforated by many
foramina, which transmit nerves and vessels and is therefore
sometimes referred to as cribriform plate or lamina cribrosa.
5. Histologically, it consists of bundle of coarse fibred woven bone
fibres, running parallel to the socket wall and arranged in lamellae.
Embedded within the bone are, bundles of collagen fibres of the
periodontal ligament and hence the name bundle bone.
Thicker layer of bundle bone on the distal wall of the socket as
compared to the mesial wall due to physiological mesial migration
of teeth. It is also known as inner cortical plate.

Supporting alveolar bone

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 It surrounds the alveolar bone proper and gives additional support.
In consists of, cortical plates {outermost}, which forms outer and inner
plates of alveoli and spongiosa {middle portion} which fills the area
between the cortical plates and the alveolar bone proper.

Cortical plates
- Cortical bone is engineered to protect vital organs, to resist
biofunctional loads and to provides safe hence for
haematopoiesis
- To carry out these functions, Haversian systems or osteons in
cortical bone function as buttresses and are designed to respond
to biofunctional challenges.
- From the central canal each concentric lamella of the Haversian
system spirals first clockwise, then counterclockwise and so on,
thus ensuring maximal response to compressive and torsional
loading.
- A Haversian system consists of 4 to 20 circumferential rings of
concentrically arranged lamellae that encompass a central canal
22 to 110 μm in diameter called the Harversian canal that
contains blood vessels, lymphatics and sometimes nerves.
Average diameter of the Haversian system in humans is about
200μm.
- Each lamellar ring is populated by a number of osteocytes.
- Each osteocyte is linked to others in the same-adjacent lamellae
thro thread like cell processes traversing canaliculi.
- Volkmann’s canals penetrate cortical bone and anastomose with
Haversian systems and provide vascular and lymphatic channels
for metabolic exchange and trafficking of soluble signals like
hormones.

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 - This organizational network enables exchange of signaling
molecules among osteocytes and endosteal and periosteal lining
osteoblasts.

The cortical plates cover the vestibular and oral surfaces of the
alveolar process. Consists of a buccal and a lingual cortical plate. They
are continuous with the compact layers of maxillary and mandibular body.
They are much thinner in the maxilla, than in the mandible. They are
thickest in the premolar and molar regions in the mandible especially on
the buccal side. Most of the facial and lingual surfaces of the socket are
formed only of cortical bane cancelleous bone is found only in apical,
apicolingual and interradicular areas of the socket wall.

Cortical plates and alveolar bone proper meet at the alveolar crest,
which is usually 1.5 -2.0 mm below the CEJ of the particular teeth, which
they surround.

Spongiosa
Consists of a 3-dimensional network of trabeculae. Spatial arrangement
of these can be isotropic on anistropic. The cancellous portion of the
alveolar process lies between the cortical plates and the alveolar bone
proper, and is continues with the spongiosa of the body of mandible and
maxilla. There is less cancellous bone in the mandible due to their thicker
cortical plates.

- This is interposed between cortical bone is the spongy –looking

cancellous bone.
- It is formed by a three-dimensional lattice of trabeculae, which
is the hallmark of this structure.
- In general spatial orientation of trabeculae is random (Isotropic)

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 - In certain areas it is aligned in a direction to sustain loading –
spatial orientation is directional (Anisotropic).
- Unlike cortical bone, which is engineered for loading, cancellous
bone is designed to respond to physiologic requirements.
- This is why cancellous bone has a 20 times more surface area
and cell density per unit volume compared to cortical bone.

Interdental septum
Consists of cancellous bone bordered by the socket wall cribriform
plates of neighboring teeth and the facial and lingual cortical plates. The
cribriform plate carries the nutrient canals Zuckerkandl and Hirschfield. If
interdental space in narrow, the septum consists of only the cribriform
plate. For example the space between the mandibular 2 n d premolars and
first molars consists of cribriform plates and cancellous bone in 85% of
the cases and only cribriform plate in the remaining 15%.

Between maxillary molars, the septum consists of cribriform plate

and cancellous bone in 66.6% of cause and has fenestration in 12.5% of
case. If roots are to close together an irregular “window” can appear in
the bone between adjacent roots. Mesiodistal angulation of the crest of the
interdental septum usually parallels a line drawn between the CEJ’s of the
approximating teeth. The distance between crest of the alveolar bone and
the CEJ in young adults varies between 0.75 and 1.49 mm. This distance
increases with age to an average of 2.81 mm. This is more due to
periodontal disease and not due to age.

Medisodistal and faciolingual dimensions and shape of the

interdental septum are governed by

a) Size and convexity of crowns of approximately teeth

b) Position of teeth in jaws and

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c) Degree of eruption

Osseous topography
Topography of bone depends on the prominence of the roots with
intervening vertical depressions. On teeth in labial version, margin of
bone is located more apically Bone margin is thinned to a knife-edge and
present s an accentuated arc in the direction of the apex. On teeth in
lingual version, the facial bony plate is thicker than normal. Margin is
blunt and rounded and horizontal rather than arcuate.

