DEPARTMENT OF PERIODONTICSCOLLEGE OF DENTAL SCIENCES

A Seminar On

Alveolar Bone in Health and Disease

Presented by, Dr. Sunitha .J

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CONTENTS:

1) Introduction

2) Classification

3) Composition

4) Development

5) Structure of alveolar bone

6) Morphology

7) Radiographical features

8) Cell types in bone

9) Matrix components

10) Ultrastructural organization

11) Physiologic remodelling of alveolar bone

12) Bone formation

13) Bone resorption

14) Blood supply

15) Internal reconstruction of bone

16) The implant - bone interface

17) Etiology of bone loss

18) Factors Responsible for Bone Resorption

19) Bone destruction patterns in periodontal disease

20) Bone loss in periodontitis

21) Benign and malignant tumors of the bone

22) Peri-implantitis and bone loss

23) Conclusion

24) References

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INTRODUCTION

Bone is a mineralized connective tissue. It is unique in body in that it

exists both as a tissue and as an organ. An example for Organ is maxilla

and mandible. Each of the bony organs that are collectively called

Skeleton, which is primarily composed of a tissue i.e called bone.

Therefore the bony skeleton is constructed from the same basic building

material which is called bone mass.

The structural organization and composition of bone reflects the activity

of the cells involved in the formation of the organic matrix.

Alveolar bone: 3

The part of the maxilla or mandible that supports and protects the teeth is known as alveolar

bone. An arbitrary boundary at the level of the root apices of the teeth separates the alveolar

processes from the body of the mandible or the maxilla.

Like bone in other sites, alveolar bone functions as a mineralised supporting tissue,

giving attachment to muscles, providing a framework for bone marrow, and acting as a

reservoir for ions (especially calcium).Apart from its obvious strength, one of the most

important biological properties of bone is its "plasticity', allowing it to remodel according to

the functional demands placed upon it. Alveolar bone is dependent on the presence of teeth

for its development and maintenance. Where teeth are congenitally absent (as in anodontia),

alveolar bone is poorly developed. Alveolar bone requires functional stimuli to maintain

bone mass. Thus, following tooth extraction, it atrophies.

CLASSIFICATION : 3

A) DEVELOPMENTALLY,(1) Endochondral bone – where the bone is preceded

by a cartilaginous model which is eventually replaced by

bone.

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(2) Intramembranous bone – where the bone forms

directly within a vascular fibrous membrane.

B) HISTOLOGICALLY, according to its density, mature bone can be divided into;(1) Compact (cortical) bone(2) Cancellous (spongy) bone

COMPOSITION: 5

DEVELOPMENT: 10

At the late bell stage, bony septa and bony bridge start to form, and separate the

individual tooth germs from another, keeping individual tooth germs in clearly outlined

bony compartment. At this stage, the dental follicle surrounds each tooth germ, which is

located between a tooth germ and its bony compartment. Even prior to root formation, the

Inorganic (65%) Organic (35%)

Hydroxyappatite

Collagen (88-89%) Noncollagenous (11-12%)

BONE

Glycoproteins (6.5-10%)

Proteoglycans (0.8%)

Sialoproteins (0.35%)

Lipids (0.4%)

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tooth germs within bony compartments show continued bodily movement in various

directions to adjust to the growing jaws. This movement causes minor remodeling of bony

compartment through bone resorption and deposition of new bone.

The major changes in the alveolar processes begin to occur with the development of

the roots of teeth and tooth eruption. As the roots of teeth develop, the alveolar processes

increase in height. Also, cells in the dental follicle start to differentiate into periodontal

ligament fibroblasts and cementoblasts responsible for the formation of the periodontal

ligament and cementum, respectively. At the same time, some cells in the dental follicle also

differentiate into osteoblasts and form the alveolar bone proper. The formation of the

alveolar bone proper is closely related to the formation of the periodontal ligament and

cementum during root formation and tooth eruption. Thus, the size and shape of the

individual developing tooth roots determine the overall structure of the alveolar bone proper.

On the other hand, the rest of bony structures in the alveolar process are achieved by

periosteal bone formation.

STRUCTURE OF ALVEOLAR BONE: 11

The maxilla and mandible of the adult human can be subdivided into two portions:

(a) The alveolar process that involves in housing the roots of erupted teeth and

(b) The basal body that does not involve in housing the roots.

The alveolar processes consist of the thin alveolar bone proper that

forms the alveolar wall of the tooth socket, the inner and outer cortical

plates, and spongy bone between the alveolar boneproper the cortical

plates. Since the alveolar processes develop and undergo remodeling

with the tooth formation and eruption, they are tooth-dependent bony

structures. Therefore, the size, shape and location and function of the

teeth determine their morphology.

The alveolar bone proper is 0.1 to 0.4 mm thick and is consisted of

a Harversian system and lamellated and bundle bone. The coronal and

apical regions of the alveolar bone proper have a sieve-like structure.

These openings connect the periodontal ligament to the bone marrow

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spaces and correspond to Volkmann’s canals through which blood

vessels, lymphatic vessels and nerve fibers pass.

Anatomically no distinct boundary exists between the body of

maxilla or the mandible and their respective alveolar process. As a result

of its functional adaptation, two parts of the alveolar process can be

distinguished. 5

The FIRST consists of thin lamellae of bone that surrounds the root

of the tooth and gives attachment to the principal fibers of periodontal

ligament. This is ALVEOLAR BONE PROPER.

The SECOND part is the bone, which surrounds the alveolar bone

proper and gives support to the socket. This has been called

SUPPORTING ALVEOLAR BONE, which in turn consists of 2 parts.

1) CORTICAL PLATE, which consists of compact bone and forms

outer and inner plates of alveolar processes.

2) SPONGY BONE, which fills area between these plates and

alveolar bone proper, also known as cancellous bone.

CORTICAL PLATES: 5

Cortical plates are continous with compact layer of the maxillary

and mandibular body, and are generally much thinner in maxilla than in

mandible. They are thickest in the premolar and molar regions of the

lower jaw, especially on buccal side. In the lower jaw the cortical bone is

of the alveolar process is dense. In the maxilla the outer cortical plate is

perforated by many small openings through which blood and lymph

vessels pass. In the region of the anterior teeth of both the jaws, the

supporting bone is usually very thin. No spongy / cancellous bone is

found here, and the cortical plate is fused with the alveolar bone proper.

In such areas, notably in premolars and molar regions of the maxilla,

defects of the outer alveolar wall are fairly common.

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Histologically, cortical plates consist of longitudinal lamellae and

haversian system. In the lower jaw, circumferential or basic lamellae

reach the body of the mandible into the cortical plates.

INTERDENTAL SEPTA: 1, 2

Interdental septa consist of cancellous bone bordered by the socket

wall cribriform plates of approximating teeth and facial and lingual

cortical plates. The interdental septa are bony partition that separate

adjacent alveoli coronally at cervical region, the septa are thinner and

here the cortical plates are fused and cancellous bone is frequently

missing. If the interdental space is narrow, the septum may consist of

only the cribriform plate. If roots are too close together, an irregular

window can appear in the bone between adjacent roots. Determining root

proximity radiographically is important. The mesiodistal angulation of the

crest of the interdental septum usually parallels a line drawn between CEJ

of the approximating teeth. Distance between crest of the alveolar bone

and CEJ in young adults is 0.75-1.49mm (avg.1.08mm). This distance

increases with age to an average of 2.81mm.The mesiodistal and

faciolingual dimension and shape of the interdental septum are governed

by the size and convexity of the crowns of the approximating teeth , as

well as by the position of the teeth in the jaw and their of eruption.

The interdental and interradicular septa contain the perforating

canals of Zuckerkandl and Hirschfeld which house interdental or

interradicular arteries, veins, lymph vesels and nerves. 5

SPONGY / CANCELLOUS BONE: 5

It fills the area between the cortical plates and the ABP.

Radiographic studies permit the classification of spongiosa of the alveolar

process into two main types;

Type 1: The interdental and interradicular trabeculae are regular and

horizontal in a ladder like arrangement. This type of architecture is seen

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most commonly in the mandible and fits well into the general idea of

trajectory pattern of spongy bone.

Type 2: Shows irregularly arranged numerous delicate interdental and

interradicular trabeculae. Although, functionally satisfactory, lacks a

distinct trajectory pattern which seems to be compensated by greater

number of trabeculae in any given area. This type of arrangement is

more common in maxilla. Wide variations occur in trabecular pattern

which is affected by occlusal forces. Maxilla has more cancellous bone

than mandible. 1, 2

Both types show a variation in thickness of trabaculae and the size

of marrow spaces. These trabeculae are less prominent in upper jaw

because of proximity to nasal cavity and maxillary sinus.5

In the body as a whole, about 85% of bone is of the cortical variety while about 15%

is spongy. However, these figures are likely to vary according to site and age. Although it

only occupies a small percentage of bone volume, spongy bone has a far higher turnover

rate than cortical bone: cortical bone is said to remodel about 3% of its mass each year,

while spongy bone remodels about 25%. The cortical bone functions mainly in

mechanical/protective role, while the spongy bone has a more metabolic function. 3

MORPHOLOGY: 4, 5

Alveolar bone structure varies greatly and an understanding of the range

of the variation is essential for diagnosis of bone defects. Generally the

form of the alveolar bone can be predicted on the basis of 3 general

principles.

1) The position, state of eruption, size and shape of the teeth

determine to a great extent the form of the alveolar bone.

2) When subjected to forces within normal physiologic limits bone

undergoes remodeling to form a structure that best resolves the

forces applied.

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3) There is a finite thickness below which bone will not survive but will

be resorbed.

The alveolar margin usually follows the contour of the

cementoenamel line. Thus, scalloping of the bony margin is prominent

on the facial aspect of the anterior teeth than on the molar and the

interproximal bone between the molars is flat buccolingually. The

interproximal bone between adjacent teeth that are erupted to the

different planes of occlusion will be inclined toward the root of the less

erupted tooth. Teeth that are rotated will exhibit a bone margin that is

located more coronally and is less scalloped than that of adjacent

normally positioned teeth. The size, position and shape of the roots

have a major influence upon bone form.

BUNDLE BONE (LAMINA DURA) AND CRIBRIFORM PLATE: 4, 5

Bundle bone is the part of alveolar bone, into which the fiber

bundles of the PDL insert. The ABP appears as an opaque line called

LAMINA DURA. The apparent density is due to thick bone without

trabeculations that x-ray must penetrate and not due to any increase in

mineral content. Embedded within this bone are the extrinsic collagen

fiber bundles of PDL. In general the lining of alveolar bone is fairly

smooth in youngsters. With age, the socket lining become rougher and is

seen in histologic section to have a ragged outline.

The alveolar bone is perforated by many openings through which

the blood vessels, lymphatics and nerves of PDL pass. It is referred to as

cribriform plate because of perforation. The outer cortical plate is

covered by a fibrous and cellular periosteum. The inner cortical plate

(ABP) contains sharpy’s fibers that are the endings of embedded PDL.

HAVERSIAN SYSTEM (BONE ORGANISATION): 3, 4

Bone is deposited in layers, or lamellae, each lamella being about 5ųm thick.

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Three distinct types of layering are recognized:

a) Circumferential lamellae enclose the entire adult bone, forming its outer perimeter.

b) Concentric lamellae make up the bulk of compact bone and form the basic

metabolic unit of bone, the osteon.

The osteon is a cylinder of bone, generally oriented parallel to the long axis of

the bone. In the center of each is a canal, the Haversian canal, which is lined by a

single layer of bone cells that cover the bone surface; each canal houses a

capillary. Adjacent Haversian canals are interconnected by Volkmann canals,

channels that, like Haversian canals, contain blood vessels, thus creating a rich

vascular network throughout compact bone.

Recently formed osteons that have not become remodeled are called primary

osteons, which become partially resorbed and replaced by adjacent osteons, they

become secondary osteons, which is indicative of old bone.

c) Interstitial lamellae are interspersed between adjacent concentric lamellae and

fill the spaces between them. They are actually fragments of preexisting

concentric lamellae and can take a multitude of shapes.

There may be between 4 and 20 concentric lamellae within each Haversian system,

the number being limited by the ability of nutrients to diffuse from the central vessel to the

cells in the outermost lamella. The longitudinally running Haversian canals are connected by

a series of horizontal ones (interconnecting canals).

In adult bone, as a result of remodelling, fragments of previous Haversian systems

may be present (the interstitial lamellae; ) which can contain old remnants of circumferential

lamellae as well as osteonal remnants.

In spongy bone the lamellae are apposed to each other to form trabeculae about 50

ųm thick. The trabeculae are not arranged randomly but aligned along lines of stress so as

best to withstand the forces applied to the bone while adding minimal to mass. The

trabeculae surround the marrow spaces from which they derive their nutrition and only

infrequently are seen to possess Haversian canals.

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BONE MARROW: 1, 2

In the embryo and 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 the adult, the marrow of the jaw is normally of

the latter type, and red marrow is found only in the ribs, sternum, vertebrae, skull and

humerus. However foci of red marrow are occasionally seen in the jaws often accompanied

by resorption of bony trabeculae. Common locations are the maxillary tuberosity, the

maxillary and mandibular molar and premolar areas, and the mandibular symphysis and

ramus angle, which may be visible radiographically as zones of radiolucency.

PERIOSTEUM AND ENDOSTEUM: 1, 2

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

Tissue covering outer surface of bone is termed Periosteum, where as tissue lining the

internal bone cavities is called Endosteum.

The periosteum consists of an inner layer composed of osteoblasts surrounded by

osteoprogenitor cells, which have the potential to differentiate into osteoblasts, and an outer

layer rich in blood vessels and nerves and composed of collagen fibers and fibroblasts.

Bundles of periosteal collagen fibers penetrate the bone, binding the periosteum to

the bone. The endosteum is composed of a single layer of connective tissue. The inner

layer is the osteogenic layer, and the outer layer is the fibrous layer.

Cellular events at the periosteum modulate bone size through out an individual’s life

span, and change in bone size is probably the result of the balance between periosteal

osteoblastic and osteoclastic activities.

RADIOGRAPHICAL FEATURES: 7

LAMINA DURA: A radiograph of sound teeth in a normal dental arch demonstrates

that the tooth sockets are bounded by a thin radiopaque layer of dense bone. Its name,

lamina dura ("hard layer"), is derived from its radiographic appearance. This layer is

continuous with the shadow of the cortical bone at the alveolar crest.

Its radiographic appearance is caused by the fact that the x-ray beam passes

tangentially through many times the thickness of the thin bony wall, which results in its

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observed attenuation. Developmentally the lamina dura is an extension of the lining of the

bony crypt that surrounds each tooth during development.

