The document discusses the causes and mechanisms of periodontal bone defects, detailing the extent of bone destruction due to gingival inflammation and trauma from occlusion. It outlines patterns of bone destruction, classification of defects, and the impact of periodontal disease on bone morphology, including various types of bone loss and treatment approaches. The document emphasizes the importance of understanding these factors for effective diagnosis and management of periodontal conditions.

1. PERIODONTAL
BONE DEFECTS
Dr. Heenal Adhyaru

2. CONTENT
Causes of bone destruction:
 Bone destruction caused by extension of gingival inflammation
 Bone destruction caused by trauma from occlusion
Factors determining bone morphology in
periodontal disease
Bone destruction patterns in periodontal disease
Bone defects with particular disease
Diagnosis
Treatment
References
2

3. BONE DESTRUCTION
Bone
formation
Bone
resorption
3

4. The level of bone is the consequence of past
pathologic experiences, whereas changes in the
soft tissue of the pocket wall reflect the present
inflammatory condition.
When resorption exceeds formation, both bone
height and bone density may be reduced.
The destruction of bone is responsible for tooth
loss.
4

5. PATHWAYS OF
INFLAMMATION FROM
THE GINGIVA INTO THE
SUPPORTING
PERIODONTAL TISSUES
5
The pathway of the
spread of inflammation
of critical because it
affects the pattern of
bone destruction in
periodontal disease.

6. 1. EXTENSION OF
GINGIVAL
INFLAMMATION
6
Periodontitis is always
preceded by gingivitis,
but not all gingivitis
progresses to
periodontitis.
Factors responsible:
 Bacterial component
 Host component

7. Bacterial component
Change in composition
of bacteria
Pathogenic potential of
bacterial
Host component
Cellular composition of
the infiltrated
connective tissue
changes
Resistance of host:
 Degree of fibrosis: width of
attached gingiva
 Reactive fibrogensis and
osteogensis
7

8. HISTOPATHOLOGY
An area of inflammation
extending from the
gingiva into the
suprabony area
Inflammation that
extends from the pocket
area (top) between the
collagen fibers.
8

9. Reformation of
transseptal fibers above
the bone margin
However, root progression
of bone destruction
progress.
Prichaid F in 1961: Dense
transspetal fibers are of
clinical importance when
surgical procedure are
used to eradicate
periodontal pockets. They
form a firm covering over
the bone, which is
encountered after the
superficial granulation 9

10. The cortical layer at the top of
the septum has been destroyed,
and the inflammation penetrates
into the marrow spaces
Osteoclasts and Howship
lacunae in the resorption of
crestal bone.
10

11. RADIUS OF ACTION
Garant and Cho suggested that locally produced
bone resorption factors may need to be present in
the proximity of the bone surface to exert their
action.
Page and Schroeder: 1.5 mm to 2.5 mm
Beyond 2.5 mm, there is no effect; interproximal
angular defects can appear only in spaces that are
wider than 2.5 mm, because narrower spaces would
be destroyed entirely.
Aggressive types of periodontitis: presence of
bacteria in the tissues. 11

12. 12
A. Horizontal resorption
B. Horizontal resorption, incipient vertical resorption
C. Vertical resorption, bony pocket

13. RATE OF BONE LOSS
Loe and colleagues in 1986 in Sri Lankan tea
laborers with no oral hygiene and no dental care
found the rate of bone loss to average about
0.2 mm per year for facial surfaces and about
0.3 mm per year for proximal surfaces when
periodontal disease was allowed to progress
untreated
Gutman in 1978 stated that loss of attachment can
be equated with loss of bone, although attachment
loss precedes bone loss by about 6 to 8 months.
13

14. Loe and colleagues also identified the following
three subgroups of patients with periodontal
disease on the basis of the interproximal loss of
attachment and tooth mortality:
1. Approximately 8% of persons had a rapid
progression of periodontal disease that was
characterized by a yearly loss of attachment of
0.1 mm to 1.0 mm.
2. Approximately 81% of individuals had moderately
progressive periodontal disease with a yearly loss
of attachment of 0.05 mm to 0.5 mm.
3. The remaining 11% of persons had minimal or no
progression of destructive disease with a yearly
loss of attachment of 0.05 mm to 0.09 mm. 14