COMPOSITION
Bone is a hard mineralized tissue. The tissue chemistry of bone is
clarified by consideration of some histological and ultrastructural
concepts. Bone cells are usually distributed through out bone, separated
from each other by mineralized extracellular material (ECM).
Ultrastructurally this ECM shows two distinct phases, an organic
and an inorganic phase. The inorganic phase is discontinuous and consists
of very small discrete crystals and amorphous material. These are
surrounded by a continuous organic phase consisting ultrastructurally of
collagen fibrils and relatively structureless inter fibrillar material. Bone
consists of weight of 33% organic matrix, 28% type I collagen and 5%
non-collagenous proteins. This organic matrix is permeated by hydroxy
apatite, which make up remaining 67% of bone.

MICROSTRUCTURE
Bone may be categorized into four microstructural components
namely,
a) Cells
b) Organic matrix
c) Inorganic matrix

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 d) Soluble signaling factors

CELLS
The most important cell phenotyes in bone are osteoblasts,
osteocytes, and osteoclasts.

Osteoblasts
- These are derived from mesenchymal cells.
- Progression from undifferentiated mesenchymal cells to
osteoblasts can take 2 routes, one leading to determined
osteoprogenitor cells and the other to inducible osteoprogenitor
cells.

Osteo progenitor cells

- The determined cells are associated with cell condensations,
which may be responsible for bone formation during
embryogenesis.
- During fracture repair the inducible population may be
susceptible to soluble inductive morphogens.
- When bone is injured due to surgical intervention and trauma, a
population of local cells restores osseous form and function
through recapitulation of embryologic events.
- The local cells are determined osteoprogenitor cells, present in
the cambial layers of the periosteum and endosteum.
- The inducible osteoprogenitor cells like pericytes arrive at the
injury locus about 3 to 5 days after injury via transit in
developing capillary sprouts.
- Therefore osteoblasts are metabolically active secretory cells
that express soluble signaling factors (e.g, BMP’s TGF- β,
insulin like growth factor, I and II, IL-1 and PDGF) and osteoid.

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- The mineralization of this osteoid occurs due to accumulation of
non-collagenous bone matrix proteins that bind calcium.
- The active life span for human osteoblasts is believed to range
from 1 to 10 weeks
- After this they disappear by apoptotic mechanisms, but some
however become lining cells and bout 15% become osteocytes.

Osteocytes
- These are inactive cells, yet their subdued metabolic activity is
crucial to bone viability and to sustain homeostasis.
- Vitality of bone is ensured through a network of osteocytic
cytoplasmic processes that traverse canaliculi.
- Through this system osteocytes interact with osteoblasts through
gap junctions and signal transmissions.
- Osteocytes are end stage cells and are not capable of renewal.
- Life span is many years, even decades.

Osteoclasts
- Granulocytic macrophage precursors found in bone marrow enter
circulation as monocytes and through asynchronous fusion,
produce a multinucleated cell up to 100 μm in diameter and an
average of 10 to 12 nuclei known as an osteoclast.
- They have a ruffled border, possess calcitonin receptors, produce
acid phosphatase and lack F C and C3 receptors.
- IL-1,3,6,11, TNF- α, TGF-α are important for development of
osteoclasts.
- IL-11 may be the major controlling factor.
- Parfitt et al have shown a dynamic inter play between soluble
factors and osteoblast and osteoclast formation. This is called
coupling.

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 - 1,25-dihydroxy vitamin D3 or PTH binds to osteoblasts and leads
to expression of an osteoblast differentiation factor that is
effective on osteoclast progenitors that have been primed by
exposure to soluble factors such as ILs.
- Therefore osteoblasts serve as a source of cofactors to promote
formation and function of osteoclasts.
- A multinucleated giant cell must be attached to bone and display
a ruffled border to qualify as an osteoclast.
- There has to be interaction between osteoblasts and osteoclasts
for resorption to occur.
- When osteoblasts disperse from bony surfaces in response to
PTH, an exposed osteoid –mineralized runway provides
osteoclasts with an opportunity to attach. This attachment
involves surface adhesion molecules (integrins) and proteins.
Osteopontin a sialophosphoprotein promotes attachment.
- In this zone of attachment the ruffled border develops and
enzymatic breakdown of the bone surface occurs. Enzymes such
as acid phosphatase, aryl sulphatase, β-glucuronidase, β-
glycerophosphatase, metalloproteases, collagenase and
stromeolysin are involved. A microenvironment with a decreased
pH is created here, that promotes solubilization of the inorganic
matrix of calcium and phosphate and exposing the organic matrix
to these proteolytic enzymes. When the organic constituents are
broken down, large resorption cavities called Howships lacunae
are formed.

MATRIX
Composition of ECM is similar to other bone tissues. Formed from a
scaffold of interwoven collagen fibers within and between which small,
uniform plate – like crystals of carbonate and hydroxyapatite are
deposited.

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Organic
- 35% of dry weight of bone is organic matrix. Type I collagen
makes up about 90% of the organic matrix. The remaining 10%
consists of non-collagenous components. Type I collagen forms
fiber bundles that provide basic structural integrity to bone. In
addition to this type V, III & XII are also present. Type III
collagen is present in relation to Sharpey’s fibers.
- Type I, V & XII are produced by osteoblasts and type III is
produced by fibroblasts.
- In rapidly forming bone (woven) that is produced during early
development and in repair sites, the fibers are extensively
interwoven with a large volume of interfibrillar space that is
occupied by mineral crystals.
- In mature lamellar bone, the collagen fibers form highly
organized sheets in which successive layers of fibers are oriented
perpendicular to each other with little interfibrillar space.