ALVEOLAR CREST: The gingival margin of the alveolar process that extends between

the teeth is apparent on radiographs as a radiopaque line, the alveolar crest. The level of this

bony crest is considered normal when it is not more than 1.5 mm from the cementoenamel

junction of the adjacent teeth. Radiographs can demonstrate only the position of the crest;

determining the significance of its level is primarily a clinical problem.

The image of the crest varies from a dense layer of cortical bone to a smooth surface

without cortical bone. In the latter case the trabeculae at the surface are of normal size and

density. In the posterior regions this range of radiodensity of the crest is presumed to be

normal if the bone is at a proper level in relation to the teeth. The absence of an image of

cortex between the incisors, however, is considered by many to be an indication of incipient

disease, even if the level of the bone is not abnormal.

CANCELLOUS BONE:

The cancellous bone (also called trabe.cular bone, or spon-giosa) lies between the

cortical plates in both jaws. It is composed of thin radiopaque plates and rods (trabec-ulae)

surrounding many small radiolucent pockets of marrow. The radiographic pattern of the

trabeculae shows considerable intrapatient and interpatient variability, which is normal and

not a manifestation of disease.

The trabeculae in the anterior maxilla are typically thin and numerous, forming a

fine, granular, dense pattern, and the marrow spaces are consequently small and relatively

numerous. In the posterior maxilla the trabecular pattern is usually quite similar to that in the

anterior maxilla, although the marrow spaces may be slightly larger.

In the anterior mandible the trabeculae are somewhat thicker than in the maxilla,

resulting in a coarser pattern, with trabecular plates that are oriented more horizontally. The

trabecular plates are also fewer than in the maxilla, and the marrow spaces are

correspondingly larger. In the posterior mandible the periradicular trabeculae and marrow

spaces may be comparable to those in the anterior mandible but are usually somewhat

larger. The trabecular plates are oriented mainly horizontally in this region also.

CELL TYPES IN BONE: 3

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Several cell types are responsible for the synthesis, maintenance and resorption of

bone. These can be regarded as belonging to two main families, one mesenchymal and the

other haemopoietic. The osteoblasts, osteocytes and bone lining cells are derived from a

mesenchymal (or ectomesenchymal) stem cell. These stem cells reside in the bone marrow

and in a region of proliferating cells adjacent to the osteoblast layer in the periosteum, In the

pcriodontal ligament and other bone-forming tissues the osteogenic precursors may be

associated with small blood vessels. The osteoclasts, however, belong to a different lineage.

They form part of the haemopoietic system, being derived from the mononuclear/phagocyte

system (including monocytes and macrophages.

OSTEOBLASTS: 3, 11

Osteoblasts are specialised fibroblast-like cells of mesenchymal origin. A cuboidal

layer of these cells is prominent on a bone surface where there is active bone formation.

Unlike cartilage, which grows interstitially, bone can be deposited (or resorbed) only at

surfaces. Active osteoblasts appear cuboidal and exhibit a basophilic cytoplasm that is

related to the extensive endoplasmic reticulum within the cells.

At the innermost surface of the tooth alveolus, the positional

arrangement of alveolar bone osteoblasts must accommodate the

interdigitating portions of the periodontal ligament collagen fibers known

as Sharpey’s fibers that insert into the bone. Thus, in three dimensions,

these cells form an extensively perforated sheet of otherwise contiguous

osteoblasts which, in addition to producing alveolar bone matrix proper,

must additionally embed continuously remodeling periodontal ligament

fibers in a rather precise manner.

At the ultrastructural level, active osteoblasts (like periodontal fibroblasts) contain

rough endoplasmic reticulum (which is even more extensive and arranged in parallel stacks)

and numerous mitochondria and vesicles: the Golgi complex is localised and extensive. The

cells contact one another by means of adherens and gap junctions. These are functionally

connected to micro-filaments and enzymes (such as protein kinases) associated with

intracellular secondary messenger systems. This complex arrangement provides for

intercellular adhesion and cell-cell communication, helping to ensure that the osteoblast

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layer completely covers the osteoid surface and that the osteoblasts function in a co-

ordinated manner.

The osteoblast secretes the organic matrix of bone, which initially is represented by

an unmineralised layer known as OSTEOID, about 5-10 um thick. Osteoid consists of type

1 collagen fibres arranged more or less parallel to bone surface, embedded in a complex

ground substance of proteoglycans, glycoproteins and other protein molecules. The

biochemical changes occurring at the mineralising front are poorly understood, when

alveolar bone is first formed, initial mineralisation may be controlled by osteoblasts from

whose cell membrane matrix vesicles are budded off into the osteoid, within which the first

crystals are formed. The cell membrane around these first crystals breaks down to form the

seed around which further mineralisation can occur by epitaxy.

The intrinsic collagen fibrils lie parallel to the bone surface. At the surface of

alveolar bone adjacent to the periodontal ligament, extrinsic Sharpey's fibres pass into the

osteoid layer more perpendicularly. About 15% of osteoblasts become embedded in the

organic matrix as osteocytes.

The osteoblast secretes the various endogenous components of the bone matrix.

Some, such as collagen type I, are widely distributed and not unique to osteoblasts. Others

are specific to cells of the osteoblast lineage and provide useful markers of the osteoblast

phenotype. These include osteocalcin and the recently described osteoblast transcription

factor, cbfa-1. Alkaline phosphatase activity, although not entirely specific to bone, is easy

to identify and is a reliable indicator of osteoblastic differentiation.

In addition to its obvious involvement in bone formation, the osteoblast has a

controlling influence in activating the bone-resorbing cells, the osteoclasts. It is a source of

factors involved in this process (such as colony-stimulating factors, prostaglandins and the

recently described protein osteo-protegerin ligand). The osteoblast, and not the osteoclast,

contain receptors for parathyroid hormone and regulates the osteoclastic response to this

hormone.

OSTEOCYTES: 3, 5

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Osteocytes are the cells lying within the bone itself and are 'entrapped' osteoblasts.

There are about 25000 osteocytes per cubic millimetre of bone. Osteoblasts that become

osteocytes occupy spaces or lacunae in bone and are defined as cells surrounded by bone

matrix, whether mineralized or still part of osteoid stream.

The lacunae are regularly distributed, and many fine canals called canaliculi radiate

from them in all directions. The canaliculi allow the diffusion of substances through the

bone. Numerous cell processes from the osteocytes run in the canaliculi in all directions.

The canaiiculi of osteocytes are preferentially oriented, more being directed perpendicularly

to the bone surface than parallel to it. Osteocytes close to the cement line have more

canaliculi directed towards the bone surface than away from it.

As a result of their widespread distribution and connections osteocytes are obvious

candidates to detect stress induced in bone and are therefore regarded as the m

mechanoreceptors of bone.

Osteocytes newly incorporated into bone matrix from the osteoblast layer have high

organelle content similar osteoblasts. However, as they become more deeply situated with

continued bone formation, they appear to be less active. The cell is then seen to have a

nucleus and thin ring of cytoplasm containing few organelles, reflecting the decreased

cellular activity. It is believed by some that formative and/or resorptive activity of these

cells may vary under certain metabolic requirements, resulting in the concept of “osteocytic

osteolysis”. Numerous slender processes from the osteocyte extend into canaliculi in the

matrix. The processes of one cell are joined to those of another by gap junctions, which

allow cell-to-cell communication and ordination of activity. Osteocytes are also in

communication with osteoblasts at the surface.

BONE LINING CELLS: 3

When bone surfaces are neither in the formative nor resorptive phase, the bone

surface is completely lined by a layer of flattened cells termed bone-lining cells. These show

little sign of synthetic activity as evidenced by their organelle content. They are regarded as

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postprolifcrative osteoblasts. By covering the surface of bone, they protect it from any

resorptive activity from osteoclasts. They may also be reactivated to form osteoblasts.

OSTEOPROGENITOR CELLS: 3, 6

In order to generate the osteoblasts throughout life, a stem-cell population is

required. The stem cells have the ability maintain their numbers throughout life. When a

stem cell divides, one of the daughter cells remains as a stem cell, while the other can

differentiate into another cell type. This property of self-renewal is a unique property of

stem cells. In the case of alveolar bone, the cells that eventually give rise to osteoblasts are

termed osteoprogenitor cells and reside in the layer of cells beneath the osteoblast layer in

the periosteal region, in the periodontal ligament, or in the marrow spaces.

Initially, they are fibroblast-like cells, with an elongated nucleus and few organelles.

Their life cycle may involve up to about eight cell divisions before reaching the osteoblast

stage. There is a gradual acquirement of osteoblast-like features associated with an ordered

increase in gene expression. Initially, genes related to cell growth are expressed (such as c-

myc, c-fos and cbfa 1), followed by genes related to osteoblast products such as type I

collagen, fibronectin, some growth factors and alkaline phosphatase. Finally, genes are

expressed related to products associated with mineralisation (such as osteocalcin and

osteopontin).

Friedenstein (1973) divided osteoprogenitor cells into;

1) Determined osteogenic precursor cells are present in bone marrow, in the

endosteum and in the periosteum thet cover the surfaces of the bone. These cells

possess an intrinsic capacity to proliferate and differentiate into osteoblasts.

2) Inducible osteogenic precursor cells represent mesenchymal cells present in the

other organs and tissues (eg; muscles) that may become bone forming cells when

exposed to specific stimuli.

OSTEOCLASTS: 3

Osteoclasts are the cells responsible for bone resorption. They are derived from

haemopoietic cells of the monocyte/ macrophage lineage by fusion of mononuclear

precursors, giving rise to multinucleated cells. Resorbing surfaces of alveolar bone show

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resorption concavities (Howship's lacunae), in which lie the multinucleated osteoclasts.

Characteristically, osteoclasts may be up to 100 um in diameter and have on average 10-20

nuclei.

That part of the cell that lies adjacent to bone, and where rcsorption is occurring,

often has a foamy, striated appearance at the light microscope level (the so-called 'ruffled

border'). A useful marker for osteoclasts is tartrate-resistant acid phosphatase, although the

precise function of this enzyme is unknown. Osteoclasts are recruited only when required;

there is consequently no significant reservoir of inactive osteoclasts. The lifespan of

osteoclasts is not known with any certainty, although it is thought to be about 10-14 days.

There is evidence of apoptosis (programmed cell death) of its nuclei, indeed, as the

administration of oestrogens and bisphosphonates induces apoptosis. This may help explain

the use of such materials in combating osteoporosis and other diseases characterised by loss

of bone. The possibility exists that additional fusion of new cells may prolong the activity of

osteoclasts.

At the ultrastructural level, the ruffled border is composed of many tightly packed

microvilli adjacent to the bone surface. This border provides a large surface area for the

resorptive process. At the circumference of the ruffled border, the plasma membrane tends

to become smooth and the cytoplasm beneath it contains numerous contractile actin

microfilaments (surrounded by two vinculin rings). It has been suggested that this modified

annular zone (also referred to as clearzone) may serve to attach the cell very closely to the

surface of the bone. This provides a 'sealing zone' and thus creates an isolated

microenvironment in which resorption can take place without diffusion of the hydrolytic

enzymes produced by the cell into adjacent tissue. A distinguishing feature of osteoclasts is

the presence of receptors for calcitonin. Administration of calcitonin inhibits bone

resorption by, among other things, blocking the formation of actin rings employed in cell

attachment.

The attachment of the osteoclast cell membrane to the bone matrix at the sealing

zone is due to the presence of cell membrane proteins known as integrins (especially αvβ3).

These integrins bind to specific amino acid sequences present in proteins of the bone matrix,

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namely Arg-Gly-Asp (RGD). Interference with the formation of such integrins or the

administration of competing synthetic peptides will inhibit bone resorption.

MATRIX COMPONENTS: 11

Although alveolar bone and the alveolar process have specialized

features relating to their functional properties, the composition of the

extracellular matrix of alveolar bone appears to be similar to other bone

tissues as indicated largely by immunohistochemical analyses.

The bone matrix is formed from a scaffold of interwoven collagen

fibers within and between which small, uniform, plate-like crystals of

carbonated hydroxyapatite (Ca10[PO4]6[OH]2) are deposited. Other

proteins, including proteoglycans, acidic glycosylated and non-

glycosylated proteins associate with and regulate the formation of

collagen fibrils and mineral crystals, or provide continuity between matrix

components and between the matrix and cellular components. In

addition, small amounts of carbohydrate and lipid contribute to the

organic matrix, which comprises approximately one-third of the matrix

while the inorganic components account for the remaining two-thirds.

Calcium and phosphate in the form of poorly crystalline, carbonated

apatite, also described as dahllite, predominates the inorganic phase,

largely replacing the water component of the soft, dense connective

tissues that include the periodontal ligament and gingiva.

COLLAGEN: 11

Collagen comprises the major (~80–90%) organic component in

mineralized bone tissues. Type I collagen (>95%) is the principal collagen

in mineralized bone and, together with type V (<5%) collagen, the type I

collagen forms heterotypic fiber bundles that provide the basic structural

integrity of connective tissues. In addition to the presence of type I and V

collagens in alveolar bone, both type III and XII collagens are also

present. The type III collagen is present as mixed fibers with type I

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collagen in Sharpey’s fibers that insert from the periodontal ligament

into the lamellar bone lining the alveolus to provide a stable connection

with the tooth.

The collagen fibrils in bone are stabilized by intermolecular cross-

linking involving lysines and modified lysines that form pyridinium ring

structures (pyridinolines). These cross-links are primarily responsible for

the high tensile strength of collagen fibers, which are formed from fibrils

as higher order structures laid down in a specific orientation by the bone-

forming osteoblasts.

In rapidly forming (woven) bone that is produced during early

development and in repair sites, the fibers are extensively interwoven,

leaving a substantial volume of inter-fibrillar space that is largely

occupied by mineral crystals and associated acidic proteins. 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. In both woven and lamellar bone the mineral

crystals within the collagen fibrils are believed to form initially within the

gap region between successive collagen molecules such that their c-axes

are aligned with the long axis of the collagen fibril.

