this ppt depicts pattern of bone destruction. its a very good slide show showing the process of bone formation, bone destruction and their patterns in periodontal diseases.

1. .

4. 
The bone that forms and
supports the tooth is
called ALVEOLAR
PROCESS

Destruction of the bone
is responsible for tooth
loss.

As the tooth is shed this
bone resorbs

5. 


Facial and lingual compact bone
Socket wall consist of dense lamellated bone
and bundle bone
Interdental septum consist of cancellous
bone.

6. 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.

9. 1. INTRAMEMBRANOUS
OSSIFICATION
2. ENDOCHONDRAL
OSSIFICATION

11. Centers of Ossification
Centers of Ossification

12. ENDOCHONDRAL OSSIFICATION

13. ENDOCHONDRAL OSSIFICATION

14. 
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.

16. BONE DESTRUCTION
PATTERN
Horizonal bone loss
Bone deformities
Vertical or angular defect
Osseous craters
Bulbous bone contour
Reversed architecture
Ledges
Furcation involvement
FACTORS CAUSING
DESTRUCTION OF
BONE
Extension of gingival inflammation
Trauma from occlusion
Systemic disorders
FACTORS DETERMINIG
BONE MORPHOLOGY
Normal variation in alveolar bone
Exostoses
Trauma from occlusion
Buttressing bone formation
Food impaction
Aggressive periodontitis

17.  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.


18. 1. Interproximally from gingiva
into bone
2. From bone into periodontal
ligament
3. From gingiva into periodontal
ligament

19. 1.
Facially and lingually
from gingiva along the
outer periosteum.
2.
From periosteum into
bone
3.
From gingiva into
periodontal ligament

20. Gingival inflammation
Marrow spaces
Replaced by leucocytes and fluid exudates, new blood vessels and
proliferating fibroblasts
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

21. 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
process.
Extension of inflammation to crestal bone surface.

22.  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
defects.

Large defects exceeding 2.5mm can be seen in
localised juvenile periodontitis and Pappilon-lefevre
syndrome

23. 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
present.

Rapid progression
8%
Loss of attachment of 0.1 to 1.0mm
Moderate
progression
81%
Loss of attachment of 0.05mm to
0.5mm
Minimal or no
progression
11%
0.05mm to 0.09mm yearly

24. 
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

25. 
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.

26. 

(a) bacterial
(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
direct effect.

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.

29. Normal variation in alveolar bone:
The anatomic feautres that affect bone destructive
pattern in periodontal disease includes:
 The thickness,width and crestal angulation of
interdental septa
 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

30. 
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
these.

Exostoses have been described in rare
cases «is developing after the
placement of free gingival grafts

31. 
Trauma from occlusion may be
a factor in determining the
dimension and shape of bone
deformities.

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

32. 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
formation.

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
angular detects


33. 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

34. 







Horizontal bone loss
Vertical or angular defect
Osseous defects
Osseous craters
Bulbous bony contours
Reversed architecture
Ledges
Furcation involvement

35. 



The most common
pattern
Bone is reduced in
height
Bone margins remain
perpendicular to tooth
surface
Interdental septa, facial
and lingual cortical
plates are affected.

37. 



Occur in adults
Have been reports in
skulls with primary
dentition..
Presence is suggested
on radiographs
Careful probing and
surgical exposure of
areas is required.

38. Occur in oblique direction
Leaves a hollowed out trough in
the bone alongside root
 Base of defect is apical to the
surrounding bone.
 Angular defect and intrabony
periodontal pocket


Classified on basis of number of
walls:
one wall defect
two walled defect
three walled defect
combined osseous defect

39. Three bony walls
Combined
osseous defect
Two wall defect
One wall defect

41. 





Concavities in the crest of alveolar
bone
Confined to facial and lingual walls
Resons for high frequency
interdental craters:
interdentally area collects plaque
and is difficult to clean.
The normal flat or even concave
faciolingual shape of interdental
septum in lower molars favours
plaque formation.
Vascular patterns from gingiva to
crest-pathway for inflammation.

42. 
Bony enlargements
caused by exostoses,
adaptation to
function or
buttressing bone
formation.

Maxilla> Mandible

43. 


Defects produced
by loss of
interdental bone
Includes facial
plates and lingual
plates without
concomitant loss
of radicular bone.
Maxilla more
common

44. 
These are plateau like bone margins caused
by resorption of thickened bony plates.

45. 



It refers to the involvement of
bifurcations and trifurcations
of multirooted teeth by
periodontal disease.
Most common in mandibular
molars.
Least common in maxillary
premolar.
Furcation anatomy:
area of root separation
Surface coronal to root
separation
Root furcation

46. GRADEI :
Also called as early lesion.
Suprabony pocket involving soft tissue
Radiographic changes not usually found
as bone loss is minimal, but increase in
probing depth
GRADEII:
Bone destroyed in one or more surfaces
of furcation
Part of PDL, alveolar bone remains intact,
allows partial penetration of bone.
Radiograph may or may not show presence

47. 

GRADEIII :
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

48. 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)

50. Mandibular Molars
Buccal Furcation
Place the probe between
the two buccal roots from
the buccal aspect
Mandibular Molars
Lingual Furcation
Place the probe between
the two lingual roots from
the lingual aspect

51. 
Should include both
periapical and bitewing

Location of the
interdental bone and bone
level within the root
complex should be
examined

53. THANK
YOU..