Non-collagenous components
- These have been categorized by Robey et al into proteoglycans
and glycoproteins.
- Proteoglycans (PGs) have a core protein to which one or more
heteropolysaccharides called Glycosaminoglycans (GAGs) are
covalently linked.
- The GAG’s consist of repeating carbohydrate units that are
sulfated, such as chondroitin sulfate, dermatan sulflate, keratan
sulfate and heparin sulfate
- Examples of PG’s include versican, decorin, biglycan,
fibromodulin, osteoglycin and osteoadherin. These may be
involved in growth factor regulation.

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 - The major PG’s in alveolar bone are expressed with chondroitin
sulfate side chains, dermatan sulfate forms are expressed by
undifferentiated bone cells.
- Decorin and biglycan are the 2 important PG’s found in alveolar
bone. They bind to TGF- β and collagen and regulate
fibrillogenesis.
- Decorin and biglycan are associated with the collagen matrix of
bone.
- There also exist numerous bound PG’s such as osteoadhesin that
have mineral binding properties.
- Lysyl oxidase and tyrosine-rich acidic matrix protein (TRAMP)
are important components of demineralized bone.
- Lysyl oxidase is critical for collagen cross-linking. TRAMP is a
recently discovered ECM protein with proteoglycan and cell –
binding properties. It is also known as dermatopontin and binds
decorin and TGF- β and regulates cellular response to TGF- β.
- Other proteins found in bone include procollagen peptides such
as thrombospondin, fibronectin and vitronectin that modulate
cell attachment and regulate enzyme alkaline phosphatase for
mineralization to occur.
- Glycoproteins in alveolar bone include osteonectin,
thrombospondin, osteopontin and bone sialoprotein, osteocalcin.

OSTEOCALCIN
- Also known as bone gla protein was the first non collageneous
bone protein to be characterized.
- It is a 5.8 KDa acidic protein that is modified by vitamin k-
dependent carboxylating enzymes that convert two to three
glutamic acids into γ- carboxyglutamic acids (gla groups).

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 - The gla groups formed on the pro-osteocalcin prior to secretion
bind calcium ions strongly and increase the affinity of
osteocalcin for bone mineral.
- Osteocalcin is said to play a role in mineral maturation and bone
resorption since it is regulated by vitamin D3 and PTH and acts
as a chemo attractant to osteoclast precursors.

OSTEOPONTIN AND BONE SIALOPROTEIN

- Were originally called Bone sialoproteins I and II. Both these

proteins are heavily glycosylated and phosphorylated with high
levels of acidic amino acids.
- Glutamic acid is predominant in Bone sialoprotein and apartate
in osteopontin.
- These proteins are implicated in hydroxyapatite binding, cell
attachment and activation of cell signaling pathways.
- Osteopontin also plays a role in bone resorption by inhibiting
hydroxyapatite crystal growth and mediating attachment of
osteoclasts.
- Expression of both these proteins is stimulated by factors that
stimulate bone formation such as TGF-β.

SPARC/OSTEONECTIN
- Is a 40 KDa glycoprotein that is predominantly bound to
hydroxyapatite. SPARC can comprise as much as 25% of the
non-collagenous proteins. SPARC has also been characterized in
basement membranes as BM40.
- It is a secreted calcium-binding glycoprotein, which interacts
with a range of extracellular matrix molecules.
- SPARC has a high affinity calcium-binding site and several low
affinity calcium-binding sites.

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 - The low affinity sites involve glutamate and aspartate groups.
- SPARC molecule has 4 domains. Domain I is responsible for
numeral binding and inhibition of hydroxyl apatite crystal
growth. Domain II is rich in cysteines and stabilizes the protein
structure.
- Domain III is susceptible to proteolysis. Domain IV contains the
high affinity Ca binding site.
- SPARC is associated with rapidly remodeling tissues; it is a
counter adhesive protein that modulates interactions of cells with
ECM.

PERIOSTEUM
The periosteum is a fibrous membrane, which ensheathes a bone
everywhere except at cartilage covered surfaces and where tendons and
ligaments are attached. It serves for muscle attachment, as a bed for
blood vessels and as a major agent for bone growth and repair.
Periosteum has two layers, an outer dense fibrous layer and an inner
much less fibrous layer containing plump osteoprogenitor cells,
osteoblasts and osteoclasts. The outer layer becomes increasingly thick as
it approaches the ends of the bone. The inner layer continues in to the
interstices of the underlying fine cancellous bone without sharp
demarcation. The inner layer is evidently, actively engaged in bone
formation and bone resorption.

Adult periosteum contains dormant osteoprogenitor cells, which

respond to a variety of stimuli by enlargement, multiplication and
conversion in to bone forming or bone destroying cells or in some
circumstances in to cartilage forming cells.

Endosteum is the tissue lining the inernal bone cavities. It is

composed of a single layer of osteoblasts and a small amount of

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connective tissue. The inner layer is osteogenic and outer layer is fibrous.
In the newborn, the cavities of all bones are occupied by red
hematopoietic marrow. The red marrow gradually undergoes a
physiologic change to the fatty or yellow inactive type of marrow. In
adult, the marrow of the jaw is normally of the fatty type, and red marrow
is found only in the ribs, sternum, vertebrae, skull and humerus.
However, foci of red bone marrow are occasionally seen in the jaws, often
accompanied by resorption of bony trabeculae. Common locations are the
maxillary tuberosity and the maxillary and mandibular molar and premolar
areas, which may be visible radiographically, as zones of radiolucency.