NONCOLLAGENOUS PROTEINS: 11

Using dissociative extraction procedures, most of the major

noncollagenous proteins from mineralized bone have been isolated and

characterized. Although age-related differences in the relative amounts

of these proteins have been reported together with differences in various

types of bone and in bones of different species, the same proteins are

always present. Some of these proteins, typically osteocalcin and bone

sialoprotein, are essentially unique to mineralized tissues, whereas

others, such as osteonectin/ SPARC (secreted protein, acidic, rich in

cysteine) and osteopontin have a more general distribution. These

19

proteins are released from bone by demineralization, reflecting the

predominant association with the mineral phase. Other proteins are

present in bone in specifically modified forms. Thus small proteoglycans,

primarily chondroitin sulfate proteoglycans, are present in bone, whereas

their dermatan sulfate counterparts are characteristically found in soft

connective tissues. The proteoglycans are generally associated with the

collagenous matrix, although interaction with mineral crystals also occurs

through the acidic glycosaminoglycan side chains. In addition to those

proteins produced by bone-forming cells, certain proteins derived from

blood and tissue fluids are concentrated in bone, largely due to their

affinity for the mineral crystals. These include albumin, α2HS-

glycoprotein, immunoglobulins and matrix gla protein.

OSTEOCALCIN: 11

Osteocalcin, also known as bone gla protein, represents 15% of the

noncollagenous proteins and was the first noncollagenous bone protein

to be characterized. It is a small, highly conserved, 5.8-kDa acidic protein

that is characteristically modified by vitamin K–dependent carboxylating

enzymes that convert two to three glutamic acids into g-carboxyglutamic

acids (gla groups), linking this protein with a family of blood coagulation

factors.The human osteocalcin gene comprising 4 exons is located on

chromosome 1 and codes for a 125-amino-acid prepro- osteocalcin that

includes a 26-amino-acid signal peptide.

Despite extensive studies, the role for osteocalcin in bone

formation and remodeling is not entirely clear. Abrogation of

carboxylating activity by treatment with the vitamin K antagonist

warfarin reduces osteocalcin levels in bone, which becomes

hypermineralized. However, the regulation of osteocalcin by osteotropic

hormones, such as 1,25- dihydroxyvitamin D3 (vitamin D3) and

parathyroid hormone, together with the ability of a carboxy- terminal

segment to act as a chemoattractant to osteoclast precursors, also

suggests a role in bone resorption.

20

OSTEOPONTIN AND BONE SIALOPROTEIN: 11

Osteopontin and bone sialoprotein, originally characterized as bone

sialoproteins I and II, are expressed in alveolar bone and have been

localized using immunohistochemistry and immunogold labeling. These

proteins share a number of biochemical and biophysical properties that

have been detailed in recent reviews. Thus, the genes for human

osteopontin and bone sialoprotein comprise 7 exons, spanning ~11.1 kb

and ~15 kb respectively, and are located within 340 kb on the long arm

of chromosome 4.

Both proteins are heavily glycosylated and phosphorylated, with

high levels of acidic amino acids; glutamic acid is predominant in bone

sialoprotein and aspartate predominant in osteopontin. A stretch of

aspartate residues in osteopontin and two to three stretches of

glutamate in bone sialoprotein are implicated in hydroxyapatite binding.

Despite the structural similarities, these proteins have clearly

different functional roles. Whereas bone sialoprotein is essentially

restricted to mineralizing tissues, osteopontin has a more general

distribution that reflects a broader biological role. Similar to blood

clotting factors, osteopontin is also susceptible to thrombin, indicative of

an origin in the blood or blood-forming organs. Thrombin digestion occurs

close to the RGD sequence and generates two large fragments with

altered biological activities.

SPARC / OSTEONECTIN: 11

SPARC / Osteonectin, a 40-kDa glycoprotein that is predominantly

bound to hydroxyapatite, was one of the first proteins to be isolated from

bone by combined dissociative extraction and demineralization. SPARC,

which has also been characterized in basement membranes as BM40, is

a secreted calcium- binding glycoprotein that interacts with a range of

extracellular matrix molecules. It is widely expressed during

21

embryogenesis, and in vitro studies have suggested roles in the

regulation of cell adhesion and proliferation, and in the modulation of

cytokine activity. SPARC has been characterized as a counteradhesive

protein that modulates interactions of cells with the extracellular matrix.

Recent studies have indicated a role for SPARC in early

development and that it has a signaling function, which may involve

effects on the nuclear matrix following endocytosis and transportation to

the nucleus. Human SPARC, which is on chromosome, has 10 exons that

code for a ~300-amino-acid nascent protein that includes a 17-amino-

acid signal sequence.

The major proteoglycans in bone, including alveolar bone, are

characteristically expressed with chondroitin sulfate side chains,

reflecting the lack of an epimerase activity in osteoblastic cells that

converts glucuronic acid into iduronic acid found in dermatan sulfate.

Notably, dermatan sulfate forms of proteoglycan are expressed by

undifferentiated bone cells, indicating that the epimerase activity can be

used as a differentiation marker for osteogenesis.

A large 1000-kDa chondroitin sulfate proteoglycan, that is similar to

versican, has been extracted from the non-mineralized bone matrix,

while two small proteoglycans, biglycan (chondroitin sulfate proteoglycan

I) and decorin (chondroitin sulfate proteoglycan II), are found

predominantly in ethylenediaminetetraacetic acid-extracts of bone, while

a third small proteoglycan (chondroitin sulfate proteoglycan) is entirely

associated with the mineral crystals.

Biglycan (Mr ~350 kDa) has a 46-kDa protein core with two

chondroitin sulfate chains of ~150 kDa each, attached near the amino

terminus. Biglycan is more prominent in developing bone and has been

localized to pericellular areas.

22

Decorin (Mr~120–200 kDa) also has a protein core of

approximately 46 kDa with a single chondroitin sulfate chain of variable

size attached at the amino terminus. Decorin is known to bind within the

gap region of collagen fibrils and, as suggested by its name, decorates

the fibril surface.

Together, decorin and biglycan can comprise, 10% of the non-

collagen proteins in bone, but this decreases with maturation of the

bone.

Lysyl oxidase and tyrosine-rich acidic matrix protein are

prominent components of the demineralized bone and dentin matrix.

While lysyl oxidase is known to be a critical enzyme for collagen cross-

linking, tyrosine-rich acidic matrix protein (TRAMP) is a recently

discovered 22-kDa (183 amino acids with a 18-amino-acid signal

sequence) extracellular matrix protein with proteoglycan and cell-binding

properties that is located on human chromosome 1. Tyrosine-rich acidic

matrix protein, which is also known as dermatopontin, binds decorin and

transforming growth factor- β, and together these proteins can regulate

the cellular response to transforming growth factor-β.

Other proteins that are found in bone include procollagen peptides,

thrombospondin, fibronectin and vironectin, proteins that modulate cell

attachment and the enzyme alkaline phosphatase, which is important for

mineralization to occur.

ULTRASTRUCTURAL ORGANIZATION: 11

The organic matrix of bone serves a major biomechanical function

in housing the solid, inorganic calcium-phosphate mineral phase of bone.

The geometrical complexity of multi-rooted teeth within the alveolar

bone, and the response of these tissues to mastication and other unique

forces within the oral cavity, results in an intricate pattern of bone

remodeling that do not involve classic Haversian remodeling. Continuous

23

accommodation of remodeling Sharpey’s fibers further complicates the

remodeling pattern.

Extracellular matrix in bone can be arbitrarily and broadly divided

into several spatially distinct compartments that conceptually allow for a

useful description of the sequence of events comprising the synthesis,

secretion, accumulation and mineralization of bone matrix. Following

synthesis and release of organic molecules by the cellular compartment

(osteoblasts), a collagenous stroma called the osteoid is formed that

ultimately acts as a scaffolding for apatite mineral deposition and the

accumulation of noncollagenous and plasma proteins and proteoglycans.

These latter events occur predominantly at what is known as the

mineralization front – a site where mineralization propagates extensively

throughout and between the collagen fibrils. Although the first mineral to

appear may be found at small, discrete foci within the osteoid seam, the

precise nucleation sites of this, and the subsequent deposition of more

confluent mineral at the mineralization front of the mineralized bone

matrix proper (the mineralized bone compartment), remain controversial.

With recent developments in the molecular characterization of

individual bone proteins, and with the production of specific antibodies to

these purified molecules, it has been possible to localize these proteins

with high resolution in situ using ultrastructural immunocytochemical

techniques. Thus, immunocytochemical studies have been able to

identify components of the organic material described above and to

reveal its ultrastructural association with sites of mineralization

throughout the tissue noncollagenous proteins typically found at sites of

mineralization includes bone sialoprotein and osteopontin.

PHYSIOLOGIC REMODELLING OF ALVEOLAR BONE: 11

Complete remodeling of the alveolar bone occurs when the primary

dentition is replaced by succedaneous teeth. The alveolar bone

24

associated with the primary tooth is completely resorbed together with

the roots of the tooth while new alveolar bone is formed to support the

newly erupted tooth. Significant remodeling of the alveolar process also

occurs as part of this process. The ability of the alveolar bone to remodel

rapidly also facilitates positional adaptation of teeth in response to

functional forces and in the physiological drift of teeth that occurs with

the development of jaw bones. From a clinical perspective, the rapid

remodeling of the alveolar bone facilitates movement of teeth within the

jaw bone by the application of orthodontic forces. However, the

application of force on bone tissues can also influence the remodeling

rate. Formation of alveolar bone is a prerequisite for the regeneration of

tissues lost through periodontal disease and for osseointegration of

implants used in restorative dentistry. Bone remodeling involves the co-

ordination of activities of cells from two distinct lineages, the osteoblasts

and the osteoclasts, which form and resorb the mineralized connective

tissues of bone, respectively.

Specific factors are believed to regulate each step in the

remodeling process and to integrate the development of osteoblast and

osteoclasts and their activities as well as modulate control that is exerted

through the endocrine system. The associations between bone formation

and remodeling and inflammatory response systems are further

emphasized by the recent identification of ‘‘master genes’’ involved in

the generation of osteoblasts and osteoclasts that belong to families of

transcription factors with prominent roles in the development of immune

responses. The regulated remodeling of alveolar bone is anticipated to

follow the general principles of bone formation and resorption described

below.

BONE FORMATION: 11

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

to maintain bone mass, involves the proliferation and differentiation of

25

stromal stem cells along an osteogenic pathway that leads to the

formation of osteoblasts. The process of cellular differentiation is

controlled by a cascade of events that involves a combination of genetic

programming and gene regulation by various hormones, cytokines and

growth factors.

The alkaline phosphatase and collagen I expression are

characteristic of the osteogenic lineage and their synthesis continues to

increase while the expression of type II collagen is lost and type III

progressively diminishes. The formation of a collagen substratum

appears to trigger the differentiation of pre-osteoblastic cells into

osteoblasts through interactions with the α2β1 receptor.

Expression of developmentally regulated genes and transcription

factors that regulate the expression of differentiation-associated genes

appear to be the most useful for defining the early stages of

osteodifferentiation. Many of the developmental genes, including

homeobox genes such as hoxa-2, hoxd-13 and hoxa-13, dlx5, msx-1 and

msx-2, are common to various forms of organogenesis. Similarly,

different classes of transcription factors involved in osteogenesis have

broad targets of regulation. However, recent studies have identified a

runt domain-related gene core binding factor a1/PEBP2α A/AML-3 as a

bone-restricted transcription factor that has been described as a

potential ‘‘master gene’’ for osteogenic differentiation.

Expression in developing odontoblasts, cementoblasts and

ameloblasts indicate that core binding factor a1 may also have a

functional role in the differentiation of all mineralizing tissue cells.

Deletion of the core binding factor a1 gene results in the complete

absence of ossified tissues and heterozygous mutations of the gene in

humans.

Regulation of bone formation: 11

26

Bone formation is regulated by factors that affect either the

production of osteoblastic cells or their activity. Many of these factors

also affect bone resorption either directly or indirectly. Thus, parathyroid

hormone, which regulates serum calcium levels by stimulating bone

resorption, can also have anabolic effects in vivo that appear to be

mediated through transforming growth factor-b and insulin-like growth

factor-I.

The seco-steroid vitamin D3 also has paradoxical effects in bone

remodeling. While stimulating bone resorption, it is essential for normal

bone growth and mineralization and has a primary function in calcium

absorption from the intestine. Vitamin D3 also strongly stimulates the

synthesis of osteocalcin and osteopontin by osteoblastic cells while

suppressing collagen production. In contrast, insulin and growth hormone

have anabolic effects on bone. Insulin targets osteoblasts directly,

stimulating bone matrix formation and mineralization, and indirectly

affects bone formation through a stimulation of insulin-like growth factor-

I produced in the liver. Growth hormone is required for attaining normal

bone mass, the anabolic effects apparently being mediated through the

local production of insulin-like growth factor-I. As with other hormones,

the effects of glucocorticoids are complicated by secondary effects

initiated in response to the primary effects. Thus, the ability of

glucocorticoids to promote differentiation of osteoblastic cells and to

stimulate bone matrix formation has been well established in vitro.

However, prolonged treatment with glucocorticoids in vivo results in

bone loss, which can be attributed to increased parathyroid hormone

production in response to the inhibitory effects of glucocorticoids on

calcium absorption and perhaps also to the depletion of osteogenic

precursor cells. Thyroid hormone and the sex steroids are also necessary

for normal growth and development of bones, but they appear to act

indirectly and the mechanisms are poorly defined.

27

Of the many growth and differentiation factors that influence bone

formation, the bone morphogenetic proteins have the most profound

effect on bone formation. These cytokines, which belong to the

transforming growth factor-b family, can induce chondrogenic and

osteogenic differentiation in undifferentiated mesenchymal cells, their

prolonged presence being required to generate endochondral bone in

ectopic sites. However, bone morphogenetic proteins do not have

marked effects on bone matrix formation. In contrast, transforming

growth factor-b can act as a potent inhibitor of osteogenic induction by

bone morphogenetic protein while strongly stimulating expression of

matrix proteins by osteoblastic cells. The anabolic effects of transforming

growth factor-b are augmented by a suppression of matrix degradative

activity through the inhibition of matrix metalloproteinase expression and

the enhanced expression of tissue inhibitor of matrix metalloproteinases.

The acidic, and particularly the basic, fibroblast growth factors,

which are characteristically expressed early in skeletal development,

exert their effects on bone formation primarily through increased

proliferation of osteoprogenitors and promotion of osteogenic

differentiation. Platelet-derived growth factor has similar effects to

fibroblast growth factors in promoting osteogenesis, but also influences

the expression of other cytokines as part of a more generalized role that

platelet-derived growth factor has in wound and fracture healing.

BONE RESORPTION: 11

Resorption of mineralized tissues requires the recruitment of a

specialized cell, the osteoclast, which is produced by the

monocyte/macrophage lineage of hematopoietic cells that are derived

from bone marrow. Osteoclasts develop from a pluripotential

mononuclear precursor (colony forming unit–granulocyte/macrophage)

which is stimulated to proliferate and differentiate under the influence of

monocyte-macrophage colony-stimulating factor. A variety of soluble and

28

membrane bound factors play a critical role in regulating osteoclast

formation, including growth factors, systemic hormones, and cells in the

marrow microenvironment, such as osteoblasts and marrow stromal

cells. Cell-to-cell interactions are important in both the formation and

activity of the osteoclast.

