Alveolar bone

Deepak Kumar
MDS 1st Year
Dept. of Oral & Maxillofacial Pathology
BIDSH
CONTENTS

 Introduction;
 Classification;
 Composition;
 Structure of bone;
 Histology;
 Bone formation;
 Bone resorption;
 Bone remodelling;
 Vascular supply;
 Lymphatic drainage;
 Nerve supply;
 Bone marrow;
 Clinical application.
INTRODUCTION

 Bone is a specialized, rigid, mineralized connective tissue.

 Highly vascular.

 Forms the body skeleton.

 It is the hardest structure of the body.

 The human skeleton is the internal framework of the body. It
is composed of 270 bones at birth – this total decreases
to 206 bones by adulthood after some bones have fused
together. The bone mass in the skeleton reaches maximum
density around age 30.
FUNCTIONS
 It forms framework and shape to the body;

 Protects the soft tissue and vital organs;

 Gives attachment to muscles and tendons;

 Provides leverage for movement;

 Acts as a reservoir for metabolic calcium and phosphate;

 Acts as a site of production and storage of red blood cells;

 Provides resilience and resists stress to the body.

 CLASSIFICATION

BASED ON BASED ON BASED ON

MICROSCOPIC SHAPE DEVELOPMENT
STRUCTERE
LONG
IMMATURE ENDOCHONDRAL
SHORT

FLAT INTRA-MEMBRANOUS
MATURE

IRREGULAR

SESAMOID
BASED ON MICROSCOPIC
STRUCTURE
 MATURE BONE:

I. COMPACT BONE (CORTICAL/LAMELLAR)

 Tightly packed osteons or haversian systems;

 Arranged in layers;

 Combination of cortex and medullary canal of long bones

provides strength and low weight.

 II.CANCELLOUS BONE
(SPONGY/TRABECULAR)
 Honeycomb appearance;

 Large marrow cavities;

 Bony elements or trabeculae arranged in form of bars or

plates;

 Provides additional strength to cortices;

 Supports bone marrow.

IMMATURE BONE
 WOVEN BONE:

 First formed bone;

 Irregularly oriented collagen fibers;

 Forms rapidly;

 Seen in alveolar bone and during healing of fractures.

BASED ON SHAPE
 Long bone
 Longer than wider;

 Shaft-diaphysis;

 Ends-epiphysis;

 Diaphysis -central cavity (yellow

marrow);

 Epiphysis- compact bone at the

periphery, spongy bone at the
centre.
 Epiphysial line (remnant of
epiphysial line) is present
between diaphysis and
epiphysis in adult bone.

 Very few trabeculae.

 Examples: radius, ulna,

femur, tibia .
Short bones :
 Equal in length and width.

 Cube shaped.

 Consist of spongy bone covered by thin layer of compact bone

Examples: carpels of wrist ,Tarsals of ankle.
■ Flat bones :
Thin, flat, curved;

No marrow cavity;

Spongy bone present between upper and lower layer of

compact bone;

Example: sternum, scapula, roof of skull .

Irregular bones
Complex shapes

Notched or with ridges

Spongy bone covered with thin

layer of compact bone

Example: mandible
Sesamoid bone

Develop in tendons where there

is pressure, tension, friction.

Example: patella
COMPOSITION
ALVEOLAR BONE

 It is defined as the part of the maxilla and the mandible that

forms and supports the sockets of teeth.

 Alveolar bone is subjected to continual and rapid remodeling

associated with tooth eruption and subsequently the functional
demands of mastication.

 The size, shape , location and function of the teeth determine

the morphology of the alveolar bone.

 Functions:

 Houses the roots of teeth

 Anchors roots of teeth to alveoli with the help of sharpey’s
fibers
 Supplies vessels to PDL;
 Organizes eruption of teeth;
STRUCTURE OF ALVEOLAR
BONE
Alveolar Cancellous
Cortical bone
bone proper trabeculae
• An external • Inner socket • Interdental
plate wall septum
• Haversian bone • Enclosed
and compacted
• Thin
bone lamellae compact within a
bone compact
• Radiographs: bone
lamina dura
Socket wall
It consists of dense, lamellated bone, which is arranged in
Haversian system and bundle bone.