REMODELING
Although it looks very rigid, alveolar bone is the least stable of the
periodontal tissues because its structure is in a constant state of flux. A
considerable amount of internal remodeling takes place by means of
resorption and formation that are regulated by local and systemic
influences. Local influences include funcitional reauirements on the tooth
and age-related changes in bone cells. Systemic influences are probably
hormonal (eg parathyroid hormone, calcitonin or Vit. D3)
Remodelling of the alveolar bone affects its height, contour and
density and it is manifested in the following three areas.
1. Adjacent to the PDL.
2. In relation to the periosteum of the facial and lingual plates and
3. Along the endosteal surface of the marrow spaces.

Remodeling is the major pathway of bony changes in shape,

resistance to forces, repair of wounds, and Ca and Phosphate hemeostasis
in the body. Bone contains 99% of Ca ions of the body and is the major
source for calcium release when blood calcium levels decrease. This is
regulated by PTH hormone. PTH stimulates osteoblasts to release IL-1&6.
IL-1&6 stimulate monocytes to migrate into the bone area. Leukemia

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inhibiting factor (LIF) secreted by osteoblasts, coalesce monocytes into
multinucleated osteoclasts, which then resorb bone, releasing calcium ions
from hydroxyapatite into the blood. This normalizes blood calcium levels,
which turns off the parathyroid gland secretion of PTH.

Osteoclasts also resorb organic matrix along with hydroxyapatite.

Breakdown of collagen from organic matrix releases osteogenic substrates
bound to collagen. These osteogenic substances stimulate the
differentiation of osteobasts, which ultimately deposit bone. This
interdepency of osteoblasts and osteoclasts in remodeling is called
COUPLING.

During the process of remodeling, osteoblasts and osteoclasts

engage in a dynamic interaction. Signalling factors such as vitamin D,
PTH, IL’s and granulocyte colony stimulating factor (GCSF) influence
bone cell phenotypes. In response to PTH, osteoblastss vacate osteoid,
leaving it susceptible to osteoclastic resorption. Soluble signaling factors
(IL’s and GCSF) promote differentiation of monocytes, pericytes and
mesenchymal stem cells.

Bone formation and factors affecting formation

The final mineral deposit is crystalline hydroxyl apatite.
Amorphous calcium phosphate that is present early in mineralization
undergoes progressive transformation in to crystalline state. Under
normal conditions ca and po4 ions in blood and tissue fluid is insufficient
for ca3po4 to convert in to crystalline form. Two theories have been put
forward for how the bone is formed and calcified.
1 s t theory:
Matrix vacuoles, which are produced as an outgrowth of osteoblasts
or chondroblasts or odontoblasts are responsible for calcification.

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They Contain alkaline phosphatase which,
1. Can hydrolyse organic phosphate containing substrates
2. Can release Ca and Phosphate from calcium-p-glycerophosphate at
ph 7.4.
3. Hydrolyses the pyrophosphate and other naturally occurring
polyphosphates; that are capable of inhibiting calcification.

2 n d theory
According to this theory,
Macromolecular constituents of bone and cartilage matrix directly
implicates in calcification.

Proteoglycans and glycoprotein aggregates of bone matrix undergo

modification, to release Ca ++ and also provide space, to accommodate
bone mineral deposition, following partial degradation of inhibiting
proteoglycans.

Factors that can affect the bone formation

1. Platelet derived growth factor:
Is a cationic heparin binding polypeptide, which is of three types AA, AB,
BB. They are produced by osteoblasts but also derived from serum and
platelets. It stimulates DNA synthesis and cell replication in osteoblasts,
increased collagen synthesis and rate of bone apposition. It also causes
bone resorption and collagen degradation.

2. Acidic fibroblast growth factors and basic fibroblast growth factor are
mitogenic and increase collagen protein synthesis.

3. Insulin like growth factor is of two types, IGF-I{stomatomedin c} IGF-

II{stimulating factor}. They increase preosteoblasts replication and have

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stimulatory effect on osteoblastic collagen synthesis. They are produced
in liver.

4. Transforming growth factor: TGF-α is not produced by osteoblasts as it

stimulates bone resorption. It is responsible for hypercalcemia in
malignancy. TGF-β is formed by osteoblasts.

5. Bone morphogenetic proteins (BMPs):

During bone repair several osteoinductive substances are released and are
called as BMPs. They are required for healing.

Resorption of bone
It is done by,
I. Solubilization of mineral phase
II. Dissolution of organic matrix

These two processes take place extra cellularly.

1. The minerals are dissolved by acid secretion, which is brought about by
electrogenic hydrogen ion transportation in to the resorption zone. It
seems likely that to buffer the local acidity, the relatively insoluble Ca
salt in bone mineral get converted in to acid salts that are steadily passed
in to solution because they are more soluble.

This produce suitable ph for lysosomes results in cysteine

proteinase enzyme activity, which demineralise bone matrix. They
degrade the proteoglycans & non-helical terminal portion of collagen
molecule.

2. According to Tencate,

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 1. Attachment of osteoclasts to the mineralized surface of bone.
2. Creation of sealed acidic environment through actions of the proton
pump, which demineralizes bone and exposes the organic matrix.
3. Degradation of the exposed organic matrix to its constituent
aminoacids by the actions of released enzymes, such as acid
phosphatase and cathepsin.
4. Sequestering of mineral ions and aminoacids with in the osteoclast.

