The bone that forms and
supports the tooth is
Destruction of the bone
is responsible for tooth
As the tooth is shed this
Facial and lingual compact bone
Socket wall consist of dense lamellated bone
and bundle bone
Interdental septum consist of cancellous
Average distance of alveolar bone
and Cemento-enamel junction:
Young Adult: 0.75mm - 1.49mm
Old age: 1.08mm – 2.81mm
Mesiodistal angulation of crest of
interdental septum usually parallels a
line drawn between Cementoenamel
junction of approximating teeth.
The height and density of alveolar bone is
normally maintained by an equilibrium,
regulated by loacal and systemic factors
between bone resorption and bone formation
When this resorption exceeds formation both
bone height and density are reduced.
In periodontal disease, even the bone
morphology is altered.
Horizonal bone loss
Vertical or angular defect
Bulbous bone contour
Extension of gingival inflammation
Trauma from occlusion
Normal variation in alveolar bone
Trauma from occlusion
Buttressing bone formation
The most common pathway
The inflammatory invasion of bone surface and the initial bone
loss marks the transition from gingivitis to periodontitis.
This transition is associated with changes in composition of
bactrerial host and resistance og host.
In advances stages of disease, the number of motile organism
and spirochete increases, whereas the coccoid rods and
straight rods decreases.
The lesion presents with most pathogenic bacteria,
inflammatory cell infiltrate, lesion becoming more destructive
with conversion of T- lymphocyte to B-lymphocytic lesion.
1. Interproximally from gingiva
2. From bone into periodontal
3. From gingiva into periodontal
Facially and lingually
from gingiva along the
From periosteum into
From gingiva into
Replaced by leucocytes and fluid exudates, new blood vessels and
Increase in osteoclasts and mononuclear cells
Thinning of bone trabeculae and enlargement of marrow spaces
Destruction of bone and reduction of bone height
Replacement of fatty bone marrow with fibrous type
Area of inflammation extends from gingiva into suprabony area.
Extension of inflammation occurs along blood vessels and
between collagen bundles.
Inflammation extending from pocket area between collagen
fibres, which are partially destroyed.
Extension of inflammation into centre of interdental septum.
Inflammation from gingiva penetrates transseptal fibres and
enters the bone around blood vessels in the centre of septum.
Cortical layer at the top of septum are destroyed and
inflammation penetrates into bone marrow.
Re-formation of trans-septal fibres. Recreated transseptal fibres
above the bone margin, partially infiltrated by inflammatory
Extension of inflammation to crestal bone surface.
1.5 to 2.5mm within which a bacterial plaque can
induce loss of bone.
For interproximal angular defect space have to be
greater than 2.5 mm because in narrow spaces bone
is entirely destroyed leading to horizontal bone
Large defects exceeding 2.5mm can be seen in
localised juvenile periodontitis and Pappilon-lefevre
in individual with no oral hygiene
facial surface: 0.2mm a year
proximal surface: 0.3 mm a year
Bone loss may vary depending on the type of disease
Loss of attachment of 0.1 to 1.0mm
Loss of attachment of 0.05mm to
Minimal or no
0.05mm to 0.09mm yearly
Occurs in episodic, intermittent manner with
period of inactivity or quiescence.
Results in loss of collagen and alveolar bone
resulting in deepening of periodontal pocket.
The reason for onset, not elucidated.
Some theories have been put forward
subgingival ulceration and an acute inflammatory reaction,
resulting in rapid loss of alveolar bone.
this coincides with the conversion of a predominantly Tlymphocyte lesion to one with a predominantly Blymphocyte–plasma cell infiltrate.
Microbiologically they are associated with an increase of the
loose, unattached, motile, gram-negative, anaerobic pocket
flora, while periods of remission coincide with the formation
of a dense, unattached, nonmotile, gram-positive flora with
a tendency to mineralize.
the onset of periods of destruction coincide with tissue
invasion by one or several bacterial species and is followed
by an advanced local host defense that controls the attack.
(b) host mediated.
Bacterial plaque products induce the differentiation of bone progenitor cells into osteoclasts and
stimulate gingival cells to release mediators that have the same effect.
Plaque products and inflammatory mediators can also act directly on osteoblasts or their progenitors,
inhibiting their action and reducing their numbers.
In addition, in rapidly progressing diseases such as aggressive periodontitis, bacterial microcolonies or
single bacterial cells have been found between collagen fibers and over the bone surface, suggesting a
Several host factors released by inflammatory cells are capable of inducing bone resorption in vitro
and play a role in periodontal disease. These include host-produced prostaglandins and their
precursors, interleukin-1α (IL-1α) and IL-β, and tumor necrosis factor alpha (TNF-α).