Recent molecular biological studies have identified transcription

factors, such as c-Fos and PU.1 that are required for osteoclast

differentiation. The identification of a novel receptor, termed

osteoprotegerin (OPG), has recently uncovered a key regulatory

mechanism in osteoclast differentiation and activity. The osteoprotegerin

ligand (OPGL), which has been identified as the putative osteoclast

differentiation factor that is expressed on the surface of stromal/bone

cells, has been shown to signal osteoclast differentiation through a tumor

necrosis factor- α –related receptor known as either tumor necrosis factor

receptor (TNFR), osteoclast differentiation and activation receptor

(ODAR) or receptor activator of nuclear factor kB (RANK).

Typically, formation of osteoclasts involves fusion of monocytic

precursors which occurs at the site of bone resorption. Demineralization

of the bone matrix, which is a prerequisite for matrix degradation, is

achieved through the acidification of a protected environment beneath

the ruffled border. A specific type of electrogenic adenosine

triphosphatase pumps protons generated by type II carbonic anhydrase

activity, into the resorption bay, which also receives lysosomal enzymes

and thereby acts as a functional secondary lysosome. Following the

dissolution of the mineral phase in the acidic environment, the lysosomal

enzymes can degrade matrix macromolecules, including collagen, in a

manner similar to that described for the phagocytic degradation of

matrix. Matrix metalloproteinases, which can be activated under the

acidic conditions, have also been observed in resorption lacunae and

could, contribute to matrix degradation. Following resorption, osteoclasts

may undergo apoptosis, which provides a mechanism for limiting

29

resorptive activity. While factors such as transforming growth factor-b,

estrogen and bis-phosphonates promote apoptosis, parathyroid hormone

and interleukin-1 act as suppressors, prolonging osteoclast activity. Thus,

the formation, activity and survival of osteoclasts are all potential targets

for regulation of osteoclast-mediated bone-resorptive activity.

Tencate, described the sequence of events in the resorptive process is

as follows:1, 2, 4

1) Attacment of osteoclats to the mineralized surface of bone.

2) Creation of a sealed acidic environment through the action of the

proton pump, which demineralizes bone and exposes the organic

matrix.

3) Degradation of exposed organic matrix to its constituent amino

acids by the action of released enzymes, such as acid phosphatase

and cathepsin B.

4) Sequestering of mineral ions and amino acids within the osteoclast.

Regulation of osteoclast activity: 11

The primary factors that stimulate bone resorption through

osteoclasts include parathyroid hormone, vitamin D3, interleukin-1,

interleukin-6, tumor necrosis factor α, and transforming growth factor- α,

whereas calcitonin, transforming growth factor-β, estrogen and

interferon-γ inhibit osteoclastic bone resorption. Parathyroid hormone,

parathyroid hormone–related protein, vitamin D3, transforming growth

factor-a and pro-inflammatory cytokines, such as interleukin- 1 and

tumor necrosis factor α, all promote differentiation of osteoclasts.

Arachidonic metabolites are also important modulators of bone cell

function. In particular, prostaglandins of the E-series can act as powerful

mediators of bone resorption and can also influence bone formation.

Estrogen is believed to suppress the production of bone-resorbing

cytokines, including interleukin-1 and interleukin-6. In addition to their

effects on osteoclast development, interleukin-1, tumor necrosis factor-α

30

and the functionally related, lymphotoxin, also stimulate osteoclastic

activity.

BLOOD SUPPLY: 15

It receives from inferior and superior alveolar arteries for mandible

and maxilla, respectively and reaches PDL from three sources; apical

vessels, penetrating vessels from the alveolar bone and anastomosing

vessels from gingiva.

VENOUS DRAINAGE:

It accompanies arterial supply. Venules receive blood via abundant

capillary network, there are also AV anastomoses that bypass the

capillaries. More frequently in apical and interradicular region and their

significance is unknown.

LYMPHATICS:

Those draining region just beneath the JE pass into PDL and

accompany vlood vessels into periapical region. From there they pass

through alveolar boneto inferior dental canal in mandible or infraorbital

canal in maxilla and then to submaxillary lymphnodes.

INTERNAL RECONSTRUCTION OF BONE: 5

The bone in the alveolar process is identical to bone elsewhere in

the body and is in a constant state of flux. During the growth of maxilla

and the mandible, bone deposited on the outer surfaces of the cortical

plates. In the mandible, with its thick, compact cortical plates, bone is

deposited in the shape of basic or circumferential lamellae. When the

lamellae reach certain thickness, they are replaced from inside by

haversian bone. This reconstruction is correlated to the functional and

nutritional demands of the bone. In the haversian canals, closest to the

surface osteoclasts differentiate and resorb the haversian lamellae and

the part of circumferential lamellae. The resorbed bone is replaced by

proliferating loose connective tissue. This area of resorption is sometimes

called the cutting cone or the resorption tunnel. After a time the

31

resorption ceases and the new bone is opposed onto the old. The

scalloped outline of houship’s lacunae thet turn their convexity toward

the old bone remains visible as a darkly stained cementing line, a

reversal line. This is in contrast to those cementing lines that

correspond to a rest period in an otherwise continous process of bone

apposition. They are called resting lines. Resting and reversal lines are

found between layers of bone of varying age.

Moreover, periods of resorption alternate with periods of rest and

repair. It is during these periods of repair that the bundle bone is formed,

and detached periodontal fibers are again secured. Islands of bundle

bone are separated from the lamellated bone by reversal lines that turn

their convexities toward the lamellated bone.

During these changes, compact bone may be replaced by spongy

bone or spongy bone may change into compact bone. This type of

internal reconstruction of bone can be observed in physiologic mesial

drift or in orthodontic mesial or distal movement of teeth.

BONE RESORPTION-FORMATION; COUPLING : 3

There is clearly a close relationship between bone deposition and bone resorption.

During the growing phase of a child, the amount of deposition exceeds that of resorption,

giving an increase in bone mass. During the adult phase, the amount of bone deposition is

equivalent to that of bone resorption and bone mass is more or less constant. In old age,

the amount of bone deposition is generally less than that of bone resorption and there is an

overall decrease in bone mass. In postmenopausal women particularly this loss may be

sufficient to lead to the clinical condition of osteoporosis.

Many of the factors that result in bone resorption are known to have no direct

effect on osteoclasts. but act indirectly through osteoblasts. Most of the receptors to

bioactive molecules that cause bone resorption are present on osteoblasts [e.g. receptors to

PTH and PTHrP). Indeed, the main receptor found in osteoclasts is related to calcitonin.

There are several mechanisms whereby osteoblasts might promote bone resorption:

32

By the local release of substances such as cytokines and growth factors (e.g.

macrophage colony-stimulating factor, osteoprotegerin and interleukins),

osteoblasts could stimulate the production of osteoclasts,

By releasing enzymes (such as MMPs) to degrade the unmineralised osteoid layer

covering forming bone, osteoblasts could help expose mineralised matrix on which

osteoclasts could attach and commence resorption.

By bioactive molecules present within bone (e.g. cytokines, BMPs. TC.F-|3) that

could be activated as a result of osteoclastic bone resorption and subsequently have

an effect on remodelling.

Reversal lines mark the position where bone activity changes from resorption to

deposition. Such lines are darkly stained and irregular in outline, being composed of a

series of concavities that were once the sites of the resorptive Howship's lacunae. They

may be seen lo contain the enzyme acid phosphatase.

On account of collagen degradation occurring during bone resorption, analysis of its

special cross links retained in urine (pyridinoline fragments) is used clinically as a

marker to indicate rates of bone remodelling.

There are a considerable number of factors that can influence bone remodelling. The

complexity of the topic is illustrated by the fact that certain reagents can produce opposite

effects, depending on concentration.

THE IMPLANT - BONE INTERFACE : 1, 2, 6

The relationship between endosseous implants and bone consistas of one of the

two mechanism:

Osseointegration: when the bone is in intimate but not not ultrastructural cntact

with implant or,

Fibrosseous integration, in which soft tissues such as fibers and/or cells, are

interposed between the two surfaces.

Osseointegration concept proposed by Branemark et al and called functional ankylosis

by Schroeder states that there is an absence of connective tissue or any non-bony tissue

in the interface between the implant and the bone.

33

Implant insertion into a hole will lead to bone apposition on to the implant

surface if the latter is nontoxic. A coupling occurs between bone resorption and the bone

formation; latter can occur only if an intercellular matrix is produced that favors apatite

crystal integration in the collagen network. The critical temperature for bone cells is as

low as 47o c at an exposure time of 1 minute. This corresponds to denaturing temperature

of alkaline phosphatase, the main bone cell enzyme.

First, woven bone is quickly formed in the gap between the implant and bone.

Second, after several months, this is progressively replaced by lamellar bone under the

load stimulation. Third, a steady state is reached after about 1 ½ years. Often for oral

implants, occlusal load is allowed as soon as 2-3 months, while mostly woven bone is

present.

Bone has a limited elasticity, with an elasticity modulus of about 10 GPa/m 2 for

the cortex and 1-5 GPa/m2 for cancellous bone. Assuming an implant that is 4mm

diameter and 10mm long, the minimal width of the jaw bone needs to be 6-7mm, and the

minimal height should be 10mm (12mm for posterior mandible, where additional margin

of safety is required over the mandibular nerve). This dimension is desired to maintain at

least 1.0 to 1.5mm of bone around all surfaces of the implant after preparation and

placement.

ETIOLOGY OF BONE LOSS

EXTENSION OF INFLAMMATION: 1, 2

34

The extension of inflammation to the supporting structures 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 gingiva, probably the width of the attached gingiva, and the reactive

fibrogenesis and osteogenesis that occur peripheral to the inflammatory lesion. A fibrin

fibrinolytic system has been mentioned as “walling off” the advancing lesion. The pathway

of the spread of inflammation is critical because it affects the pattern of bone destruction in

periodontal disease.

Pathway of Inflammation: 1, 2

Gingival inflammation extends along the collagen and fiber bundles and follows the

course of the blood vessels through the loosely arranged tissues around them into the

alveolar bone. Although the inflammatory infiltrate is concentrated in the marginal

periodontium, the reaction is a much more diffuse one, often reaching the bone and eliciting

a response before there is evidence of crestal resorption or loss of attachment. In the upper

molar region, inflammation can extent to the maxillary sinus, resulting in thickening of the

sinus mucosa.

Interproximally, inflammation spreads in the loose connective tissue around the

blood vessels, through the transeptal fibers, and then into the bone through vessel channels

those perforate the crest of the interdental septum. The site at which the inflammation enters

the bone depends on the location of the vessel channels. It may enter the interdental septum

at the center of the crest, toward the side of the crest, or at the angle of the septum, and it

may enter the bone through more than one channel. After reaching the narrow spaces, the

inflammation may return from the bone into the periodontal ligament. Less frequently, the

inflammation spreads from the gingival directly into the periodontal ligament and from there

into the interdental septum.

Facially and lingually, inflammation from the gingiva spreads along the periosteal

surface of the bone and penetrates into the marrow spaces through vessel channels in the

outer cortex. Along its course from the gingiva to the bone, the inflammation destroys the

gingiva and transseptal fibers, reducing them to disorganized granular fragments

interspersed among the inflammatory cells and edema. However, there is a continuous

tendency to recreate transseptal fibers across the crest of the interdental septum farther along

35

the root as the bone destruction progresses. As a result, transseptal fibers are present, even

in cases of extreme periodontal bone loss.

The dense transseptal fibers are of clinical importance when surgical procedures are

used to eradicate periodontal pockets. They form a firm covering over the bone, which is

encountered after the superficial granulation tissue is removed.

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. Mutlinuclear osteoclasts and mononuclear phagocytes

are increased in number, and the bone surfaces are lined with cove-like resorption 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. Normally fatty bone marrow is partially or

totally replaced by a fibrous type of marrow in the vicinity of the resorption.

Bone destruction in periodontal disease is not a process of bone necrosis. It involves

the activity of living cells along viable bone. When tissue necrosis and pus are present in

periodontal disease, they occur in the soft tissue wall of periodontal pockets, not along the

resorbing margin of the underlying bone.

The amount of inflammatory infiltrate correlates with the degree of bone loss but not

with the number of osteoclasts. However, the distance from the apical border of the

inflammatory infiltrate to the alveolar bone crest correlates with both the number of

osteoclasts on the alveolar crest and the total number of osteoclasts.

Radius of Action: 1, 2

Garant and Cho(1979) suggested that locally produced bone resorption factors may

have to be present in the proximity of the bone surface to be able to exert their action.

Locally produced bone resorption factors may have to be present in the proximity of the

bone surface to be able to exert their action. Page and Schroeder (1982) on the basis of

36

Waerhaug’s measurements made on human autopsy specimens, postulated that there is a

range of effectiveness of about 1.5 to 2.5 mm within which bacterial plaque can induce loss

of bone. Beyond 2.5 mm there is no effect; interproximal angular defects can appear only in

spaces wider than 2.5 mm because narrower spaces would be destroyed entirely. Tal (1984)

corroborated this with measurements in human patients.

Large defects far exceeding 2.5 mm from the tooth surface may be caused by the

presence of bacteria in the tissues.

Rate of Bone Loss: 1, 2

Loe and associates(1986) conducted a study on Srilankan tea labourer with no oral

hygiene and no dental care, they found the rate of bone loss to average about 0.2 mm a year

for facial surfaces and about 0.3 mm a year for proximal surfaces when periodontal disease

was allowed to progress untreated. However, the rate of bone loss may vary, depending on

the type of disease present. Loe and coworkers (1978) identified three subgroups of patients

with periodontal disease based on interproximal loss of attachment and tooth mortality.

1. Approximately 8% of persons had rapid progression of periodontal disease,

characterized by a yearly loss of attachment 0.1 to 1 mm.

2. Approximately 81% of individuals had moderately progressive periodontal disease,

with a yearly loss of attachment of 0.05 to 0.5 mm.

3. The remaining 11% of persons had minimal or no progression of destructive disease

(0.05 to 0.9 mm yearly).

Mechanisms of Bone Destruction: 1, 2

Many investigations have been conducted and many explanations considered, but the

mechanism or mechanisms by which inflammation and/or plaque derived products destroy

bone in inflammatory periodontal disease have not yet been determined.