Factors associated with mechanism of bone destruction:

1. Interleukin 1(IL-I)
They are of two types, IL-1 alpha and IL-1 beta, are responsible for
resorption. It stimulates production and release of prostaglandin PGE2.
There is direct action of IL-1 on osteoclasts. It inhibits bone formation in
vivo and in vitro.

2. Interleukin-6 (IL-6)
No effect on bone resorption. Some says it stimulates resorption. It can
stimulate osteoclastic phenotypes. Osteoblasts can produce IL-6.

3. Tumor necrosis factor and lymphotoxin;

These are multifunction cytokines produced by lymphocytes. Their role in
osteoclastic bone resorption, part of TNF alpha effect is mediated by
PGE2 as well as IL-6.

4. Gamma interferon
It is a multifunctional cytokine similar to TNF alpha or IL-1. It also
inhibits bone resorption.

5. Colony stimulating factors:

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They can differentiate osteoclast precursors in to osteoclasts.

6. Prostaglandins and other arachidonic metabolites:

PGE2 series can cause bone resorption. They are slow acting powerful
mediators.
7. Sex steroids:
Androgens can affect bone resorption

BLOOD SUPPLY
The blood supply to the alveolar bone comes from branches of the
alveolar artery. The major supply comes from the alveolar vessels the
pass up to the center of the alveolar septum, sending branches laterally
from the marrow spaces, and by way of canals through the cribriform plate
to the periodontal ligament. The blood supply depends upon the nature of
bone either spongy or compact bone.

The blood supply of spongy bone is afforded by the blood vessels of

marrow spaces. Which are generally equidistant from surrounding bone
trabeculae. In compact bone the blood vessels occupy the network of
longitudinal Haversian and connecting Volkmann’s canals. The blood
vessels in the canals are in communications with those in periosteum and
marrow. Most of the blood vessels inside the compact bone are
capillaries. Often two blood vessels are found in one Haversian canal of
which is narrow arterial capillary and other wider venous capillary.

The blood supply of a bone is derived principally from two different

sources. Smaller or larger arteries enter the bone by perforating the
compact outer layer and ramify in the bone marrow. The second groups of
arteries supply primarily the compact bone. These arteries are from
periosteal network and enter the bone as arterioles or prearterioles in
numerous Volkmans canals. The veins of the bone follow arteries.

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Radiographic features
The normal alveolar bone supporting the dentition has characteristic
radiographic appearance. A thin layer of opaque cortical bone often
covers the alveolar crest. The height of the crest lies at a level
approximately 1-1.5 mm below the level of the CEJ of adjacent teeth.
Between the anterior teeth the alveolar crest is usually pointed and has a
dense cortex. Between posterior teeth the alveolar crest will also be
parallel with a line connecting adjacent CEJ. The alveolar crest is
continuous with the lamina dura of adjacent teeth.
CLINICAL CONSIDERATION
1.Physiologic migration of the teeth. 2.External forces and the
periodontium.
PHYSIOLOGIC MESIAL MIGRATION
With time and wear
The proximal contact areas of the teeth are flattened
The teeth tend to move mesially
By the age of 40 years,this process results in a reduction of about 0.5cm
in the length of the dental arch from the midline to the third molars.
ORTHODONTIC TOOTH MOVEMENT
Occurs when there is increased orthodontic forces within the physiological
limit. More common in adult patients.
Osteoblasts and newly laid osteoid line the socket in areas of tension.
New layers of bundle bone are formed in areas of tension on the distal
surfaces.
Osteoclasts and bone resorption occurs in the areas of pressure.
Bone resorption is increased in areas of pressure along the mesial surface
of the teeth.

ALVEOLAR BONE IN DISEASE

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 Periodontitis is an infectious disease of the gingival tissue. Changes
that occur in bone are crucial because it is the destruction of bone that it
is responsible for tooth loss. The height of the alveolar bone is normally
maintained by equilibrium, regulated by local and systemic influences
between bone formation and bone resorption. The reduction in the height
of the alveolar bone, termed physiologic and senile atrophy, occurs with
aging.

Bone destruction as relates to the periodontium is caused by,

1) Extension of gingival inflammation
2) Trauma From Occlusion (TFO)
Bone loss caused by extension of gingival inflammation is
responsible for reduction in the height of the alveolar bone, whereas TFO
causes bone loss lateral to the root surface.

The level of bone is the consequence of past pathologic experiences,

whereas changes in the soft tissue of the pocket wall reflect the present
inflammatory condition.

BONE DESTRUCTION CAUSED BY EXTENSION OF GINGIVAL

INFLAMMATION

Chronic inflammation is the most common cause of bone destruction

in periodontal disease due to the extension of inflammation from the
marginal gingiva into the supporting periodontal tissues.

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 Periodontitis is always preceded by gingivitis, but not all gingivitis
progresses to periodontitis. The factors that are responsible for the
extension of inflammation of the supporting structures and that bring
about the conversion of gingivitis to periodontitis are not known.

The transition from gingivitis to periodontitis is associated with

changes in the composition of bacterial plaque.

The cellular composition of the infiltrated connective tissue also

changes with increasing severity of the lesion. Fibroblasts and
lymphocytes predominate in stage I gingivitis, whereas the number of
plasma cells and blast cells increase gradually as the disease progresses.
Seymour and associates have postulated a stage of contained gingivitis in
which T-lymphocytes are predominant.