Bundle bone is the term given to bone adjacent to the

periodontal ligament that contains a great number of
sharpey’s fibers.

It is characterized by thin lamellae arranged parallel to the

root.
 Most of the facial and lingual portions of

the sockets are formed by compact bone.

 The cancellous portion of the alveolar

bone consists of trabeculae that encloses

irregularly shaped marrow spaces lined

with layer of thin, flattened endosteal

cells.

 Cancellous bone is predominantly in the

inter - radicular and Interdental spaces

and in limited amounts facially or

lingually, except in the palate .
 The bone which covers the root

surfaces is considerably thicker at the

palatal than at the buccal aspect of the

jaw.

 The walls of the socket are lined by

cortical bone and the area between

the socket and between the compact

jaw bone wall is occupied by

cancellous bone
 The alveolar process contains a
region of compact bone adjacent to
the periodontal ligament called
LAMINA DURA.
 It is attached to the cementum of
the roots by the periodontal
ligament.
 Is the bone lining the alveolus.

 In clinical radiographs, it
commonly appears as a dense white
line.
PERIOSTEUM
INNER LAYER
 Composed of Osteoblasts surrounded by Osteoproginator
cells, which have the potential to differentiate into
osteoblasts.

 Inner layer is osteogenic layer.

OUTER LAYER
 This layer is rich in blood vessels and nerves and composed
of collagen fibers and fibroblasts.

 Outer layer is the fibrous layer.

PERIOSTEUM AND
ENDOSTEUM:

Layers of differentiated
osteogenic connective tissue
cover all the bone surfaces.

The Tissue covering the outer

surface of the bone is
periosteum.

The Tissue lining the internal

bone cavities is called
endosteum.
Sharpey's fibers are the terminal
ends of fibers that insert into the
cementum and into the periosteum
of the alveolar bone.

Sharpey's fibers intensifies the

continuity between the periodontal
ligament fiber and the alveolar

bone.
INTERDENTAL
SEPTUM:
The interdental septum consists of

cancellous bone bordered by

socket wall cribriform plates of

approximating teeth and the facial

and lingual cortical plates.

If the interdental space is narrow,

the septum may consists of only

the cribriform plate.

HISTOLOGY OF BONE
 RESTING LINES
This lines has more regular
appearance which denotes
period of rest during bone
formation.

 REVERSAL LINES/
CEMENTING LINES :
This lines has irregular lines
which indicates area of bone
resorption
Like other connective tissues, bone tissue contains an abundant
matrix surrounding the cells. The matrix is about 25% water,
25% protein fibres and 50% mineral salts.

There are 4 types of cells in bone tissue.

OSTEOPROGENITOR cells are unspecialized cells derived

from mesenchyme, the tissue from which all connective tissues
are derived. They undergo mitosis and develop into osteoblasts.
They are found in the periosteum, endosteum and in canals that
contains blood vessels.
 OSTEOBLASTS are the cells that form bone, but they have
lost the ability to divide by mitosis. They secrete collagen
and other organic components needed to build bone tissue.
 The differentiation of osteoprogenitor cells into osteoblast is
accelerated by some hormones and some bone proteins
called Skeletal growth factors.
FUNCTIONS:
 Role in formation of bone matrix,
 Role in calcification ( through the alkaline phosphatase
enzymes)
 Synthesis of proteins.
 OSTEOCYTES these cells are concerned with maintenance
of bone.
 Small flattened and rounded cells embedded in bone lacunae.
 Derived from mature Osteoblast

FUNCTIONS
 Help to maintain the bone as living tissue because of there
metabolic activity.
 Maintain the exchange of calcium between the bone and ECF
 OSTEOCLASTS : Concerned with bone resorption.
 Giant phagocytic multinucleated cells found in the lacunae of
bone matrix.
 Derived from hemopoietic stem cells via monocytes.( CFU-M)

FUNCTIONS
 Responsible for bone resorption during bone
remodelling.
 Synthesis and release of lysosomal enzymes necessary for bone
resorption in to bone resorbing compartment.
REGULATION OF OSTEOBLAST ACTIVITY
FACTORS AFFECTING OSTEOCLAST
ACTIVITY
 BONE FORMATION

 Formation of bone, which appears to be linked with bone

resorption to maintain bone mass, involves the proliferation and
differentiation of stromal stem cells along an osteogenic pathway
that leads to the formation of osteoblasts.