There are several possible pathways by which products in plaque absorbed by

periodontal tissues could cause alveolar bone loss as described by Hausman E (1974)

1. Absorbable products from plaque could stimulate bone progenitor cells in the

periodontium to differentiate into osteoclasts, which resorb alveolar bone.

37

2. Absorbable products from plaque as, for example, complexing agents and hydrolytic

enzymes could destroy alveolar bone through non-cellular mechanisms by dissolving

bone mineral and hydrolyzing the organic matrix.

3. Absorbable products from plaque could stimulate cells within the gingival to release

mediators, which in turn could trigger bone progenitor cells to differentiate into bone

resorbing osteoclasts.

4. Gingival cells in response to plaque products could release agents which by

themselves have no effect on bone, but could potentiate as co-factors for other bone

resorptive agents.

5. Gingival cells could release agents, which destroy bone by direct chemical action

without osteoclasts.

Periods of Destruction: 1, 2

Periodontal destruction occurs in an episodic, intermittent fashion, with periods of

inactivity or quiescence. The destructive periods result in loss of collagen and alveolar bone

with deepening of the periodontal pocket. The reasons for the onset of destructive periods

have not been totally elucidated, although the following theories have been offered.

1. Bursts of destructive activity are associated with subgingival ulceration and an acute

inflammatory reaction, resulting in rapid loss of alveolar bone.

2. Bursts of destructive activity coincide with the conversion of a predominantly T-

lymphocyte lesion to one with predominance of B lymphocyte – plasma cell

infiltrate.

3. Periods of exacerbation are associated with an increase of the loose, unattached,

motile, gram negative, anaerobic pocket flora, and periods of remission coincide

with the formation of a dense, unattached, non-motile, gram positive flora with a

tendency to mineralize.

4. Tissue invasion by one or several bacterial species is followed by an advanced local

host defense that controls the attack.

Table : Bone resorbing factors that act via the osteoblasts

Agent Source

Parathyroid hormone Parathyroid

Vitamin D3 Liver via kidney from skin

38

Interleukin – 1 Monocytes (major source)

Many other cell types including

keratinocytes, fibroblasts and tumour

cells

Tumour necrosis factor Monocytes

Factors Inhibiting bone resorption

Agent Function / Use

Calcitonin Acts directly on osteoclasts

Glucocorticoids Inhibits eicosonoids synthesis

Biphosphonates Inhibits osteoclastic bone resorption probably

by making the mineralized surface

inaccessible to the cell by binding to the

hydroxyl apatite crystals.

Indomethacin and

Aspirin

Inhibits prostaglandin synthesis

Interferon Inhibits both proliferation and differentiation

of osteoclast progenitors

TGF- Inhibits both proliferation and differentiation

of osteoclast progenitors

Interleukin-1 receptor

antagonist (IL-1ra)

Binds to IL-1 receptors effective against TNF

as well.

39

FACTORS CAUSING BONE RESORPTION

ctors Responsible for Bone Resorption :

Factors Responsible for Bone Resorption:

Hormones Regulating Bone Resorption: 1, 2, 3, 4

Parathyroid Hormone:

Systemic Factors Parathyroid hormone

Parathyroid related peptide

Vitamin D3

(1, 25, dihydrocholecalciferol)

Thyroid hormone

Local factors Prostanoids

Lipooxygenase metabolites

Cytokines : Interleukin-1

Interleukin – 1

Tumour necrosis factor alpha

(Cachectin)

Tumour necrosis factor –

(Lymphotoxin)

Interleukins

Growth Factors Epidermal growth factor

Transforming growth factor alpha

Transforming growth factor beta

Platelet derived growth factor

Bacterial factors Lipopolysaccharides

Muramyl dipeptides

Capsular material

Peptidoglycans

Lipoteichoic acids

40

It has been known for 70 years that parathyroid hormone (PTH) affects bone-cell

function, may alter bone remodeling, and cause bone loss. It is now apparent that PTH acts

on both bone-resorbing cells and bone-forming cells. The net effect of the hormone depends

on whether it is administered continuously or intermittently. When administered

continuously, it increases osteoclastic bone resorption and suppresses bone formation.

However, when administered in low doses intermittently, its major effect is to stimulate

bone formation, a response that has been called the anabolic effect of PTH.

PTH stimulates osteoclasts to resorb bone. In organ cultures, PTH increases

osteoclast activity, with resultant degradation of bone matrix. PTH activates mature

osteoclasts to resorb bone, whereas other agents exert their effects by increasing the

formation of new osteoclasts.

It stimulates mature, multinucleated osteoclasts to form ruffled borders and resorb

bone. However, the precise molecular mechanism by which PTH exerts its effects on

these cells is still not known. The effect of PTH on osteoclast precursors is combined with

direct effects on the cell itself, with an indirect effect of regulating other cells to produce

local factors that influence the osteoclast precursor cells, such as regulating cells of the

granulocyte-macrophage type, to produce granulocyte-monocyte-colony-stimulating factor

(GM-CSF).

The effect of PTH on mature osteoclasts is also indirect because osteoclasts will not

resorb bone unless osteoblasts are present, suggesting that PTH may stimulate osteoclastic

bone resorption by interacting with cells in the osteoblast lineage.

The mechanisms used by cells of the osteoblast phenotype to communicate with

osteoclasts are still not known. It has been suggested that osteoblasts may prepare the bone

surface for osteoclastic bone resorption by producing proteolytic enzymes. However, this

theory is still questionable.

1,25-Dihydroxycholecalciferol (1, 25 (OH)2 D) :

41

The active metabolites of vitamin D3 have complex effects on calcium homeostasis

and bone regulation. 1,25(OH)2 D3 stimulates osteoclastic bone resorption in vitro and in

vivo.

It has a very slow onset of action, with a shallow dose-response curve. It increases

both osteoclast number and activity, with an increase in ruffled border size and clear-zone

volume. Mature osteoclasts do not have receptor for 1, 25 (OH)2 D3 which increases both

osteoclast number and activity, with an increase in ruffled border size and clear-zone

volume. Mature osteoclasts do not have receptors for 1, 25 (OH)2 D3. Thus, the effects of

this hormone on mature osteoclasts are most likely mediated indirectly through other cells.

The major effect of 1, 25 (OH)2 D3 on osteoclastic bone resorption may be to stimulate the

fusion of differentiation of committed osteoclast progenitors to form mature cells. Use of l,

25 (OH)2 D3 influences and modulates cytokine production by immune cells.

Calcitonin:

Calcitonin has been demonstrated to inhibit osteoclastic bone resorption. The effect

of calcitonin on osteoclasts is mediated through cyclic AMP. Calcitonin decreases osteoclast

activity.

The effects of calcitonin on bone resorption are short-lived, however, osteoclasts

eventually lose their responsiveness to calcitonin after continuous exposure, a phenomenon

referred to as escape.

One explanation for this phenomenon may involve a decrease in receptor number

after long periods of exposure. Another possible explanation is that, a second population of

osteoclasts, which is not responsive to calcitonin emerges.

It is believed that it inhibits bone resorption transiently when bone turnover is not

needed for calcium homeostasis.

Estrogens:

Estrogen clearly inhibits the increase in bone resorption associated with

menopause. Following estrogen withdrawal, an initial increase in bone turnover can be

observed. Later, bone resorption occurs faster than bone formation, with a net effect of

bone loss.

42

The effects of estrogen are mediated by a combination of direct and indirect effects.

The direct effect is mediated by specific receptors found in cells of the osteoblast and

osteoclast lineages. The effects of estrogen on osteoclasts are in part direct and in part

mediated through osteoblasts. Some indirect effects of estrogen result from its enhancing the

expression of growth factors like insulin like growth factor (IGF-1) and transforming growth

factor- (TGF-), and of cytokines, others from its inhibition of prostaglandin production

by bone cells.

Thus, the major effect of estrogen may be to inhibit bone resorption, but it may also

have the additional effect of stimulating bone formation.

Interleukin-1 (IL-1):

IL-1 is a powerful and potent bone-resorbing cytokine. IT has been found that IL-1α

and IL-1β are equally potent in stimulating bone resorption and probably exert their effects

on bone-resorbing cells in several ways. They stimulate proliferation of precursor cells, but

also probably act indirectly on mature cells to stimulate bone resorption. The effects of IL-1

probably occur by two mechanisms. One mechanism is the stimulation of the production

and release of PGE2, which in turn stimulates bone resorption. The second mechanism

involves the direct action of IL-1 on the osteoclast, which is independent of prostaglandin

synthesis, through an 80,000 Dalton receptor.

IL-1 has complex and apparently paradoxical effects on bone formation. The

continued presence of IL-1 inhibits bone formation in vivo and in vitro. IL-1 appears to

stimulate proliferation of cells at early stages of differentiation in the osteoblast lineage, but

inhibits functions characteristic of the fully differentiated state. In contrast, transient

exposure to IL-1 has been shown to stimulate bone formation by osteoblasts.

Interleukin-6 (IL-6):

In some experimental models, IL-6 appears to have no effect son bone resorption.

However, in others, it stimulates bone resorption. IL-6 is also responsible for the formation

of cells with an osteoclastic phenotype. Bone cells also have the ability to produce IL_6,

which seems to be greater when the stimulus is by another cytokine.

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Tumor Necrosis Factor (TNF) and Lymphotoxin:

Lymphotoxin and TNF are two closely related cytokines that have equivalent effect

son bone cells. They are both multifunctional cytokines produced by activated

lymphocytes, and they share the same receptor. Their major effect on bone is to stimulate

osteoclastic bone resorption. It has been suggested that part of the effect of TNF is mediated

by PGE2, as well as by IL-6. TNF also affects cells with osteoblast phenotypes and inhibits

differentiated function and stimulates cell proliferation. Production of TNF in some tumors,

like squamous cell carcinomas, may be responsible for paraneoplastic syndromes.

Gamma Interferon (IFN-γ)

Gamma interferon is a multifunctional cytokine, which in most biological systems

ahs effects similar to TNF or IL-1. However, it has an effect on bone resorption that is

opposite that of IL-1 and TNF. Gamma interferon is more effective in inhibiting IL-1 or

TNF induced bone resorption than systemic hormones like PTH or 1,25-(OH)2D3. Further,

it has been found in long term marrow cell cultures that gamma interferon inhibits the

formation of cells with the osteoclast phenotype.

Colony Stimulating Factors (CSFs) :

CSF has the ability to stimulate differentiation of osteoclast precursors into mature

osteoclasts. Recently, it was found that there are a number of human and animal tumors

associated with granulocytosis in which increased production of CSFs are involved. In

many of these tumors, hypercalcemia is associated with increased bone resorption.

It is possible that CSFs mediate their effects on osteoclast formation indirectly. For

example, early studies showed that CSF stimulates IL-1 production, which stimulates

prostaglandin synthesis.

Prostaglandins and Other Arachidonic-Acid Metabolites:

A number of arachidonic acid metabolites act as modulators of bone cell function.

These factors are produced by immune, marrow, and bone cells. Prostaglandins of the E

series were some of the first described and best tested stimulators of osteoclastic bone

resorption. PGEs are slow acting, but powerful, mediators of bone resorption and affect

both active mature osteoclasts, as well as differentiated osteoclast precursors. The effect of

44

PGE is local and has been shown to mediate the effects of other factors like epidermal

growth factor (EGF) and transforming growth factor –β (TGF-β).

PGE is produced by osteoblasts and has effects not just on bone resorption, but on bone

formation as well. In vitro it has been found that high doses of PGE are inhibitory, while

low doses stimulate bone formation. However, in vivo it appears that the effect of PGE is

clearly associated with an increase in periosteal bone formation. There have also been

recent reports that other arachidonic acid metabolites stimulate bone resorption.

Arachidonic acid can be metabolized by an alternative enzyme system, 5-lipoxygenase,

which also produces metabolites capable of stimulating bone resorption.

BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE

Nomenclature of Deformities of the alveolar process: 1, 2, 14

The proposed system of nomenclature for bony deformities caused by non-uniform

loss of bone is based on the following basic terms:

Osseous Craters:

Osseous craters are concavities in the crest of the interdental bone confined within the

facial and lingual walls. Craters have been found to be made up about one third of all

defects and about two thirds of all mandibular defects. They are twice as common in

posterior segment as in anterior segments. The following reasons for the high frequency of

interdental craters have been suggested.

The interdental area collects plaque and is difficult to clean.

The normal flat or even concave facio-lingual shape of the interdental septum in

lower molars may favour crater formation.

Vascular patterns from the gingiva to the center of the crest may provide a pathway

for inflammation.

Hemisepta:

The remaining half of an interdental septum forming the proximal wall of a one-

walled infrabony defect.

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Reversed Architecture:

These defects are produced by loss of interdental bone, including the facial and/or

lingual plates, without concomitant loss of radicular bone, thereby reversing the normal

architecture. Such defects are more common in the maxilla.

Ledges:

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

Buttressing Bone formation (Lipping):

Bone formation sometimes occurs in an attempt to buttress bony trabeculae

weakened by resorption. When it occurs within the jaw, it is termed as central buttressing

bone formation. When it occurs on the external surface, it is reformed to as peripheral

buttressing bone formation. The latter may cause bulging of the bone contour, termed

lipping, which sometimes accompanies the production of osseous craters and angular

defects.

Bulbous Bone Contours:

These are bony enlargements caused by exostoses, adaptation to function, or

buttressing bone formation.

Exostoses:

Are outgrowths of bone of varied size and shape. They can occur as small nodules,

large nodules, sharp ridges, spike-like projections, or any combination of these.

Fenestrations and Dehiscence:

Isolated areas in which the root is denuded of bone and the root surface is covered

only by periosteum and overlying gingiva are termed fenestrations. In these instances the

marginal bone is intact. When the denuded areas extend through the marginal bone, the

defect is called as dehiscence. They occur more often on the facial bone than on the lingual,

are more common on anterior teeth than on posterior teeth, and are frequently bilateral.

Prominent root contours, malposition, and labial protrusion of the root combined with a thin

46

bony plate are predisposing factors. Fenestration and undehiscence are important, because

they may complicate the outcome of periodontal surgery.

Furcation Involvement:

The term furcation involvement refers to the invasion of the bifurcation and

trifurcation of multirooted teeth by periodontal disease. The mandibular first molars are the

most common sites, and the maxillary involvements increase with age.

The denuded furcation may be visible clinically or covered by the walls of the

pocket. The extent of involvement is determined by exploration with a blunt probe, along

with a simultaneous blast of warm air to facilitate visualization.

Furcation involvement has been classified as Grade I, II, III and IV according to the

amount of tissue destruction29.