They believe that as the lesion becomes a B-lymphocyte lesion, it

becomes progressively destructive.
The extension of inflammation to the supporting structure of a tooth
may be modified by the pathogenic potential of plaque (or) by the
resistance of the host. The latter includes immunologic activity and other
tissue-related mechanisms such as the degree of fibrosis of the gingival,
probably the width of the attached gingiva, and the reactive fibrogenesis
and osteogenesis that occur peripheral to the inflammatory lesion. The
pathway of the spread of inflammation is critical, because it affects the
pattern of bone destruction in periodontal disease.

Gingival inflammation extends along the collagen fiber bundles and

follows the course of the blood vessels through the loosely arranged
tissues around the alveolar bone. Although the inflammatory infiltrate is
concentrated in the marginal periodontium, the reaction is a much more

25
diffuse one, often reaching the above eliciting a response even before
there is evidence of crestal resorption (or) loss of attachment.

Interproximally, inflammation spreads in the loose connective tissue

around the blood vessels, through the transseptal fibers and then into the
bone through vessel channels that perforate the crest of the interdental
septum.

Facially and lingually, inflammation from the gingiva spreads along

the outer periosteal surface of the bone and penetrates into the marrow
spaces through vessels channels in the outer cortex.
After inflammation reaches the bone by extension from the gingiva
it spreads into the marrow spaces and replaces the marrow with a
leukocytic and fluid exudates, new blood vessels and proliferating
fibroblasts. Multinuclear osteoclasts and mononuclear phagocytes are
increased in number and the bone surfaces are lined with cove-like
resorption lacunae called Howships lacunae.

In the marrow spaces, resorption proceeds from within causing first

a thinning of the surrounding bony trabeculae and enlargement of the
marrow spaces followed by destruction of the bone and a reduction in
bone height.

It has been hypothesized that 2 cell types are involved in bone

resorption.
1. The osteoclast which removes the mineral portion of the bone
2. Mononuclear cell which plays a role in organic matrix degradation.

Radius of Action

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 Grant and Cho suggested that locally produced bone resorption
factors may have to be present in the proximity of the surface to be able to
exert their action.

Page and Schroeder on the basis of Waerhug’s measurements made

on human autopsy specimens postulated that there is range of
effectiveness of about 1.5 to 2.5 mm which bacterial plaque can induce
bone loss. Interproximal angular defects can appear only in spaces wider
than 2.5 mm.

Rate Of Bone Loss

Loe et al studied Srilankan tea labourers with no oral hygiene and
found the rate of bone loss to be about 0.2mm annually for facial surfaces
and 0.3 mm a year for proximal surfaces when periodontal disease is
untreated.
.
Pharmacologic agents and bone resorption:

Ibuprofen, a non-steroidal anti inflammatory drug, is a potent

inhibitor of cyclooxygenase pathway of arachidonic acid metabolism.
Flurbiprofen sloes bone loss in naturally occurring periodontal disease in
humans; this effect occurs without changes in gingival inflammation and
rebounds 6 months after cessation of administration of drug.

Bone destruction caused by systemic disorders:

Osteopenia / osteoporosis:
Osteopenia is characterized by a reduction in bone mass, whereas
osteoporosis is the most severe degree of osteopenia which leads to pain,
deformity, or fracture. Osteoporosis is a physiological, gender, and age-

27
related condition resulting from bone mineral content loss and structural
change in bones. The rate of bone mineral loss is approximately two times
greater in women than men. In women, post-menopausal osteoporosis is a
heterogeneous disorder which begins after natural or surgical menopause

Alveolar Bone Loss Progression in Diabetes:

Taylor et al suggested that poorer glycemic control leads to both an

increased risk for alveolar bone loss and more severe progression over
those without type 2 DM.
Factors potentially contributing to development of periodontal
disease as per the Position Paper on Diabetes and Periodontal Diseases
published in the August 1999.
1. Polymorphonuclear Leukocyte Function.
2. Collagen Metabolism and Advanced Glycation End products.

Vitamin D deficiency:
Vitamin D or calciferol is essential for the absorption of calcium
from the gastrointestinal tract and the maintenance of the calcium
phosphorous balance.
Experimental studies in animals showed that in osteomalacia, there
is rapid, generalized severe osteoclastic resorption of alveolar bone,
proliferation of fibroblasts that replace bone and marrow, and new bone
formation around the remnants of unresorbed bony trabeculae.
Radiologically there is generalized partial to complete loss of lamina dura
and reduced density of supporting bone, loss of trabeculae. Increased
radiolucence of trabecular interstices and increased prominence of
remaining trabeculae.

Hyperparathyroidism:

28
 Oral changes include malocclusion and tooth mobility, radiographic
evidence of alveolar osteoporosis with closely meshed trabeculae,
widening of the lamina dura, and radiolucent cyst like spaces. Bone cysts
become filled with fibrous tissue with abundant hemosiderin- laden
macrophages and giant cells. They have been called brown tumors,
although they are not really tumors but reparative giant cell granulomas.
This disease is called osteitis fibrosa cystica or Von Recklinghausen’s
disease. Other diseases in which it may occur are Paget’s disease, fibrous
dysplasia, and osteomalacia.