 Osteoblasts synthesize the collagenous precursors of bone matrix

and also regulate its mineralization.

 The process by which bone forms is called OSSIFICATION.

 The skeleton of a human embryo is composed of fibrous

connective tissue membrane formed by embryonic connective
tissue (mesenchyme) and hyaline cartilage that are loosely shaped

like bones. They provide supporting structure for ossification.

 Ossification begins around the 6th or 7th week of embryonic life

and continues throughout adulthood.
 Bone formation follows one of 2 patterns;

1. Intramembranous ossification- refers to the formation of bone

directly on or within the fibrous connective tissue membranes.

2. Endochondral ossification - refers to the formation of bone in

hyaline cartilage

• Maxilla forms by intramembranous ossification.

• Mandible forms partly by intramembranous and partly by intra
cartilaginous ossification.

• Greater part of body, ramus, condyloid and coronoid process are

intramembranous in origin.

• Only the tip of condyloid and coronoid process are of

endochondral origin.
INTRAMEMBRANOUS
OSSIFICATION
 At the site where bone will develop, mesenchymal cells become

vascularized, cluster and differentiate, First into osteoprogenitor

cells and then into osteoblasts. The site of such a cluster is called a

Centre of ossification.

 Osteoblasts secrete the organic matrix of bone and gets

surrounded to become osteocytes. Later calcium & other minerals

are deposited and tissue calcifies .
 As the bone matrix forms, it develops into Trabeculae. As
trabeculae develop in various ossification centres, they fuse with
one another to create the open latticework appearance of spongy

bone. Connective tissue in trabecular spaces differentiates into

red bone marrow.

 On the outside of bone, vascularized mesenchyme develops into

Periosteum . Eventually, Some of the spongy bone is replaced

by the cortical bone. This will remodeled to reach its adult size
& shape.
ENDOCHONDRAL OSSIFICATION

1) Development of the cartilage model.

• Mesenchymal cells differentiateinto chondroblasts which form

the hyaline cartilage model.

• A membrane called perichondrium develops around the

cartilage.
2) Growth of the cartilage model

• Cartilage model grows by interstitial & appositional growth;

• Chondrocytes in mid-region calcify the matrix;

• Vacated lacunae formssmall cavities;

• Osteoblastsin perichondrium produce periosteal bone collar

(once perichondrium starts to form bone, it is known as
periosteum.
3) Development of primary ossification center

Near the middle of the model, capillaries of the periosteum

grow into the disintegrating calcified cartilage.

These vesselsand the osteoblasts,osteoclasts & red marrow

cells, are known as the Periosteal bud.

With the development of periosteal bud, primary ossification

center and medullary cavity forms.
4) Development of the diaphysis and epiphysis

• The diaphysis, which was once asolid mass of hyaline cartilage,

is replaced by compact bone.

• When blood vessels(epiphyseal arteries) enterthe epiphysis,

secondary ossification centers develop. ( usually around the time

of birth)
BONE RESORPTION
 Removal of the mineral and organic components of extracellular
matrix of bone under the action of osteolytic cells especially
osteoclasts .

 Sequence of bone resorption:

 1st phase :

Formation of osteoclast progenitors in hematopoietic tissues.

 Their vascular dissemination.

 Generation of resting preosteoclasts and osteoclast in bone.

 2nd phase

Activation of osteoclasts at the surface of bone.

 3rd phase

Activated osteoclasts resorbing bone.

Alterations in osteoclasts
 Osteoclasts create cavities called howships lacunae which are
shallow troughs with an irregular shape.