Grade I is incipient bone loss

Grade II is partial boneloss (cul-de-sac)

Grade III is total bone with through-and-through opening of the furcation.

Grade IV is similar to grade III, but with gingival recession exposing the furcation to

view.

The destructive pattern in a furcation involvement varies in different cases and with

the degree of involvement. Bone loss around each individual root may be horizontal or

angular, and very frequently a crater develops in the interradicular area.

Marginal Defects:

Thickened Margin:

A linear enlargement of facial or lingual marginal alveolar plate, instead of a thin,

tapering, or slightly rounded bony margin.

Irregular Bone Margin:

Where there are abrupt irregularities in the scalloped level of marginal bone and interdental

septa.

47

Marginal Gutter:

A shallow linear defect between marginal bone of the radical cortical plate or

interdental crest, extending the length of one or more root surfaces.

Horizontal Bone Loss:

This is the most common pattern of bon eloss in periodontal disease. The bone is

reduced in height, but the bone margin remains roughly perpendicular to the tooth surface.

The interdental septa and facial and lingual plates are affected, but not necessarily to an

equal degree around the same tooth.

Vertical Bone Loss or Angular Defects:

Vertical or angular defects are those that occur in an oblique direction, leaving a

hollowed out thorough 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; such pocket always have an underlying angular defect. Angular defects

are classified as follows :

Three wall bony defects are bordered by one tooth surface and three osseous

surfaces.

Two walls bony defects (interdental craters) are bordered by two tooth surfaces and

two osseous surfaces (one facial and one oral).

One wall bony defects are bordered by two tooth surfaces, and osseous surface

(facial or oral) and soft tissue.

The one wall vertical defect is also called hemiseptum vertical defects occurring

interdentally can generally be seen on the radiograph. Angular defects can also appear on

facial and lingual or palatal surfaces, but these defects are not seen on radiographs. Surgical

exposures are the only sure way to determine the presence and configuration of vertical

osseous defects.

48

Classification of Bone Deformities:

Goldman and Cohen (1958) 12

1.Three osseous walls

A. Proximal, buccal and lingual walls

B. Buccal, mesial and distal walls

C. Lingual, mesial and distal walls

2.Two osseous walls

D. Buccal and lingual (crater) walls

E. Buccal and proximal walls

F. Lingual and proximal walls

3.One osseous wall

G. Proximal wall

H. Buccal wall

I. Lingual wall

2. Combination

A. Three walls plus two walls

B. Three walls plus two walls plus one wall

Classification by Clarke M.A. (1971)13

A. Vestibular, lingual or palatal structures or defects

1. Normal anatomic structures

a) External oblique ridge

b) Retromolar triangle

c) Mylohyoid ridge

d) Zygomatic process

2. Exostoses and Tori

a) Mandibular lingual tori

b) Buccal and posterior palatal exostoses

3. Dehiscence

4. Fenestrations

5. Reverse Osseous architecture

B. Vertical Defects

1. Three walls

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2. Two walls

3. One wall

4. Combination with a different number of walls at the various levels of the

defects.

C. Furcation Defects

1. Class I or incipient

2. Class II or partial

3. Class III or through and through

BONE LOSS IN PERIODONTITIS: 1, 2

Periodontitis the most common type of periodontal disease. It results from extension

of the inflammatory process initiated in the gingiva to the supporting structures of the tooth.

Chronic Periodontitis:

Clinical Features:

The characteristic findings in slowly progressive periodontitis are gingival

inflammation, which results from the accumulation of plaque, and loss of periodontal

attachment and alveolar bone, which results in formation of a pocket.

Pocket depths are variable, and both horizontal and angular bone loss can be found.

Tooth mobility often appears in advanced cases when bone loss has been considerable.

Therefore, can be diagnosed clinically by the detection of chronic inflammatory

changes in the marginal gingiva and the presence of periodontal pockets; it is diagnosed

radiographically by evidence of bone loss.

When trauma from occlusion coexists, a higher incidence of infrabony pockets,

angular bone loss, widening of the periodontal ligament, and earlier and more severe tooth

mobility are found.

Types:

Mild periodontitis is usually characterized by probing attachment loss of 2 to 4 mm,

minimal furcation invasions, and little tooth mobility. Radiographic evidence of bone loss is

minimal (usually less than 20% of the total attachment). This stage of involvement can be

localized to several teeth or generalized to many areas throughout the mouth.

50

Patients with moderate periodontitis exhibit 4 to 7 mm of probing attachment loss,

early to moderate furcation invasions, and slight to moderate tooth mobility.

Radiographically evident bone loss is usually horizontal and may consist of upto 40% of the

total possible periodontal attachment on the tooth.

Patients with severe periodontitis have a probing attachment loss of 7 mm or more

with significant furcation invasions, often through and through. Radiographic bone loss

exceeds 40%, and angular bony defects are seen. Purulent exudates can be present, along

with bleeding on probing.

AGGRESSIVE PERIODONTITIS:

Localized:

Previously known as localized juvenile periodontitis, it affects both males and

females and is seen most frequently in the period between puberty and 20 years of age.

Clinical Findings:

Clinically characterized by localized first molar / incisor presentation with

interproximal attachment loss on atleast two permanent teeth, one of which is a first molar,

and involving no more than two teeth other than first molars and incisors. The most striking

feature of early juvenile periodontitis the lack of clinical inflammation, despite the presence

of deep periodontal pockets.

Clinically, there is a small amount of plaque, which forms a thin film on the tooth

and rarely mineralizes to become calculus. The most common initial symptoms are mobility

of the first molars and distolabial migration of the incisors. Bone loss is about 3-4 times

faster than in chronic periodontitis. The progression of bone loss and attachment loss maybe

self-arresting.

Radiographic Findings:

Vertical loss of alveolar bone around the first molar and incisors in otherwise healthy

teenagers is a diagnostic sign of classic juvenile periodontitis. Radiographic findings

include an “arc-shaped’ loss of alveolar bone extending from the distal surface of the second

premolar to the mesial surface of the second molar. There is evidence that the bone loss is

not the result of any development or congenital absence or defect. Alveolar bone in patients

51

in this age group develops normally with tooth eruption, and only subsequently does it

undergo resorptive changes.

Generalized:

Clinical Findings:

Clinically characterized by generalized interproximal attachment loss effecting

atleast three permanent teeth other than first molars and incisors.

Two types of gingival tissue responses can be found. One is severe, acutely

inflamed tissue, often proliferating, ulcerated, and fiery red. Bleeding may occur

spontaneously or with slight stimulation. Suppuration may be an important feature. This

tissue response is considered to occur in the destructive stage, in which attachment and bone

are actively lost. In other cases, the gingival tissues may appear pink, free of inflammation,

stippling may or may not be present. This tissue response coincides with the periods of

quiescence in which bone level remains stationary.

The age at onset of this disease ranges from the middle to late teens and to 30 years

old. By 30 to 35 years of age, patients will have progressed to advanced bone loss.

Radiographic Findings:

The radiographic picture can range from severe bone loss associated with minimal

number of teeth, to advanced bone loss affecting the majority of teeth.

Necrotizing Ulcerative Periodontitis:

This type of periodontitis occurs after repeated long-term episodes of acute

necrotizing ulcerative gingivitis. The inflammatory infiltrate in lesions of ANUG,

especially in long standing cases, can extend to the underlying bone, resulting in deep, crater

like osseous lesions, most often located in interdental areas. These cases are diagnosed as

NUP.

NUP is characterized by deep interdental osseous craters, but deep “conventional”

pockets are not found. Lesions of NUP can lead to advanced bone loss, tooth mobility and

tooth loss.

52

TRAUMA FROM OCCLUSION:

When occlusal forces exceed the adaptive capacity of the tissue, tissue injury results.

The resultant injury is termed trauma from occlusion.

Thus trauma from occlusion refers to the tissue injury, not the occlusal force. An

occlusion that produces such injury is called a traumatic occlusion. Excessive occlusal

forces may also disrupt the function of the masticatory musculature and cause painful

spasms, injure the temporomandibular joints, or produce excessive tooth wear, but the term

trauma from occlusion is generally used in connection with injury in the periodontium.

Trauma from occlusion also tends to change the shape of the alveolar crest. The

change in shape consist of a widening of the marginal periodontal ligament space, a

narrowing of the interproximal alveolar bone, and a shelf-like thickening of the alveolar

margin. Therefore although trauma from occlusion does not alter the inflammatory process,

it changes the architecture of the area around the inflamed site. Thus in the absence of

inflammation, the response to trauma from occlusion is limited to adaptation to the

increased forces. However, in the presence of inflammation, the changes in the shape of the

alveolar crest may be conductive to angular bone loss, and existing pockets may become

intrabony.

Radiographic signs of trauma from occlusion may include the following :

1. Increased with of the periodontal space, often with thickening of the lamina dura

along the lateral aspect of the root, in the apical region and in bifurcation areas.

These changes do not necessarily indicate destructive changes because they may

result from thickening and strengthening of the periodontal ligament and alveolar

bone, constituting a favourable response to increased occlusal forces.

2. A “vertical” rather than “Horizontal” destruction of the interdental septum.

3. Radiolucence and condensation of the alveolar bone.

4. Root resorption

PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC

DISEASES: 1, 2

Papillon-lefevre syndrome:

This syndrome is characterized by hyperkeratotic skin lesions, severe destruction of

the periodontium, and in some cases, calcification of the dura.

53

Periodontal involvement consists of early inflammatory changes that lead to bone

loss and exfoliation of teeth. Primary teeth are lost by 5 or 6 years of age. The permanent

dentition then erupts normally, but within a few years the permanent teeth are lost owing to

destructive periodontal disease. By the age of 15 years, patients are usually edentulous

except for the third molars. These, too, are lost a few years after they erupt.

Hypophosphatasia:

This is a rare familial skeletal disease characterized by rickets, poor cranial bone

formation, craniostenosis, and premature loss of primary teeth, particularly the incisors.

Patients have a low level of serum alkaline phosphatase, and phosphoethanolamine is

present in serum and urine.

Teeth are lost with no clinical evidence of gingival inflammation and show reduced

cementum formation. In patients with minimal bone abnormalities, premature loss of

deciduous teeth may be the only symptom of hypophospahtasia. In adolescents, this disease

resembles localized aggressive periodontitis.

Diabetes Mellitus:

Is a complicated metabolic disease characterized by hypofunction of or lack of

function of the B cells of islets of Langerhans in pancreas, leading to high blood glucose

levels and excretion of sugar in the urine.

Periodontal disease in diabetics follow no consistent pattern. Very severe gingival

inflammation, deep periodontal pockets, rapid bone loss, and frequent periodontal abscesses

often occur in diabetic patients with poor oral hygiene. The distribution and severity of local

irritants affects the severity of periodontal disease in diabetics. Diabetes does not cause

gingivitis or periodontal pockets, but there are indications that it alters the response of the

periodontal tissues to local irritants, hastening bone loss and retarding post surgical healing

of the periodontal tissues.

HEMATOLOGICAL DISEASES: 1,2

LEUKEMIA:

The leukemia are “malignant neoplasias” of white blood cell precursors,

characterized by;

(1) Diffuse replacement of the bone marrow with proliferating leukemic cells

54

(2) Abnormal numbers and forms of immature white cells in the circulating blood, and

(3) Wide spread infiltrates in the liver, spleen, lymphnodes and other sites throughout the

body.

Types: a) acute b) subacute c) chronic

Leukemic cells can infiltrate the gingiva and, less frequently, the alveolar bone.

Monocytic leukemia is an extremely rare form of the disease leukemic gingival enlargement

consists of a basic infiltration of the gingival corium by leukemic cells that creates gingival

pockets where bacterial plaque accumulates, initiating a secondary inflammatory lesions that

contributes also to the enlargement of the gingiva.

The PDL and alveolar bone may also involved in acute and subacute leukemia. PDL

may be infiltrated with mature and immature leukocytes. The marrow of alveolar bone

exhibits a variety of changes, such as localized areas of necrosis, thrombosis of blood

vessels, infiltration with mature and immature leukocytes, occasional RBCs and

replacement of the fatty marrow by fibrous tissue.

ANEMIA:

Anemia is a deficiency in the quantity and quality of the blood, as manifested by a

reduction in the number of erythrocytes and in the amount of hemoglobulin.

Types:

1) macrocytic hyperchromic (pernicious) anemia

2) microcytic hypochromic ( iron deficiency) anemia

3) sickle cell anemia

4) normocytic normochromic ( hemolytic or aplastic anemia )

Sickle cell anemia is a hereditary form of chronic hemolytic anemia. Oral changes include

generalized osteoporosis of jaws, with a peculiar stepladder alignment of trabeculae of the

interdental septa, along with pallor and yellowish discoloration of the oral mucosa.

Periodontal infections may precipitate sickle cell crisis.

LAZY LEUKOCYTE SYNDROME:

Characterized by susceptibility to severe microbial infections, neutropenia, defective

chemotactic response by neutrophils, and an abnormal inflammatory response.

Individuals with this are susceptible to aggressive periodontitis with destruction of

bone and early tooth loss.

55

CHEDIAK-HIGASHI SYNDROME: 8

Chediak-Higashi syndrome (CHS) is a rare disease with an autosomal recessive

mode of inheritance. A structural defect, the fusion of azurophil and specific granules into

giant granules called megabodies, is characteristic of neutrophils from individuals with this

disease. Functional neutrophil defects include decreased chemotaxis, degranulation, and

micorbicidal activity. As a result, killing of ingested micro-organisms is delayed.

Aggressive periodontitis has been described in this patient. A biochemical defect, the

relative lack of neutral serine proteases, has also been observed in CHS.

AGRANULOCYTOSIS: 1, 2, 8

Agranulocytosis is characterized by a reduction in the number of circulating

granulocytes and results in severe infections, including ulcerative necrotizing lesions of the

oral mucosa, skin, and gastrointestinal and gastorurinary tracts. Less severe forms of the

disease are called neutropenia or granulocytopenia.

The absence of a notable inflammatory reaction caused by lack of granulocytes is a

striking feature. Oral features may include gingival hemorrhage, necrosis, increased

salivation, and fetid odour. The occurrence of rapidly destructive periodontitis has been

described in cyclic neutropenia.

The microscopic features show hemorrhage into the periodontal ligament with

destruction of the principal fibers, osteoporosis of the cancellous bone with osteoclastic

resorption, small fragments of necrotic bone in the hemorrhagic periodontal ligament,

hemorrhage in the marrow adjacent to the teeth, areas in which periodontal ligament is

evidenced and consist of dense fibrous tissue with fibers parallel to the tooth surface, and

the formation of new bony trabeculae.