15. PERIODS OF
DESTRUCTION
Periodontal destruction occurs in an episodic,
intermittent manner, with periods of inactivity or
quiescence.
Theories:
1. Schoder-1980; Page RC-1982: Bursts of destructive
activity are associated with subgingival ulceration and
an acute inflammatory reaction, resulting in rapid loss
of alveolar bone.
2. Saymore GJ-1979: Bursts of destructive activity
coincide with the conversion of a predominantly T-
lymphocyte lesion to one with a predominantly B-
lymphocyte–plasma cell infiltrate 15

16. 3. Newman MG-1979: Periods of exacerbation are
associated with an increase of the loose,
unattached, motile, gram-negative, anaerobic
pocket flora, whereas periods of remission
coincide with the formation of a dense,
unattached, nonmotile, gram-positive flora with
a tendency to mineralize.
4. Saglie-1987: The onset of periods of destruction
coincides with tissue invasion by one or several
bacterial species and that this is followed by an
advanced local host defense that controls the
attack.
16

17. MECHANISMS OF
BONE DESTRUCTION
SCHWAR Z. MECHANISMS OF ALVEOLAR BONE DESTRUCTION IN
PERIODONTITIS. PERIODONTOLOGY 2000. 1997;14 : 158-172 17

18. 2. TRAUMA FROM
OCCLUSION
The zone of irritation and the
zone of co-destruction
according to Glickman.
In trauma from occlusion, the
inflammatory infiltrate
spreads directly into
periodontal ligament
LINDHE J. CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY
4TH EDITION 18

19. The changes caused by trauma from occlusion vary
from increased compression and tension of the
periodontal ligament.
Persistent trauma from occlusion results in funnel-
shaped widening of the crestal portion of the
periodontal changes which may cause the bony
crest to have an angular shape, represent
adaptation of the periodontal tissues aimed at
“cushioning” increased occlusal forces, but the
modified bone shape may weaken tooth support
and cause tooth mobility.
19

20. Widening of PDL space
(Arrow)- “cushioning”
effect
These changes are
reversible in that they
can be repaired if the
offending forces are
removed.
20

21. FACTORS DETERMINING
BONE MORPHOLOGY IN
PERIODONTAL DISEASE
Normal variation in alveolar bone
 The thickness, width, and crestal angulation of the
interdental septa
 The thickness of the facial and lingual alveolar plates
 The presence of fenestrations and dehiscences
 The alignment of the teeth
 Root and root trunk anatomy
 Root position within the alveolar process
 Proximity with another tooth surface
21

22. NORMAL VARIATION
IN ALVEOLAR BONE
22

23. EXOSTOSES
23

24. BUTTRESSING BONE
FORMATION
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.
(Lipping)
24

25. 25

26. BONE DESTRUTION
PATTERNS IN
PERIODONTAL
DISEASEPeriodontal disease alters the morphologic features
of the bone in addition to reducing bone height.
An understanding of the nature and pathogenesis
of these alterations is essential for effective
diagnosis and treatment.
26

27. CLASSIFICATION
Pritchard (1965)
Interproximal craters.
Inconstent margins.
Hemisepta.
Furcation involvement.
Intra bony defect (with
three osseous walls).
Combination of above.
Fenestration.
Dehiscence.
Glickman (1964)
Osseous craters.
Intra bony defect.
Bulbous bony contours.
Hemisepta.
In consistent margins.
Ledges.
Horizontal bone loss
27

28. HORIZONTAL BONE
LOSS
28

29. VERTICAL OR
ANGULAR DEFECTS
29

30. Suprabony Pocket Infrabony Pocket
Base of pocket coronal to level of
alveolar bone.
Base of pocket is apical to crest of
alveolar bone.
Pattern of bone destruction is
horizontal.
Pattern of bone destruction is
vertical.
Interproximally transseptal fibers
are arranged horizontally in the
space between the base of the
pocket and the alveolar bone.
Interproximally transseptal fibers
are oblique rather than horizontal.
On the facial and lingual surface,
the PDL fibers beneath the pocket
follow their normal horizontal
oblique course between the
healthy cementum of the tooth
and the alveolar bone.
On the facial and lingual surface,
the PDL fibers follow the angular
bone pattern of the adjacent bone.
They extend from the healthy
cementum between the base of the
pocket along the base and over the
crest to join with the outer
periosteum (over the bone).
30

