- introduction - bone resorption - factors causing bone destruction in periodontal disease -- destruction by extension of gingival inflammation --- histopathology --- pathways of spread of inflammation --- radius of action --- periods of destruction ---- mechanism of destruction -- bone destruction caused by TFO -- bone destruction caused by systemic disorders - factors determining bone morphology in periodontal disease -- normal variation of alveolar bone -- exostosis -- butressing bone formation -- food impaction -- agressive periodontitis - patterns of bone destruction -- horizontal bone loss -- vertical or angular defects -- osseous craters -- bulbous bone contours -- reversed architecture -- ledges - furcation involvement -- classification -conclusion

2.  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

3.  The height and density of alveolar bone are
normally maintained by an equilibrium.
 Regulated by local and systemic influences between
bone formation and resorption.
 When resorption exceeds formation, both bone
height and density is reduced

4. 1) Extension Of Gingival Inflammation
2) Trauma from occlusion(TFO)
3) Systemic disorders

5. BONE DESTRUCTION CAUSED BY
EXTENSION OF GINGIVAL
INFLAMMATION
 Most common cause
 The inflammatory
invasion of bone surface
and the initial bone loss
marks the transition from
GINGIVITIS to
PERIODONTITIS
 “Periodontitis is always
preceded by gingivitis, but
not all gingivitis progress
to periodontitis”

6.  Extension of inflammation from marginal
gingiva to supporting tissues
 The transition from gingivitis to
periodontitis is associated with changes in
composition of bacterial plaque.
Composition of plaque
GINGIVITIS PERIODONTITIS
Coccid rods,
straight rods Motile organisms and
spirochetes
cells
Plasma cells PMNLs

7. HISTOPATHOLOGY
 Area of inflammation extending from gingiva into suprabony
area.
 course : along collagen bundle fibres, blood vessels, loosely
arranged tissues
 Extension of inflammation into centre of interdental septum.
 Cortical layer at top of septum are destroyed and inflammation
penetrates into bone marrow

8. PATHWAYS OF SPREAD OF
INFLAMMATION
 Facially and Lingually:
1. Gingiva to outer periosteum
2. Periosteum to bone
3. Gingiva to PDL
 interproximally:
1. from gingiva along the outer
periosteum
2. from gingiva into
periodontal ligament
3. from periosteum into bone

9. • gingival inflammation
• Replaced by leucocytes and fluid exudates, new blood vessels
and proliferating fibroblasts
• Increase in osteoclasts and mononuclear cells
• Resorption proceeds from within
• 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

10. RADIUS OF ACTION

11. RATE OF BONE LOSS
In individuals with no oral hygiene :
FACIAL SURFACE: 0.2mm/year
PROXIMAL SURFACE: 0.3mm/year

12. PERIODS OF DESTRUCTION
Periodontal destruction occurs
in episodic and intermittent
manner
Periods of inactivity and
destruction
Results in loss of collagen and
alveolar bone resulting in
deepening of periodontal pocket
Followed by an advance host
defense that controls the
attack

13. MECHANISM OF BONE
DESTRUCTION
BONE
DESTRUCTION
BACTERIAL
Differentiation of
bone progenitor
cells into
osteoclasts
Inhibit action of
osteoblasts
HOST MEDIATED
Release PGE2,
IL-α,IL-β,TNF-α

14. BONE DESTRUCTION CAUSED
BY TRAUMA FROM OCCLUSION
 Periodontal response to the
external force.
 TFO can occur in presence
or absence of inflammation.
 In the absence, effects on
alveolar bone ranges from
resorption to necrosis.
 Persistent TFO results in
angular defects of the bone.

15. o When combined with inflammation- ZONE OF CO-
DESTRUCTION
plaque induced inflammation entering into the zone
of trauma results in angular bone defects, BIZARRE
BONE PATTERN

16. BONE DESTRUCTION CAUSED
BY SYSTEMIC DISORDERS
 Possible relationship between periodontal bone
loss and systemic disorders.
 OSTEOPOROSIS : loss of bone mineral content and
structural bone changes. Risk factors ageing,
smoking, etc
 OSTEOPENIA : tooth mobility and tooth loss
 Hyperparathyroidism, leucopenia

17. 1) Normal variation of alveolar bone:
 thickness width, crestal angulations of
interdental septa
 thickness of facial and lingual septa
 presence of fenestrations and dehiscence
 root and trunk anatomy

18. 2) Exostoses:
 Exostoses are outgrowths of bone in varied
shapes and sizes
 They can occur as small nodules, sharp ridges,
spike like projections, or a combination of
these

19. 3) Buttressing bone formation:
 bone formation sometimes occurs in an
attempt to buttress bony trabeculae weakened
by resorption.
 When this occurs within the jaw it is termed as
central buttressing bone
 when it occurs on external surface it is is
termed as peripheral buttressing formation

20. 4) Food impaction:
 interdental bone defects occur where proximal
contact is abnormal or absent. In such areas
food impaction results in inverted bone
architecture
5) aggressive periodontitis:
 vertical or angular bone defects

21.  Horizontal bone loss
 Vertical bone loss
 Osseous craters
 Bulbous bone contour
 Reverse architecture
 Ledges
 Furcation involvement

22. HORIZONTAL BONE LOSS
 the most common pattern
 bone height is reduced, but bone margins
remain perpendicular to tooth surface.
 interdental septa, facial and lingual cortical
plates are affected

23. VERTICAL OR ANGULAR DEFECTS
 Occurs in an OBLIQUE
DIRECTION
 leads to a HOLLOWED –OUT
trough in the alongside bone
 classified on the basis of
number of walls:
› one wall defect/one osseous
wall
› two walled defect
› three walled defect
› combined osseous defect

25. OSSEOUS CRATERS
a) concavities in the crest of
interdental
bone confined within faciolingal
walls.
b) Reasons :
 plaque accumulation and
difficulty to clean.
 normal concavity in lower
molars
 vascular patterns from gingiva
to crest, a pathway for
inflammation

26. BULBOUS BONE CONTOURS
 bony enlargement
 an adaptation to Exostoses
 adaptation to function or buttressing bone
formation.
 maxilla>mandible

27. REVERSED ARCHITECTURE
 produced by loss of
interdental bone, facial
and lingual plates
without concomitant
loss of radicular bone
 maxilla more
commonly affected

28. LEDGES
 plateau-like bony margins
 caused by resorption of thickened bony
plates

29. FURCATION INVOLVEMENT
 Involvement of bifurcation or
trifurcation of multirooted
teeth by periodontal disease.
 SITE: most common in
mandibular molars, least
common in maxillary
premolar.

30. CLASSIFICATION --
GLICKMAN’S(1953) :
 GRADE I : Incipient bone loss,
suprabony pocket involving soft
tissue, no radiographic changes
 GRADE II : partial bone loss, bone
destroyed in one or more surfaces
of furcation, parts of PDL and
alveolar bone remains intact
 GRADE III : total bone loss with
through and thro ugh opening of
furcation, facial or lingual or both
orifices of furcation cannot be seen
because of soft tissue coverage
 GRADE IV : similar to grade III
with gingival recession exposing
the furcation to view

31.  Although periodontitis is an infectious
disease of the gingival tissue , changes that
occur in bone are crucial because
destruction of bone is responsible for tooth
loss.
 Bone loss patterns associated with
periodontal disease is varied and the type of
management depends upon the type of loss.