Osteoclasts undergo changes just before resorption :

1. Development of ruffled border
Many infoldings of cell membrane resulting in fingerlike
projections of the cytoplasm creating an extensive surface suited
for resorption.
2. Sealing zone of the plasma membrane
At the periphery of the ruffled border plasma membrane is smooth
and closely apposed to bone surface.
 Cytoplasm contains contractile actin microfilaments surrounded

by 2 vinculin rings .

 This region is called sealing zone or clear zone.

 Facilitates attachment of osteoclast to resorption sites.

 Creates an isolated microenvironment for resorption.

 Osteoclasts binds to bone by Integrin and Vitronectin.

Degradation of organic
matrix

 Digestionof organic componentoccurs by

osteolytic enzymes like Cathepsin K and matrix
metalloproteinase secreted by osteoclasts.

 Cathepsin Kdegrades major amount of Type 1

collagen and non collagenous proteins.

 MMP9 required for osteoclast migration, bone

resorption and osteoclast differentiation .
 Removal of hydroxyapatite

 Dissolution of minerals takes place by HCL;

 Protons for acid arise from activity of cytoplasmic carbonic

anhydrase 2 synthesized by osteoclasts;

 Protons are released across ruffled border by a proton pump to

resorption site.
 After resorption these organic and non organic particles of
bone matrix are endocytosed into osteoclasts.

 They are packed into membrane bound vesicles and released

by exocytosis through FSD ( functional secretory domain ).

 Following resorption osteoclasts undergo apoptosis which is

facilitated by TGF β and estrogen.
 TRAP- Tartrate resistant acid phosphatase

 Active enzyme which plays an important role in bone

resorption both inside and outside osteoclast cell.
 REMODELING OF BONE

 Major pathway of bony changes in shape, resistance to forces,

repair of wounds.

 Regulates calcium and phosphate homeostasis

 Bone remodeling involves the co-ordination of activities of cells

the osteoblast and the Osteoclast.
Osteoblasts
Stimulated by parathyroid hormone

Release interleukin -1 and interleukin -6

Leads to migration of monocyte into bone
area

LIF(leukemia inhibiting factor) coalesces to

form multinucleated Osteoclasts

Resorbs bone and releases hydroxyapatite

into the blood
Feedback mechanism

Release of osteogenic
substrate

Differentiation of
osteoblast

Deposition of bone
 PHASES OF REMODELING :
1. Activation phase :
Stimuli such as-
 Micro-fracture,
 Alteration of mechanical loading
 Insulin growth factor-I (IGFI)
 Tumor necrosis factor-α (TNF-α)
 Parathyroid hormone (PTH)
 Interleukin-6 (IL-6) activate lining cells
 RANKL/ RANK interaction triggers pre-osteoclasts fusion and
differentiation toward multinucleated osteoclasts
2. Resorption phase :
Once differentiated, osteoclasts adhere to the bone surface
and begin to dissolve bone.
They resorb the haversian lamellae and a part of the
circumferential lamellae and form a resorption tunnel or cutting
cone.
This function requires two steps:
Acidification of the bone matrix to dissolve the inorganic
component
Release of enzymes such as cathepsins K and MMP
Osteoclasts undergo to apoptosis .
3. Reversal phase :
 After removal of debris produced during matrix degradation,
osteoclasts are replaced by osteoblasts

4. Formation phase:
 Bone matrix resorption leads to the release of several growth
factors:
 Bone morphogenetic proteins (BMPs)
 Fibroblast growth factors (FGFs)
 Transforming growth factor β (TGF β)
 Recruitment of the osteoblasts in the reabsorbed area
 Osteoblasts produce the new bone matrix
The entire area of osteon where active formation occurs is

termed the filling cone

The osteoblasts get entrapped in the new bone and are called

osteocytes

Thus completing the bone remodeling process

According to ten cate:
Attachment of the osteoclasts to the
mineralized surface of the bone

Acidic environment

Demineralizes the bone

Exposes organic matrix

(mediated by acid phosphatese and
cathespin

Degradation into amino acids

VITAMINS NEEDED FOR BONE
REMODELLING
 Several vitamins like vitamins D, C, A, and B12, play a role in
bone remodeling.