31. Suprabony Pocket Infrabony Pocket
31

32. CLASSIFICATION
GOLDMAN HM &
COHEN DW-1958
A. THREE WALL DEFECT. B. TWO WALL
32

33. Combined defect Five wall defect
33

34. OSSEOUS CRATERS
34

35. The following reasons for the higher
frequency of interdental craters have
been suggested:
1. The interdental area collects plaque
and is difficult to clean.
2. The normal flat or even concave
faciolingual shape of the interdental
septum in lower molars may favor
crater formation.
3. Vascular patterns from the gingiva to
the center of the crest may provide a
pathway for inflammation.
35

36. BULBOUS BONE
CONTOUR
36

37. REVERSED
ARCHITECTURE
37

38. Peaks of bone typically remain at the facial and
lingual/palatal line angles of the teeth are known as
widow’s peaks.
38

39. LEDGES
Ledges are plateau
like bone margins
caused by resorption
of thickened bony
plates.
39

40. FENESTRATIONS AND
DEHISCENCE
40

41. FURCATION
INVOLVEMENT
The term furcation involvement refers to the
invasion of the bifurcation and trifurcation of
multirooted teeth by periodontal disease.
That the mandibular/ maxillary first molars are the
most common sites and the maxillary premolars are
the least common.
Furcation involvements have been classified
according to the amount of tissue destruction.
41

42. HORIZONTAL
CLASSIFICATION:
Glickman (1953)
1. Grade I is incipient involvement into a flute
of furcation with suprabony pockets and no
interradicular bone loss
2. Grade II is any involvement of the
interradicular bone without a through-and-
through ability to probe
3. Grade III is total bone loss with through-and
through opening of the furcation
4. Grade IV is similar to grade III, but with
gingival recession exposing the furcation to 42

43. 43

44. VERTICAL
CLASSIFICATION:
Tarnow and Fletcher:
Evaluating the degree of vertical involvement:
1. Subclass A: 1–3 mm
2. Subclass B: 4–6 mm
3. Subclass C: ≥ 7 mm
44

45. BONE DEFECTS WITH
PARTICULAR
DISEASE
1. Trauma from occlusion
2. Food impaction
3. Aggressive periodontitis
45

46. FOOD IMPACTION
46

47. AGGRESSIVE
PERIODONTITIS
47

48. DIAGNOSIS
CLINICAL
“Walking” of probe For Interdental craters
48

49. Transgingival probing/ Bone sounding
49

50. FOR FURCATION
INVOLVEMENT
50

51. RADIOGRAPHIC
Radiograph suggesting
two-walled defects
(craters) between the
first molar and adjacent
teeth and distal
furcation involvement
on the second molar
(arrows).
51

52. 52

53. TREATMENT
The periodontal flap is one of the most frequently
employed procedures particularly for moderate to
deep pockets in posterior areas.
Flaps are used for pocket therapy to accomplish the
following:
1. Increase accessibility to root deposits
2. Elimination or reduce pocket depth by resection
of the pocket wall
3. Expose the area to perform regenerative
methods.
53

54. MINIMALLY INVASIVE 54

55. OSSEOUS 55

56. 56

57. BONE FILL
REGENERATIVE 57

58. ONE WALLED DEFECT 58

59. CRATER-TYPE TWO-WALLED 59

60. THREE-WALLED 60

61. FURCATION 61

62. REEVALUATION OF THE
PATIENT WITH BONE
FILLS REGENERATION
PROCEDURE
62

63. Karn et al classification-1984
• To describe irregular defects:
1. Craters: Involves only one side
2. Trench: involves 2 or 3 sides
3. Moat: involves 4 sides. Circumferential defect

64. • When both alveolar bone and outer cortical bone plates are
lost:
1. Ramp: margins at different levels.
2. Plane: margins all at a similar levels. (Zero wall defects)

65. REFERENCES
1. Carranza’s Clinical Periodontology 10th edition
2. Edward S. Cohen, Atlas of Cosmetic and
Reconstructive Periodontal Surgery, Third Edition
3. Lindhe J. Clinical Periodontology and Implant
Dentistry 4th edition
4. Schwar Z. Mechanisms of alveolar bone
destruction in periodontitis. Periodontology
2000. 1997;14 : 158-172
5. Khairnar M. Classification of Food Impaction -
Revisited and its Management. Indian J Dent Adv
2013; 5(1): 1113-1119
6. Hall WB. Critical Decisions in Periodontogy. 4th
edition 65