Beruflich Dokumente
Kultur Dokumente
A Seminar On
Presented by,
Dr. Sunitha .J
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)
12)
Bone formation
13)
Bone resorption
14)
Blood supply
15)
16)
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:
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:
A)
DEVELOPMENTALLY,
(1)
Endochondral bone where the bone is preceded by
a cartilaginous model which is eventually replaced by
bone.
3
(2)
B)
COMPOSITION:
BONE
Inorganic (65%)
Organic (35%)
Hydroxyappatite
Collagen (88-89%)
Noncollagenous (11-12%)
Glycoproteins (6.5-10%)
Proteoglycans (0.8%)
Sialoproteins (0.35%)
Lipids (0.4%)
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
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.
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:
INTERDENTAL SEPTA:
1, 2
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
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
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
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 sharpys fibers that are the endings of embedded PDL.
3, 4
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
m 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.
10
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.
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
11
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.
12
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 Sharpeys 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
13
layer completely covers the osteoid surface and that the osteoblasts function in a coordinated 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
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
14
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.
15
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 cmyc, 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
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.
16
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 v3).
These integrins bind to specific amino acid sequences present in proteins of the bone matrix,
namely Arg-Gly-Asp (RGD). Interference with the formation of such integrins or the administration of competing synthetic peptides will inhibit bone resorption.
17
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-
COLLAGEN:
Collagen
11
comprises
the
major
(~8090%)
organic
component
in
into the lamellar bone lining the alveolus to provide a stable connection
with the tooth.
18
The collagen fibrils in bone are stabilized by intermolecular crosslinking 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 boneforming 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
19
for
the
mineral
crystals.
These
include
albumin,
2HS-
OSTEOCALCIN:
11
and
remodeling
is
not
entirely
clear.
Abrogation
of
reduces
osteocalcin
levels
in
bone,
which
becomes
20
11
SPARC / OSTEONECTIN:
11
matrix
molecules.
It
is
widely
expressed
during
21
studies
have
indicated
role
for
SPARC
in
early
expressed
with
chondroitin
sulfate
side
chains,
and
decorin
(chondroitin
sulfate
proteoglycan
II),
are
found
(Mr~120200
kDa)
also
has
protein
core
of
22
ULTRASTRUCTURAL ORGANIZATION:
11
23
its
ultrastructural
association
with
sites
of
mineralization
11
24
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 coordination of activities of cells from two distinct lineages, the osteoblasts
and the osteoclasts, which form and resorb the mineralized connective
tissues of bone, respectively.
remodeling
and
inflammatory
response
systems
are
further
BONE FORMATION:
11
25
alkaline
phosphatase
and
collagen
expression
are
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/PEBP2 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
11
26
27
of
osteoprogenitors
and
promotion
of
osteogenic
BONE RESORPTION:
11
cell,
the
osteoclast,
which
is
produced
by
the
bone
marrow.
Osteoclasts
develop
from
pluripotential
28
The
identification
(OPG),
has
of
recently
novel
uncovered
receptor,
a
key
termed
regulatory
ruffled
border.
specific
type
of
electrogenic
adenosine
29
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,
11
calcitonin,
transforming
growth
factor-,
estrogen
and
15
30
colony-stimulating
factor, osteoprotegerin
32
and interleukins),
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.
33
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 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/m 2 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.
EXTENSION OF INFLAMMATION:
1, 2
34
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.
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
the root as the bone destruction progresses. As a result, transseptal fibers are present, even
in cases of extreme periodontal bone loss.
35
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.
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
Waerhaugs 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
36
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.
1. Absorbable products from plaque could stimulate bone progenitor cells in the
periodontium to differentiate into osteoclasts, which resorb alveolar bone.
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.
37
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.
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 Tlymphocyte 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.
Source
Parathyroid
Liver via kidney from skin
Monocytes (major source)
Many
other
cell
types
including
38
cells
Monocytes
Function / Use
Acts directly on osteoclasts
Inhibits eicosonoids synthesis
Inhibits osteoclastic bone resorption probably
by
making
the
mineralized
surface
Indomethacin
Aspirin
Interferon
TGF-
of osteoclast progenitors
Inhibits both proliferation and differentiation
Interleukin-1
of osteoclast progenitors
receptor Binds to IL-1 receptors effective against TNF
antagonist (IL-1ra)
as well.
39
Parathyroid hormone
Parathyroid related peptide
Vitamin D3
(1, 25, dihydrocholecalciferol)
Local factors
Thyroid hormone
Prostanoids
Lipooxygenase metabolites
Cytokines
: Interleukin-1
Interleukin 1
Tumour necrosis factor alpha
(Cachectin)
Tumour necrosis factor
(Lymphotoxin)
Growth Factors
Interleukins
Epidermal growth factor
Transforming growth factor alpha
Transforming growth factor beta
Bacterial factors
Parathyroid Hormone:
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
40
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
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.
41
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
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-1
and IL-1 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
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.
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
43
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.
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.
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 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 onewalled infrabony defect.
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.
45
Ledges:
Ledges are plateau-like bone margins caused by resorption of thickened bony plates.
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.
Furcation Involvement:
46
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 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.
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.
47
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
49
C. Furcation Defects
1. Class I or incipient
2. Class II or partial
3. Class III or through and through
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.
Patients with moderate periodontitis exhibit 4 to 7 mm of probing attachment loss,
early to moderate furcation invasions, and slight to moderate tooth mobility.
50
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
in this age group develops normally with tooth eruption, and only subsequently does it
undergo resorptive changes.
51
Generalized:
Clinical Findings:
Clinically characterized by generalized interproximal attachment loss effecting
atleast three permanent teeth other than first molars and incisors.
Two types
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.
52
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
Papillon-lefevre syndrome:
This syndrome is characterized by hyperkeratotic skin lesions, severe destruction of
the periodontium, and in some cases, calcification of the dura.
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
53
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.
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.
54
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.
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
55
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.
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
56
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 and IL-1 , TNF-
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.
appealing, the relation between osteoporosis and periodontal disease is not well understood.
NUTRITIONAL INFLUENCES:
Vitamin D Deficiency:
57
The effect of such deficiency or imbalance on the periodontal tissues of young dogs
results in osteoporosis of alveolar bone.
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.
58
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.
59
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.
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.
60
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.
Clinical forms of fibrous dysplasia of the jaws are:
Monostotic:
Polyototic:
61
-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 caf au lait
spots (Jaffeys 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.
2) The pattern is similar except that increased trabeculation renders the lesion more
opaque and typically mottled in appearance.
62
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.
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,
63
leaving deeply staining hematoxyphilic reversal lines. These lines eventuate in a jigsawpuzzle 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; Lobsteins 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.
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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.
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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
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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.
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eosinophilic cytoplasm and centrally placed nuclei with occasional multinucleated cells
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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:
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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;
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.
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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.
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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
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