 The most active form of vitamin D is calcitriol. Acting as a

hormone, it promotes removal of calcium from bone. On the
other hand, it retards calcium loss in urine, which makes it
available for deposit in bone matrix.

 Vit C deficiency causes decrease collagen production, which

retards bone growth and delays fracture healing .
 Vit A helps to control the activity , distribution, and co-ordination
of osteoblasts and osteoclasts during development. Its deficiency
results in a decreased rate of growth in the skeleton.

 Vit B12 may play a role in osteoblast activity.

VASCULAR SUPPLY
NERVE SUPPLY
BONE MARROW

 RED BONE MARROW YELLOW BONE

MARROW

Young bone Old bone

Within cavities of Epiphysis of long bones
spongy bone Accumulation of fat
Contains cells of cells
mesenchymal and Loss of haemopoetic
fibroblast type . potential
Conditions involving loss of alveolar
bone
 The various causes of alveolar bone loss are:
I. Extension of gingival inflammation
II. Trauma from occlusion
III. Systemic factors

Other factors :
I. Periodontitis
II. Periodontal abscess
III. Food impaction
IV. Overhanging restoration
V. Adjacent tooth extraction
VI. Ill-fitting prosthesis
BONE DESTRUCTION CAUSED BY
EXTENTION OF GINGIVAL
INFLAMMATION
 Most common cause of bone loss in periodontal disease is
extension of inflammation from marginal gingiva into supporting
periodontal tissues.

 Spread of inflammation from gingiva directly to PDL is less

frequent.

 The transition from gingivitis to periodontitis is associated with

changes in compostion of bacterial plaque.

 In advanced stages number of motile organisms and spirochetes

increases.
 Radius of action of plaque
 Garant &Cho suggest that bacterial plaque can induce bone loss

within range of 1.5 to 2.5 mm.

 Page and Schroeder on the basis of waerhaug’s measurements

made on human autopsy specimens, postulated that there is range

of effectiveness of about 1.5 to 2.5mm within which bacterial

plaque can induce loss of bone. This is known as radius of
action.
BONE DESTRUCTION PATTERN
IN PERIODONTAL DISEASE
1)Horizontal bone loss
2)Vertical bone loss

Horizontal bone loss:

 Most common pattern of bone loss in periodontal disease.

 Bone is reduced in height but margin remain almost

perpendicular to tooth surface not necessarily equal degree

around same tooth.

VERTICAL BONE LOSS:
 Less common pattern.

 It occurs when the pathway of inflammation travels directly into

the pdl space.

 This type of bone loss produce infrabony pocket.

 These defects are classified on bases of No. of osseous walls
present.

Three wall
defect

Two wall defect

Combined defect
One wall defect
CRATER
Bulbous bone contour (Exostosis) :
Reverse Architecture
 LEDGES
 Plateau like bone margins caused by resorption of thickened
bony plates
 TRAUMA FROM OCCLUSION
 when occlusal forces exceeds the adaptive capacity of the tissue
injury results .Trauma from occlusion;
 1) ACUTE TRAUMA FROM OCCLUSION
 2) CHRONIC TRAUMA FROM OCCLUSION

 PRIMARY TRAUMA FROM OCCLUSION:

Alteration in occlusal forces with normal periodontium with
normal height of bone.
 SECONDARY TRAUMA FROM OCCLUSION:
Due to reduced ability of tissues to resist forces .
Bone Destruction by Systemic
Disease

Vit-D deficiency;
 Diabetes;
 Hyperparathyroidism
 Paget’sdisease
 Fibrous dysplasia
 Osteoporosis
 Osteopetrosis
 VITAMIN D

 Deficiency leads to osteoporosis of alveolar bone, osteoid is

formed at normal rate but remains uncalcified, failure of

osteoid to resorb leads to its accumulation and distortion in the
growth pattern of alveolar bone.
 DIABETES

 Diabetes leads to rapid periodontal destruction.

 Defective chemotaxis, impaired host defenses and rapid

progression of infection are seen.
 Higher levels of IL-1 and PGE2 in GCF.

 Increased release of cytokines by monocyte.