Sex hormones:
Ovirectomy results in osteoporosis of alveolar bone, reduced
cementum formation, and reduced fiber density and cellularity of
periodontal ligament in young adult mice, but not in older animals. The
gingival epithelium is atrophic in estrogen- deficient animals.
Systemic administration of testesterone retards the down growth of
sulcular epithelium over cementum, stimulates osteoblastic activity in
alveolar bone; increases the cellularity of periodontal ligament; and
restores osteoblastic activity, which is depressed by hypophysectomy

Hematological disorders:
In leukemic mice , the presence of infiltrate in marrow spaces and
the periodontal ligament results in osteoporosis of alveolar bone with
destruction of the supporting bone and disappearance of periodontal
fibers.

In Sickle cell anemia generalized osteoporosis of the jaws, with a

peculiar stepladder alignment of the trabeculae of interdental septa and
pallor and yellowish discoloration of oral mucosa. On the other way
periodontal infections may precipitate sickle cell crisis.

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BONE DESTRUCTION CAUSED BY TRAUMA FROM OCCLUSION

The second cause of periodontal destruction is TFO. TFO can

produce bone destruction in the absence/ presence of inflammation.

Trauma In The Absence Of Inflammation

In the absence of inflammation, the changes caused by TFO vary
form increased compression and tension of the periodontal ligament and
increased osteoclasis of alveolar bone to necrosis of the periodontal
ligament and bone and resorption of bone and tooth structure. The
changes are reversible; they can be repaired if the offending forces are
removed.

Persistent TFO results in funnel-shaped widening of the crestal

portion of the periodontal ligament, with resorption of the adjacent bone.

Trauma Combined With Inflammation

When combined with inflammation, TFO aggravates the bone
destruction caused by the inflammation and causes bizarre bone patterns.

FACTORS DETERMINING BONE MORPHOLOGY IN

PERIODONTAL DISEASE
Normal variation in Alveolar bone

There is considerable variation in the morphologic features of

alveolar bone, which affect the osseous contours produced by periodontal
disease. The bone features that substantially affect the bone destructive
pattern in periodontal disease include the following,

30
 - The thickness, width & crestal angulation of the
interdental septa.
- The thickness of the facial & lingual alveolar plates.
- The presence of fenestrations & dehiscences.
- The increased thickness of the alveolar bone margins to
accommodate functional demands.
- The alignment of the teeth.
For e.g. angular osseous defects cannot form in facial or lingual
alveolar plates, which have little or no cancellous bone between the outer
and inner cortical layers. In such instances the entire crest of the plate is
destroyed and the height of the bone is reduced.

Exostoses

Exostoses are outgrowths of bone of varied size and shape. Palatal

exostoses have found in 40% of human skulls. They can occur as small
nodules, large nodules, sharp ridges, spike like projections, (or) any
combination of these. Exostoses have been described in rare cases as
developing after the placement of free gingival graft.

Trauma form occlusion

It refers to the tissue injury, not the occlusal force
TFO may be a factor in determining the dimension and shape of bone
deformities. It may cause thickening of cervical margin of alveolar bone
or a change in the morphology of the bone on which inflammatory changes
will later to superimposed.
e.g: Angular defects and Buttressing Bone

Buttressing Bone Formation (Lipping)

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 Bone formation sometimes occurs in an attempt to buttress bony
trabecular weakened by resorption.

When it occurring in the jaw it is called Central buttressing bone

formation. When it occurs on the external surface, it is referred to as
peripheral buttressing bone formation. The latter may cause bulging of
bone contour called LIPPING. Sometimes accompanies the production of
osseous craters and angular defects.

Food Impaction
Interdental bone defects often occur where proximal contact is
abnormal/absence. Pressure and irritation from food impaction contribute
to the inverted bone architecture. In some instances the poor proximal
relationship may be the result of shift in tooth position because of
extensive bone destruction that preceded food impaction. In such cases
food impaction is a complicating factor rather than the cause of the bone
defect.

Juvenile Periodontitis
A vertical or angular pattern of alveolar bone destruction is found
around the first molars in juvenile periodontitis. Cause is unknown.

In 1923 Gottlieb called this disease as diffuse atrophy of the

alveolar bone. This disease was characterized by a loss of collagen fibers
in the periodontal ligament and their replacement by loose connective
tissue and extensive bone resorption, resulting in a widened periodontal
ligament space.

There will be vertical loss of alveolar bone around the first molars
and incisors. Radiographic findings include an “Arc-shaped” loss of

32
alveolar bone extending from the distal surface of the 2nd premolar to the
mesial surface of the 2 n d molar.

Prepubertal Periodontitis

Occurs before 11 years of age. Periodontal involvement consists of

early inflammatory changes that lead to bone loss and exfoliation of teeth.
Primary teeth are lost by 5 to 6 years of age.

Localized Prepubertal Periodontitis

This form of periodontitis involves only a few teeth & is

characterized by minor inflammation & slower bone loss.

Slowly Progressive Periodontitis

In SPP, pocket depths are variable and both horizontal and angular
bone loss can be found. Tooth mobility often appears in advanced cases.
Three types are seen,
1) Mild Periodontitis
Probing attachment loss of 2-4 mm
Minimal furcation involvement
Little tooth mobility
X-ray shows minimal bone loss
2) Moderate Periodontitis
Probing attachment loss 4-7 mm
Early to moderate furcation involvement
X-ray shows horizontal type of bone loss.
3) Severe periodontitis
Loss of Attachment is 7mm or more
Excessive tooth mobility
Significant furcation involvement, often through & through.