IN HAND SCHULER-CHRISTIAN DISEASE:

The radiographic appearance is one of single or multiple areas of radiolucency,

mobility of the teeth results from loss of bony support.

Letterer-Siwe disease and Gaucher’s disease may have comparable changes.

Eosinophilic granulomas, appears as single or multiple radiolucent areas, which may be

unrelated to the teeth or entail destruction of the tooth supporting bone. These lesions may

simulate severe localized periodontitis.

56

OSTEOPOROSIS:

Osteoporosis is characterized by low bone mass as a result of an imbalance between

the activities of osteoclasts and osteoblasts. Initially the pattern of bone loss is consistent

with an increase in bone resorption. However, during the latter stages of development of

osteoporosis, the pattern and rate of bone loss are inconsistent with a decrease in bone

formation due to reduction in the number of osteoblasts . It may be due to either reduction

of the size of the stromal cell population or an impairment in the process of the osteogenic

commitment of the stromal cells. There is also evidence that there may be an imbalance

between the differentiation of osteoblasts and marrow adipocytes which could be a

contributory factor in the elderly. In ostoeporotic patients the volume of marrow adipose

tissue is increased at sits of marked bone atrophy and diseased bone formation.

It has been long hypothesized that individuals with osteoporosis are at increased risk

for periodontitis. These conditions share some common pathways in their pathogenesis.

For example, systemic up-regulation and increased production of IL-1 α and IL-1 β, TNF-α

and IL-6 induce osteoclastic activity and increase bone turnover rates that lead to loss of

bone mass and osteoporosis.

Increased concentrations of these cytokines in the periodontal tissue also lead to

alveolar bone loss and periodontal disease. It is possible that patients who are at risk for

osteoporosis because of a systemically upregulated cytokine response may also be more

susceptible to periodontitis in the presence of local irritants. Although this theory is

appealing, the relation between osteoporosis and periodontal disease is not well understood.

MENOPAUSE AND OSTEOPOROSIS:

During menopause there is decline in hormonal levels due to decreased ovarian

function. This is characterized by tissue changes such as desquamation of gingival

epithelium and osteoporosis which may be attributed to hormone deficiency. An alteration

in the calcium phosphate equilibrium due to deficient absorption of dietary calcium and

increased excretion due to diminished oestrogen levels can amount for some of the bone

changes seen in postmenopausal women. Although osteoporosis in postmenopausal women

may not be the cause of periodontal disease, it may affect the severity of pre-existing

disease. The circulating levels of oestrogen have been shown to influence on alveolar bone

density in post-menopausal women .

57

NUTRITIONAL INFLUENCES:

Vitamin D Deficiency:

The effect of such deficiency or imbalance on the periodontal tissues of young dogs

results in osteoporosis of alveolar bone. Osteoid forms at a normal rate but remains

uncalcified and failure of osteoid to resorb leads to its excessive accumulation, reduction in

the width of the periodontal space, a normal rate of cementum formation, but defective

calcification. Some cementum resorption, and distortion of the growth pattern of alveolar

bone.

In osteomalacic animals, 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 trebaculae.

Radiographically, there is generalized partial to complete disappearance of the

lamina dura and reduced density of the supporting bone, loss of trabecuale, increased

radiolcuency of the trabecular interstices, and increased prominence of the remaining

trabeculae.

WATER SOLUBLE VITAMINS: 1, 2

B-Complex Deficiency:

Oral manifestations of Vitamin B complex and niacin deficiency in experimental

animals include black tongue and gingival inflammation with destruction of the gingiva,

periodontal ligament, and alveolar bone. Necrosis of the gingiva and other oral tissues and

leucopenia are terminal features of niacin deficiency in experimental animals.

Vitamin C (Ascorbic acid) Deficiency:

Vitamin C deficiency (Scurvy) results in defective formation and maintenance of

collagen, retardation or cessation of osteoid formation, and impaired osteoblastic function.

Osteoporosis of alveolar bone in scorbutic monkeys results from increased osteoclastic

resorption and is not associated with periodontal pocket formation (W0aerhaug 1958).

Vitamin C deficiency is also characterized by increased capillary permeability, susceptibility

to traumatic hemorrhages, hyporeactivity of the contractile elements of the peripheral blood

vessels, and sluggishness of blood flow.

58

Acute vitamin C deficiency results in edema and hemorrhage in the periodontal

ligament, osteoporosis of the alveolar bone, and tooth mobility, hemorrhage, edema and

degeneration of collagen fibers occur in the gingiva. Vitamin C deficiency also retards

gingival healing. The periodontal fibers that are least affected by vitamin C deficiency are

those just below the junctional epithelium and above the alveolar crest, which explains the

infrequent apical down growth of the epithelium.

ENDOCRINE DISORDERS 1, 2, 7, 8

Hyperparathyroidism:

Hyperparathyroidism is an endocrine abnormality in which there is an excess of

circulating parathyroid hormone (PTH). An excess of serum PTH increases bone remodeling

in preference of osteoclastic resorption, which mobilizes calcium from the skeleton. In

addition, PTH increases renal tubular reabsorption of calcium and renal production of the

active vitamin D metabolite 1, 25 (OH)2D. The net result of these functions is in an increase

in serum calcium.

Primary hyperparathyroidism usually results from a benign tumor (adenoma) of

one of the four parathyroid glands, which produces excess PTH. Less frequently, individuals

may have hyperplastic parathyroid glands that secrete excess PTH. The combination of

hypercalcemia and an elevated serum level of PTH are diagnostic of primary

hyperparathyroidism. The incidence of primary hyperparathyroidism is about 0.1%.

Secondary hyperparathyroidism results from a compensatory increase in the output

of PTH in response to hypocalcemia. The underlying hypocalcemia may result from an

inadequate dietary intake or poor absorption of vitamin D or from deficient metabolism of

vitamin D in the liver or kidney.

Clinical Features:

Gradual loosening, drifting, and loss of teeth may occur. Definite consistent hypercakemia

is virtually pathognomonic of primary.

Radiographic features: Occasionally periapical radiographs reveal loss of the lamina

dura in patients (only about 10%) with hyperparathyroidism. Depending on the duration and

severity of the disease, loss of the lamina dura may occur around one tooth or all the

remaining teeth. The loss may be either complete or partial around a particular tooth. The

result of lamina dura loss may give the root a tapered appearance because of decreased

59

image contrast. Although PTH mobilizes minerals from the skeleton, mature teeth are

immune to this systemic demineralizing process.

Hypoparathyroidism and pseudohypoparathyroidism:

Definition:

Hypoparathyroidism is an uncommon condition in which insufficient secretion of PTH

occurs. Several causes exist, but the most common is damage or removal of the

parathyroid glands during thyroid surgery. In pseudohypoparathyroidism there is a defect in

the response of the tissue target cells to normal levels of PTH.

Clinical Features:

Both hypoparathyroidism and pseudohypoparathyroidism produce hypocalcemia, which

has a variety of clinical manifestations. Most often this includes sharp flexion (tetany) of

the wrist and ankle joints (carpopedal spasm).

Radiographic Features:

Radiographic examination of the jaws may reveal dental enamel hypoplasia, external root

resorption, delayed eruption, or root dilaceration.

BENIGN FIBRO-OSSEOUS LESIONS: 8, 9

A collection of non-neoplastic intraossseous lesions that replace normal bone and

consists of a cellular fibrous connective tissue with in which nonfunctional osseous

structures forms.

Cemento-osseous lesions:

Benign fibro-osseous lesions of the jaws closely associated with the apices of teeth

and containing amorphous spherical calcifications thought to resemble an aberrant form of

cementum; lesions are usually without signs and symptoms.

Periapical cemental dysplasia:

Asymptomatic diffuse periapical radiolucent and radiopaque areas, primarily of the

anterior mandible, in which cemento-osseous tissue replaces the normal architecture of the

bone.

60

It is not true not true neoplasm but a dysplastic condition. The teeth overlying the

lesion remain vital. Buccal or lingual expansion of the cortices is usually absent.

Radiographically, 3 stages from early formation to maturation:

1) Osteolytic: In this early stage, lesions are well-defined radiolucencies at the apex

of one or more teeth.

2) Cementoblastic: This stage displays similarly sized lesions and a demarcated

border with radiolucencies containing nodular radiopaque deposits.

3) Mature: Each radiopaque nodule has a thin radiolucent zone around its

periphery.

4)

Florid cemento-osseous dysplasia:

Diffuse asymptomatic, radiopaque and radiolucent intraosseous areas of cemento-

osseous tissue that involve one or both arches. It is more extensive form of periapical

cemental dysplasia.

The areas of dense bone have reduced vascularity and are less able to cope with the

usual transient infection. Composed of cellular connective tissue containing small and

largespherical calcificatios and large nodules of dense bone.

Radiographically; the lesions are diffusely distributed and contain faint nodular

radiopacities reminiscent of clouds or cotton balls. Lesions occupy the complete thickness of

the bone and are found from the alveolar crest to the inferior border.

A solitary lesion is occasionally present, usually in a molar region. Such a lesion has

recently designated as focal cemento-osseous dysplasia.

Fibrous dysplasia:

An asymptomatic regional alterations of bone in which the normal architecture is

replaced by fibrous tissue and nonfunctional trabeculae like osseous structures; lesions may

be monostotic or polyostotic, with or without associated endocrine disturbances.

61

Clinical forms of fibrous dysplasia of the jaws are:

Monostotic: Polyototic:

-Juvenile -Craniofacial

-Juvenile aggressive -McCune-Albright syndrome

-Adult -Jaffe syndrome

Clinical features:

Juvenile fibrous dysplasia begins early in childhood. Most common type of

monostotic dysplasia. Maxilla is affected more often than the mandible. It is a slow growing

regional distortion that usually enlarges proportionately with affected bone.

Aggressive Juvenile fibrous dysplasia grows at a faster rate than the affected bone,

producing major, often grotesque deformity that result in loss of function.

Adult monostotic dysplasia is a rare form. Affected area presents as an asymptomatic

diffuse expansion of the cortices. The clinical term “leontiasis ossea” has often been

applied when maxilla or facial bones are affected and give a patient a leonine appearance.

Polyostotic fibrous dysplasia is usually accompanied by skin pigmentation and

endocrine dysfunction. Bone lesions may be confined to the craniofacial area or distributed

diffusely throughout the skeleton. The bones most commonly affected are ribs cranium,

maxilla, femur, tibia, and humerus. Large light-brown pigmentations termed café au lait

spots (Jaffey’s type), which have a ragged periphery. In addition female patients may

exhibit precocious puberty, vaginal bleeding. When endocrine dysfunction is present it is

called McCune-Albright syndrome, which manifests in early childhood but it is

uncommon.

In Craniofacial fibrous dysplasia, lesions occur in bones of the jaws and cranium.

Radiogrphically;

Monostotic fibrous dysplasia has 3 basic patterns:

1) A lesion is generally a rather small unilocular radiolucency or a larger multilocular

radiolucency, both with rather well-circumscribed border and containing a network

of fine bony trabeculae.

62

2) The pattern is similar except that increased trabeculation renders the lesion more

opaque and typically mottled in appearance.

3) This type is quite opaque with many delicate trabeculae giving a “ground glass” or

“peau d’ orange” appearance to lesion.

In Polyostotic fibrous dysplasia , the medullary portions of the bone are rarified and present

irregular trabeculations, often a multilocular cystic appearance.

In all the types, generally cortical bone thinned because of expansile nature of growth.

Histologically;

Monostotic fibrous dysplasia is essentially a fibrous one made up of proliferating fibroblasts

in compact stroma of interlacing collagen fibers. Irregular trabeculae of bone are scattered

through out the lesion with no definite pattern of arrangement. Characteristically, some of

these trabeculae are C-shaped or Chinese character shaped.

In Polyostotic fibrous dysplasia, the lesions are composed of fibrillar connective tissue

within which are numerous trabeculae of coarse, woven fiber bone, irregular in shape but

evenly spaced, showing no relation to functional patterns.

Metabolic conditions:

Pagets disease(osteitis deformns):

Uncoordinated increase in the osteoclastic and osteoblastic activity of the bone cells

of older adults, producing larger but weaker bones, extensive pain, high levels of serum

alkaline phosphatase and urinary hydroxyproline, and an increased tendency to develop

malignant bone neoplasms.

The maxilla exhibits progressive enlargement, the alveolar ridge becomes widened and

palate is flattened. If teeth are present, they may become loose and migrate, producing some

spacing.

Radiographically; loss of normal trabeculation and appearance of irregular osteoblastic

activity giving rise to “cotton wool” appearance. Hypercementosis and often loss of a well

defined lamina dura around the teeth.

63

Histologically; most characteristic feature is the formation of “mosaic” bone, a descriptive

term which indicate the appearance of bone which has partially resorbed and then repaired,

leaving deeply staining hematoxyphilic reversal lines. These lines eventuate in a “jigsaw-

puzzle” appearance of the bone. The rapidly the bone is laid down, the more immature it is

and greater amount of osteoid. As bone formation lags and a resting phase is reached, the

bone changes from a fibrillar type to a more mature lamellar variety. The proliferation of

bone and concomitant hypercementosis sometimes result in obliteration of PDL.

Osteopetrosis:

(Marble bone disease; Albers-schonberg disease; osteosclerosis Fragilis generalisata)

Generalized hereditary condition consisting of excessive bone mineralization,

resuting in altered stature, frequent fractures, lack of bone marrow hematopoietic function,

and a tendency for severe osteomyelitis of the jaws.

2 types: (1) a clinically benign dominantly inherited form

(2) a clinically malignant recessively inherited form (more severe)

Pathological fractures, often multiple are common clinical manifestation followed by bone

pain, cranial nerve palsy. The madullary spaces of the jaws are remarkably reduced in both

dominant and recessive osteopetrosis so that there is marked predilection for the

development of osteomyelitis.

Radiographically; Medullary cavities are replaced by bone, and the cortex is thickened.

Density of the affected jaw bone may be such that the roots of the teeth are nearly invisible

on the radiograph.

Histologically; Ostopetrosis is characterized by the endosteal production of the bone with

an apperent concomitant lack of physiologic bone resorption.

Osteogenesis imperfecta:

(Brittle bones; Fragilitas ossium; Osteopsathyrosis; Lobstein’s disease)

A spectrum of diseases of bone caused by a basic alteration in the formation of bone

connective tissue matrix, resulting in an ability of the matrix to fully mineralize, a tendency

for multiple broken bones, blue sclera of the eyes, and associated dentinogenesis imperfecta.