 Decreased production of insulin lead to reduce in growth ,

proliferation and matrix synthesis by gingival and periodontal
fibroblast and osteoblast.
 HYPERTHYRODISM

 Generalized demineralization of the skeleton, increased

osteoclastic activity with proliferation of the connective tissue
in the enlarged marrow spaces.

 Alveolar bone shows osteoporosis with closely meshed

trabeculae, widening of PDL, absence of lamina dura leading
to tooth mobility and malocclusion.

 Hyperparathyroidism increases bone remodeling and

osteoclastic resorption which mobilizes calcium from the
skeleton
 FIBROUS DYSPLASIA

 Localized change in normal bone metabolism leads to

replacement of all components of cancellous bone by fibrous
tissue containing varying amounts of abnormal bone.

 Enlargement of the area with gradual blending of cortical

borders.

 Trabecular bone may show mixed radiolucent and radiopaque

areas.

 Trabeculae are shorter, thinner, irregularly shaped and more

numerous than normal.(Ground glass appearance).
 PAGET’S DISEASE

 Abnormal resorption and apposition of osseous tissue in one or

more bones.

 Intense wave of osteoclastic activity with resorption of normal

bone resulting in irregularly shaped resorption cavities followed
by increased osteoblastic activity forming woven bone.
3 stages-
1. Early radiolucent resorptive stage;
2.Granular or ground glass stage and
3.Denser more radiopaque appositional stage.

 Trabeculae are long, horizontal ,linearly or short and randomly

arranged.

 Cortical bone appears laminated. Abnormal laminadura and

hypercementosis is seen.
 Osteopetrosis

 Defect in the differentiation and function of osteoclast.

 Lack of normally functioning osteoclast results in abnormal

formation of bone and generalized increase in bone mass.

 Failure of bone remodeling results in dense, fragile bones that are

susceptible to fractures in infections, obliteration of marrow
spaces is seen.

 Radiographically there is bilaterally symmetrical increase in

bone density.

 Bones appear radiopaque and trabecular patterns of medullary

cavities are not visible. Laminadura is thicker than normal.
 Osteoporosis :

 Generalized decrease in bone mass and density.

 Imbalance between bone formation and resorption.

 Decreased bone formation results in a lower trabecular bone

volume and thinning of cortical bone and trabeculae.

 Bone mass decreases after 35-40 years of age.

Potential Therapeutic Strategies To Treat
Bone Resorption
 Osteoprotegerin (OPG) inhibits the differentiation of
osteoclasts through its action as a decoy receptor that blocks
receptor activator of nuclear factor-kappa B (NF-κB) ligand
(RANKL) and RANK juxtacrine interaction.

 Non-steroidal anti-inflammatory drugs (NSAIDs) and other

anti-inflammatory molecules can inhibit the formation of
hematoprogenitor cells to pre-osteoclasts. Antibodies to RANKL
can also block this interaction.

 Matrix metalloproteinase (MMP) inhibitors reduce the

protease degradation of the organic matrix, and anti-integrins
block the initial osteoclast adhesion to the matrix .
 Submicrobial doses of Tetracyclines helps to control bone

resorption .

 Bisphosphonates act by preventing the formation of ruffled

borders .

 Transferring growth factor beta increases OPG .

 Estrogen decreases RANK Ligand expression by osteoblasts.

 Calcitonin there is a receptor for calcitonin on osteoclasts

surface that prevents bone resorption .
 Bone grafts
 Allografts a tissue graft from a donor of same species as
recipient but not genetically identical .

 Alloplasts obtained from another human sources highly

processed bone powder.

 Xenografts obtained from animal sources .

such as Cow/pig processed animal bone or growth proteins.

 Synthetic bone grafting materials:- they help to create an
environment that facilitates the body’s regenerative process.
Natural or synthetic hydroxyapatites
Ceramics
Calcium carbonate
Silicon containing glasses
Synthetic polymers acts by osteoconductive
potential.
 CONCLUSION

 Alveolar bone is in interdependence with the dentition.

 It has a specialized function in the support of teeth.

 There are architectural specifications for alveolar bone that

relate to its functional role. The basic cellular and matrix
components are consistent with other bone tissues.
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