When injected intradermally, prostaglandin E2 (PGE2) induces the vascular changes seen in
inflammation; when injected over a bone surface, PGE2 induces bone resorption in the absence of
inflammatory cells and with few multinucleated osteoclasts.
In addition, nonsteroidal antiinflammatory drugs (NSAIDs), such as flurbiprofen and ibuprofen, inhibit
PGE2 production, slowing bone loss in naturally occurring periodontal disease in beagle dogs and
humans. This effect occurs without changes in gingival inflammation and rebounds 6 months after
cessation of drug administration.
Normal variation in alveolar bone:
The anatomic feautres that affect bone destructive
pattern in periodontal disease includes:
The thickness,width and crestal angulation of
The thickness of facial and lingual alveolar plates
Presence of fenestrations and dehiscences
The alignment of teeth
Root and root trunk anatomy
Root position within the alveolar process
Proximity with another tooth surface
Exostoses are outgrowths of bone Of
varied size and shape.
Palatal exostoses have been found in
40% of human skulls.
They can occur as small nodules,
large nodules, sharp ridges, spike-like
projections, or any combination of
Exostoses have been described in rare
cases «is developing after the
placement of free gingival grafts
Trauma from occlusion may be
a factor in determining the
dimension and shape of bone
It may cause a thickening ol
the cervical margin of alveolar
bone or a change in the
morphology of the bone on
which inflammatory changes
will later be superimposed
Bone formation sometimes occurs in
an attempt to buttress bony trabeculae
weakened by resorption.
When it occurs within the jaw, it is
termed central buttressing bone
When it occurs on the external surface,
it is referred 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
Interdental bone defects often occur where
proximal contact is abnormal or absent. Pressure
and irritation from food impaction contribute to
the inverted hone architecture.
In some instances the poor proximal
relationship may be the result of a shift in tooth
position because of extensive bone destruction
preceding food impaction
Horizontal bone loss
Vertical or angular defect
Bulbous bony contours
The most common
Bone is reduced in
Bone margins remain
perpendicular to tooth
Interdental septa, facial
and lingual cortical
plates are affected.
Occur in adults
Have been reports in
skulls with primary
Presence is suggested
Careful probing and
surgical exposure of
areas is required.
Occur in oblique direction
Leaves a hollowed out trough in
the bone alongside root
Base of defect is apical to the
Angular defect and intrabony
Classified on basis of number of
one wall defect
two walled defect
three walled defect
combined osseous defect
Three bony walls
Two wall defect
One wall defect
Concavities in the crest of alveolar
Confined to facial and lingual walls
Resons for high frequency
interdentally area collects plaque
and is difficult to clean.
The normal flat or even concave
faciolingual shape of interdental
septum in lower molars favours
Vascular patterns from gingiva to
crest-pathway for inflammation.
caused by exostoses,
by loss of
plates and lingual
of radicular bone.
These are plateau like bone margins caused
by resorption of thickened bony plates.
It refers to the involvement of
bifurcations and trifurcations
of multirooted teeth by
Most common in mandibular
Least common in maxillary
area of root separation
Surface coronal to root
Also called as early lesion.
Suprabony pocket involving soft tissue
Radiographic changes not usually found
as bone loss is minimal, but increase in
Bone destroyed in one or more surfaces
Part of PDL, alveolar bone remains intact,
allows partial penetration of bone.
Radiograph may or may not show presence
Interradicular bone completely missing. Facial and
lingual or both orifices of furation canot be seen
clinically because of soft tissue coverage.
Bone loss crater like or angular.
Radiograph at proper angulation shows furcation.
GRADE I V:
Clinically visible if gingival reseccion is present.
Radiograph reveals easy furcation involvement
DEGREE I: Horizontal bone loss less than 3mm
DEGREE II: Horizontal bone loss more than 3mm
DEGREE III: through and through horizontal lesion
Vertical bone loss is measured in mm from the roof of the furcation
Subclass A: Vertical destruction to one-third of total radicular height (1-3mm)
Subclass B: Vertical destruction reaching two-third of inter-radicular height (4-6mm)
Subclass C: Inter-radicular osseous destruction into or beyond apical third (>7mmm)
Place the probe between
the two buccal roots from
the buccal aspect
Place the probe between
the two lingual roots from
the lingual aspect
Should include both
periapical and bitewing
Location of the
interdental bone and bone
level within the root
complex should be