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 Radiographic bone loss exceeds 40% & angular
bone defects are seen.

Horizontal Bone Loss

This is the most common pattern of bone loss in periodontal

disease. The bone is reduced in height, but the bone margin remains
roughly perpendicular to the tooth surface. The interdental septa and the
facial lingual plates are affected.

Bone Deformities (Osseous Defects)

Different types of bone deformation can result from periodontal

disease. These usually occur in adults and have been reported in human
skulls with deciduous dentition. Their presence may be suggested on
radiographs, but careful probing and surgical exposure of the areas are
required to determine their exact conformation and dimensions.

Vertical/Angular Defects

These occur in an oblique direction, leaving a hollowed out trough

in the bone along side the root. The base of the defect is located apical to
the surrounding bone. In most instances angular defects have
accompanying infrabony pockets.

Angular defects are classified on the basis of the number of osseous

walls. Angular defects may have 1,2 & 3 walls. The number of walls in
the apical portion of the defects may be greater than that in its occlusal
position in these cases it is called combined osseous defect. Vertical
defects occurring interdentally can be seen on the radiograph, although

34
thick, bony plates may sometimes obscure them. Angular defects can also
occur on facial and lingual or palatal surfaces, but these defects are not
seen on radiographs. Surgical exposure is the only sure way to determine
the presence and configuration of vertical osseous defects.

Vertical defects increases with the age. Approximately 60% of

persons with interdental angular defects have only a single defect.
Vertical defects detected radiographically have been reported to appear
most commonly on the distal and mesial surfaces. However three wall
defects are more frequent on the mesial surfaces of U/L molars.

The three wall vertical defect was originally called an intrabony

defect. However this term was later expanded to include all vertical
defects. This 3-walled defect is more frequent on the mesial aspects of
second and third maxillary and mandibular molars. The one wall vertical
defect is also called hemiseptum.

Rapidly Progressive Periodontitis

RPP can follow an episodic pattern in its progression, periods of
advanced destruction followed by stages of quiescence of variable length.
The possibility of rapid periodontal destruction differentiates this form of
periodontitis from the more typical SPP.

Page & coworkers described sites in RPP points that demonstrated

osseous destruction of 25% to 60% during a 9- week period.

BONE DESTRUCTION PATTERN IN PRIODONTAL DISEASE

Periodontal disease alters the morphologic features of the bone, in
addition to reducing bone height. An understanding of the nature &
pathogenesis of these alterations is essential for effective diagnosis and
treatment.

35
Osseous Craters
These are concavities in the crest of the interdental bone confined
in the facial & lingual walls. Craters have been found to make up about
1/3 r d of all defects and bout 2/3 r d of all mandibular defects. Common in
posterior segments than in anterior segments. The following reasons for
the high frequency of interdental craters have been suggested.
1. The interdental area collects plaque & is difficult to
clean.
2. The normal flat or even concave & faciolingual shape of the
interdental septum in lower molars may favour crater formation.
3. Vascular patterns from the gingiva to the center of the crest may
provide a pathway for inflammation.

Bulbous Bone Contours

These are bony enlargements caused by exostoses, adaptation to
function or buttressing bone formation. They are found more frequently
more in than maxilla.

Reversed Architecture
These defects are produced by loss of interdental bone, including
the facial and lingual plates, without concomitant loss of radicular bone,
reversing the normal architecture. These defects are more common in the
maxilla.

Ledges
Ledges are plateau like bony margins caused by resorption of
thickened bony plates.

Furcation Involvement

36
 The furcation involvement refers to the invasion of the bifurcation
and trifurcation of multirooted teeth by periodontal disease. The
mandibular I molar are the most common sites and the maxillary
premolars are the least common. The number of furcation involvements
increases with the age.

Furcation involvement has been classified as grades.

Grade I - Incipient bone loss.
Grade II - Partial bone loss (cul-del-sac).
Grade III - Total bone loss through & through opening of the furcation.
Grade IV - It is similar to Grade III, but gingival recession exposes the
furcation to view

The destructive pattern in a furcation involvement varies in

different cases & the degree of involvement. Bone loss around each
individual root may be horizontal or angular & very frequently a crater
develops in the interradicular area.

Conclusion:
Alveolar bone is essential for a healthy periodontium.
A better understanding of the alveolar bone offers appropriate idea
for treating them.

37
 REFERENCES

1. Newman, Takei and Carranza. Clinical Periodontology. 9 t h edition.

2. Giannobile WV, Al-Shammari KF, Sarment DP. Matrix molecules
and growth factors as indicators of periodontal disease activity.
3. Palys MD, Haffajee AD, Socransky SS. Relationship between C-
telopeptide pyridinoline cross-links and putative periodontal
pathogens in periodontitis. J Clin Periodontol 1998; 25:865-871.
4. Reinhardt RA, Sanderfer VJ, Meinberg TA. Local biochemical
markers of bone turnover:Relationship to subsequent density of
healing alveolar bone defects. J Clin Periodontol; 31:223-228.
5. Sodek J, McKee MD. Molecular and cellular biology of alveolar
bone. Periodontology 2000, 24, 2000, 99-126.
6. Hollinger JO, Buck DC, Bruder SP. Biology of Bone Healing. In:
Tissue Engineer ing, p 17-53.

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