64

Teeth exhibit with bulbous crown, obliteration of the pulpal chambers, and shortened roots.

The bones have marked thinned cortices composed of immature woven bone. Bone displays

increased number of osteoblasts, osteocytes and osteoclasts, as well as decreased mineral

content.

BENIGN TUMORS:

Osteoma:

An exophytic nodular growth of dense cortical bone on or within the mandible or

maxilla. When multiple, they are often associated with gardner syndrome, which consists of

multiple intestinal polyps with malignant potential, unerupted normal and supernumary

teeth, and cysts and fibromas of the skin.

Each of the lesion is composed of dense cortical bone with lamellar pattern. The

cortical bone is sclerotic and relatively avascular. The medullary bone is denser than normal

with reduced marrow spaces. The periosteal layer is often more active in osteoma.

Osteiod osteoma and Osteoblastoma:

Benign intraosseous lesions with similar clinical, radiographic, and histopathologic

features consisting of well demarcated, rounded intraosseous swellings, each with an active

cellular central nidus surrounded by a wide zone of osteoid, with pain upon palpation.

Osteoid osteoma is small (0.5-2.0) and osteoblastoma is large (>2.0). Both are

rounded, with a well defined central radiolucency(nidus) surrounded by a zone of increased

radiopacity.

The radiographic features of osteoid osteoma and osteoblastoma are distinctive and

pathognomonic. They are rounded, with a well-defined central radiolucency (nidus)

surrounded by a zone of increased radiopacity

Histolopathology:

All lesions pass through several phases. Initially a small focus of active osteoblasts is

followed by a period in which wide zones of osteoid are deposited. In the matured stage, the

osteoid becomes well calcified, creating an atypical form of bone. The center usually

remains vascular with increased numbers of plump osteoblasts and large osteoclasts

65

Cemento-ossifying fibroma:

A well-demarcated, encapsulated, expansile intraosseous lesion of the jaws composed of

cellular fibrous tissue containing spherical calcifications and irregular, randomly oriented

bony structures.

When lesions containing the spherical calcifications occur in the sinonasal and

orbital

bones in young patients, they have been termed psammo-matoid juvenile ossifying

fibroma. Lesions of the maxilla and mandible with trabecular bone as the main histologic

feature have been referred to as trabecular juvenile ossifying fibroma

COF is most often located in the mandible posterior to the canines and only

occasionally in the maxilla and other locations. The lesion is usually painless and grows

slowly, exhibiting marked buccal and lingual bony expansion.

Radiographically; The lesions may be either unilocular or multilocular. In the early

stages the lesions are small and usually completely radiolucent. As they enlarge, increased

amounts of irregularly shaped radiopacities appear within the radiolucent area. In the later,

more mature stage, the radiopaque structures enlarge and coalesce, often forming a nearly

radiopaque lesion with a thin rim of radiolucency separating it from the surrounding normal

bone. Root resorption and displacement of teeth are frequent findings.

Histolopathology: The more radiolucent lesions are composed of cellular fibrous

connective tissue, frequently in a whorled pattern. Spherical amorphous calcifications of

various sizes (cementicles) are often present and randomly distributed. Irregularly shaped

calcified structures containing osteocytes and a wide zone of osteoid and osteoblasts are

frequentIy intermingled. A thin outer zone of fibrous connective tissue is usually present,

separating the fibroosseous tissue from the surrounding normal bone.

Lesions of the Jaws Containing Giant Cell Tissue

1. Central giant cell granuloma

2. Peripheral giant cell granuloma

3. Cherubism

4. Aneurysmal bone cyst

5. "Brown tumor" of hyperparathyroidism

66

Peripheral giant cell granuloma:

An extraosseous nodule composed of a proliferation of mononudear and

multinucieated giant cells with an associated prominent vascularity found on the gingiva or

alveolar ridge. The PGCG is the most common giant cell lesion occurring in the jaws,

arising from the connective tissue of the periosteum and periodontal membrane. PGCG most

often appears as a sessile focal purplish nodule on the gingiva. They are usually exophytic

and may encompass one or more teeth, spreading through penetration of the periodontal

membrane. Occasionally, lesions arise from the periosteum overlying edentulous areas.

Radiographically; There may be little radiographic evidence of some lesions in

teeth-bearing areas, because lesions may be small and primarily in the soft tissues. Larger

lesions exhibit a superficial erosion of the cortical bone and may demonstrate some

widening of the adjacent periodontal space. Close examination of the area may reveal small

spicules of bone extending vertically into the base of the lesion. In edentulous areas, the

cortical bone exhibits a concave area of resorption beneath the lesion, often referred to as

saucerization.

Histopathology; PGCG is composed of nodules of multinucieated giant cells in a

background of mononudear cells and extravasated red blood cells. Bands of fibrous

connective tissue stroma containing small sinusoidal spaces (especially in the periphery)

surround the nodules. Osteoid deposits or spicules of new bone are often present in the base

of the lesion. Accumulations of hemo-siderin are found throughout the lesion.

Central giant cell lesion:

An intraosseous destructive lesion of the anterior mandible and maxilla in which

larger lesions expand the cortical plates, cause movement of teeth, and produce root

resorption; it is composed of multinucleated giant cells in a background of mononudear

fibrohistiocytic cells and red blood cells.

Expansion of the buccal and lingual cortical plates is common. Some lesions exhibit

cortical perforation and resorption of root apices.

Radiographically; It consists of a radiolucency (usually relatively large) with an

indistinct line of demarcation with the adjacent normal bone. Buccal and lingual expansion

67

is usually observed on ocdusal radiographs, which often exhibit complete cortical bone loss.

Movement of associated teeth and resorption of tooth roots is commonly observed.

Histopathology; Tissue from the lesions is composed of giant cells, usually

containing 5 to 20 nuclei, against a background of mononuclear cells and fibrous tissue. In

the more granulomatous lesions, foci of new bone formation are evidenced by osteoid and

woven bone. In the more aggressive lesions, the proportion of mononuclear cells and giant

cell tissue is greatly increased, mature fibrous tissue is decreased, and foci of bone

formation are lacking.

Aneurysmal bone cyst:

An uncommon lesion located primarily in the posterior mandible and maxilla with

clinical features similar to central giant cell lesion; it contains many large blood-filled

spaces separated by connective tissue septa containing giant cell tissue.

Most lesions occur in the posterior mandible and often extend into the ramus. The

occasional lesion that occurs in the maxilla is also confined to the molar area. Lesions are

firm, diffuse swellings that produce facial deformity and mal-occlusion. ABC grows rapidly

and may perforate the cortex.

Radiographically; The radiographic features are not distinctive, consisting of an

oval or fusiform expansile radiolucency in which the cortex is thinned or eroded. Teeth are

often moved and their roots resorbed. Lesions are usually unilocular, with some exhibiting

faint trabeculation.

Histopathology; ABC tissue consists of large blood-filled spaces separated by

fibrous septa. The septa are composed of connective tissue containing osteoid deposits,

spicules of woven bone, and deposits of hemosiderin. Varying numbers of multinucleated

giant cells may be observed.

Traumatic bone cyst:

Asymptomatic intraosseous empty cavity of young patients located primarily within

the mandible and lined by a thin loose connective tissue membrane; it is adequately treated

when blood enters the space during an intraosseous biopsy.

68

Radiographically; Traumatic bone cyst appears as a well-circumscribed, solitary

radiolucency of variable size. Larger lesions frequently extend between the roots of the

associated teeth to produce a scalloped appearance that is characteristic of this lesion.

Buccal or lingual cortical expansion of the mandible is usually absent.

Histopathology; Tissue obtained from the wall of the lesion reveals a thin layer of

loose and delicate connective tissue overlying a zone of reactive bone that exhibits

remodeling. Often the soft tissue luminal surface contains a thin layer of fibrin. In areas

where healing is taking place, the connective tissue will contain mineralized deposits of new

bone with a distinctive lamellar pattern.

Langerhans cell histiocytosis:

A probable neoplastic proliferation of Langerhans type of histiocytic cells with a

wide spectrum of biologic behavior ranging from a single lesion of the mandible to diffusely

distributed bone lesions in combination with organ and other soft tissue lesions; consists of

S- 7 00 and CD 1 a positive histiocytes containing Birbeck granules and accompanying

accumulations of eosinophils.

Based on the clinical findings, LCH is grouped into three categories for treatment

and prognostic purposes:

(1) chronic focal—usually a solitary lesion in one bone but occasionally in multiple bones,

with no soft tissue or organ involvement (previously designated as "eosinophilic

granuloma")

(2) chronic disseminated—involving multiple bones, organs, lymph nodes, and

occasionally skin (previously designated as "Hand-Schuller-Christian disease")

(3) acute disseminated—involving most organs, lymph nodes, bone marrow, and skin of

infants (previously designated as "Letterer-Siwe disease").

Radiographically; reveal a solitary intraosseous punch out lesion around and

beneath the teeth roots The lesions may involve several teeth and appear as focal areas of

advanced periodontal disease in which the teeth seem to be floating in space because of the

lack of surrounding bone.

Histopathology; The tissue contains sheets of large histiocytic cells with

eosinophilic cytoplasm and centrally placed nuclei with occasional multinucleated cells

69

interspersed with other inflammatory cells. The presence of Birbeck granules when viewed

with electron microscopy confirms a diagnosis of LCH.

MALIGNANT TUMORS:

Osteogenic sarcoma:

Most common of the malignant neoplasms derived from bone cells that in the jaws

exhibit radiographic widening of periodontal membrane of teeth and histologically exhibit a

wide spectrum of findings, all of which contain atypical osteoblasts and abnormal bone or

osteoid formation.

The incidence of osteogenic sarcoma in older patients with a history of Paget disease

of bone is 1%. Association between Paget disease and osteogenic sarcoma is the result of a

single gene or two tightly linked genes on chromosome 18.

Radiographically; Lesions of the mandible and maxilla are usually first noticed as

bony, hard swellings of the buccal and lingual cortices (with or without pain) and often

associated with separation of teeth. Lesions of the well-differentiated osteo-blastic and

chondroblastic types of osteogenic sarcoma form large amounts of mineralized bonelike

tissue, producing large areas of radiopacity within a diffuse, non-defined radiolucent

background. A characteristic finding in jaw lesions is widening of the periodontal membrane

in adjacent teeth. An occlusal radiograph usually reveals a sunburst pattern of radiopacity

radiating from the periosteum.

Histopathology; Osteogenic sarcoma lesions must contain normal or abnormal

osteoid or bone that is closely associated with the malignant connective tissue cells to

distinguish them from other forms of sarcoma.

Histologic Variants of Intraosseous Osteosarcoma

Osteoblastic

Chondroblastic

Fibroblastic

Telangiectatic

Chondrosarcoma:

Uncommon malignant bone neoplasm in the jaws, usually of the anterior maxilla,

consisting of a proliferation of plump chondroblasts or spindle-shaped mesenchymal cells

and abnormal cartilage but no osteoid or bone. Lesions may be;

70

primary chondrosarcomas (arising directly from bone cells as malignant neoplasms)

secondary chondrosarcomas (arising in a preexisting benign cartilaginous lesion such as enchondroma or osteochondroma).

Nearly all lesions are confined to the anterior maxilla, where preexisting nasal cartilage is

present, and the premolar areas of the mandible, the site of the em-bryonically derived

Meckel cartilage.Lesions are expansile masses that produce distortion of the areas. In the

larger lesions, pain and paresthesia may occur. In the anterior maxilla, nasal obstruction and

breathing difficulties are often presenting signs.

Radiographically; it is variable depending on the extent of calcification of the cartilaginous

component. Commonly, it appears as an expansile "moth-eaten" radiolucent area with

indistinct boundaries containing flecks or blotchy radiopacities throughout. Widening of the

periodontal membrane of associated teeth is a common finding.

Histopathology; Most lesions exhibit a combination of abnormal cartilage surrounded by

neoplastic cells. Lesions are graded I to III , depending on the amount and maturity of the

cartilage and the proportion and anaplasticity of the connective tissue cells. In grades II and

III, areas of myxoid tissue and cystic degeneration are present.

Ewing sarcoma:

Rare malignant bone neoplasm of uncertain cell origin in young patients; the lesion

is composed of anaplastic smalt, dark, round cells containing glycogen granules and

intermediate filaments.

Ewing sarcoma is a highly malignant bone tumor thought to arise from primitive

neuroectodermal cells. The lesions consist of densely packed, small, darkly stained round

cells without prominent nucleoli or distinct cell borders.

In the jaws, patients may experience loosening teeth and, in later stages, focal

ulceration. The mandible is affected more often than the maxilla.

Radiographically; The involved bone appears "moth-eaten," simulating an osteomyelitis

with indistinct margins. The periosteum often has a lamellar layering, referred to as an

"onionskin" reaction.

The histologic features are sufficiently nonspecific.

71

PERIIMPLANTITIS AND BONE LOSS: 1, 2

Periimplantitis is defined as an inflammatory process affecting the tissues around an

osseointegrated implant in function, resulting in loss of supporting bone.

Periodic evaluation of tissue appearance, probing depth changes, and radiographic

assessment are the best means of detecting changes in bone support.

In cases with severely reduced bone support extending into the apical half of the

implant, or in cases demonstrating mobility, implant removal should be considered. After

implants are removed, the ridge defect can be reconstructed using bone graft and membrane

techniques.

CONCLUSION:

Alveolar bone has its embryological origin from the initial condensation of

ectomesenchyme around the early tooth germ. The alveolar processes are tooth dependent,

and are present as long as they house the teeth. .

Bone is continually remodeled by the combined activities of osteoblasts and

osteoclasts, and in pathological situations like chronic periodontitis there may be a

preponderance of bone resorption over formation due to a variety of factors. The bone loss

in periodontal disease occurs at local sites, but it is regulated by both systemic and local

factors. Bone resorption is probably the most critical factor in periodontal attachment loss

leading to eventual tooth loss.

Various factors (host and bacterial) that interplay in causing bone resorption are age,

local inflammation of the periodontal tissues, trauma from occlusion. Systemic diseases

example diabetes mellitus, hyperparathyroidism and systemic conditions like osteoporosis,

osteopenia, debilitating diseases such as HIV and blood dyscrasias. Iatrogenic causes might

include excessive loading of abutment teeth, overhanging restorations and use of excessive

orthodontic forces. Cysts and tumours in the alveolar region also account for the resorption.

Alveolar bone, which has interdependence with the dentition, has a specialized

function in the support of the teeth. Safe guarding the integrity of the PDL and the alveolar

bone is one of the most important challenges for the clinician

72

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15) Periodontics; Grant; 6th edn

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