Patterns of bone destruction in periodontics

1. BONE LOSS AND
PATTERNS OF BONE DESTRUCTION
1
Dr.R.Dhivya ., MDS

2. 2
INTRODUCTION
CAUSES OF BONE DESTRUCTION
1. Extension of Gingival Inflammation
- Radius of action
- Rate of bone loss
- Periods of destruction
- Mechanisms of bone destruction
- Various pathways involved
- Formation of Bone
- Bone coupling
- Bone Remodelling
2. Trauma from occlusion
3.Systemic diseases
- Osteoporosis
- Diabetes Mellitus
- Stress
- Obesity
- Reactive oxygen species
- Rhematoid Arthritis
FACTORS DETERMINING BONE MORPHOLOGY
BONE DESTRUCTION PATTERNS
THERAPEUTIC STRATEGIES TO TREAT BONE RESORPTION
CONCLUSION
REFERENCE
CONTENT

3. BONE LOSS AND PATTERNS OF BONE DESTRUCTION
Periodontitis:
Infectious disease of the gingiva
Destruction of bone
Tooth loss
3

4. BONE LOSS AND PATTERNS OF BONE DESTRUCTION
Density and height of bone
Inflammation
Local factors
Trauma from occlusion
Systemic disorders
Equilibrium of bone resorption and formation
4

5. BONE LOSS AND PATTERNS OF BONE DESTRUCTION
Bone level : experience of past inflammation
Pocket change : present inflammatory condition
- Both are not necessarily correlated
5

6. BONE DESTRUCTION CAUSED BY EXTENSION OF GINGIVAL INFLAMMATION
Bacterial composition in plaque :
- motile, spirochetes increased
- cocoid, straight rod decreased
Cell composition in infiltrated connective tissue (ICT) :
- fibroblast, lymphocyte predominant
- plasma cell, blast cell predominant
Immune reaction :
- T-cell predominant B-cell predominant
6

7. BONE DESTRUCTION CAUSED BY EXTENSION OF GINGIVAL INFLAMMATION
Extension of inflammation
1. Pathogenic potential of plaque
2. Resistance of host :
- Immunologic activity
-Tissue-related mechanisms:
1.Fibrosis of gingiva
2.Width of attached gingiva
3.Reactive fibrogenesis & osteogenesis
7

8. HISTOPATHOLOGY
Area of inflammation extending from gingiva into suprabony area.
course : along collagen bundle fibres, blood vessels, loosely arranged tissues.
Area of inflammation
extending from the gingiva
into the suprabony area.
8

9. PATHWAYS OF INFLAMMATION
Interproximally
From gingiva into the bone
From the bone into the pdl
From gingiva into pdl
Facially and Lingually
From gingiva along the outer periosteum
From periosteum into the bone
From gingiva into pdl
9

10. - Recreate transseptal fibers
- Extension of Inflammation
- Multinuclear osteoclasts and Mononuclear phagocytes
- Bone destruction - not - bone necrosis - tissue necrosis
- Inflammatory infiltrate - correlates - bone loss - not - no. of osteoclasts
- Inflammatory infiltrate - alveolar crest – correlates - No. of osteoclasts - Total No. of osteoclasts
on the alveolar crest
10

11. BONE DESTRUCTION CAUSED BY EXTENSION OF GINGIVAL INFLAMMATION
 Radius of action
 Rate of bone loss
 Periods of destruction
 Mechanisms of bone destruction
 Bone formation in periodontal diseases
11

12. RADIUS OF ACTION
Garant and Cho
Page and Shroeder
12

13. RATE OF BONE LOSS
Loe et al in 1986 , found rate of bone loss to average about
# 0.2 mm/year for facial surfaces
# 0.3 mm/year for proximal
- when periodontal disease was allowed to progress untreated.
1. Approximately 8% of persons had rapid progression of
periodontal disease, characterized by a yearly loss of
attachment of 0.1 to 1.0 mm .
2. Approximately 81% of individuals had moderately progressive
periodontal disease, with a yearly loss of attachment of 0.05 to
0.5 mm
3. The remaining 11% of persons had minimal or no progression
of destructive disease (0.05 - 0.09 mm yearly).
J Periodontal 49 : 607;1978
13

14. PERIODS OF DESTRUCTION
Periodontal destruction occurs in
episodic and intermittent manner.
Periods of inactivity & destruction.
Destructive activity , results in loss
of collagen & alveolar bone.
14

15. Bursts of destructive activity are associated with sub gingival ulceration and
an acute inflammatory reaction resulting in rapid loss of alveolar bone.
(Page RC, Schroeder HE, Lindhe J in 1982)
Bursts of destructive activity coincide with the conversion of predominantly
t - lymphocytes to lesion to one with a predominance of B –lymphocytes -
plasma cell infiltration.
(Seymour GJ, Powell RN, Davies WJR in 1979)
Periods of
exacerbation are
associated with an
increase of the loose,
unattached, motile,
gram negative flora
with a tendency to
mineralize.
(Newman MG in
1979)
Tissue invasion by one
or several bacterial
species is followed by
an advanced local host
defense that controls
the attack.
(Saglie RF, Renzende
M, Pertuiser J, et al in
1987)
15

16. MECHANISM OF BONE DESTRUCTION
Bone destruction
Bacterial
Differentiation of
bone progenitor cells
into osteoclasts
Inhibit action of
osteoblasts
Host-mediated
Releases PGE2,
IL-1α,IL-1β,TNF-α
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17. 17

18. WNT SIGNALLING PATHWAY
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19. 19

20. ROLE OF BACTERIA AND CYTOKINES ON OSTEOCLAST
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23. 23

24. Bacterial virulence factors are capable of potentiating bone resorption themselves.
Endotoxin from Gram-negative cell walls activates CD4+ T cells to stimulate resorption via their
interaction with macrophages.
Porphyromonas gingivalis :
Pg produces a fimbrial protein that is a potent osteoclast stimulator via a tyrosine
kinase mechanism .
Aa comitans :
Aa produces a 62 kDa heat shock protein associated with the ability to stimulate bone
resorption at picomolar concentrations, as well as a peptide that acts as a potent IL-6 inducer in
fibroblasts andmonocytes
24

25. 25

26. 26

27. ROLE OF APC
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28. 28
INFLAMMATORY MEDIATORS

29. DESTRUCTION OF MINERAL ORGANIC MATRIX
29

30. 30
TNF – ALPHA PATHWAY

31. 31
NF – KAPPA – B PATHWAY

32. RANKL/OPG PATHWAY
32

33. JNK PATHWAY
33

34. 34

35. 35
ROLE OF MMPS

36. BONE FORMATION IN PERIODONTAL DISEASE
 Areas of bone formation: adjacent to resorption areas, and a little away –
Buttressing bone formation.
 Intermittent pattern of resorption is seen in periodontal disease.
 The basic aim in periodontal therapy- to remove the stimulus for resorption.
36

37. Calcium
blood levels
Release of
PTH
Stimulates
osteoblast
Release IL 1
& 6
Stimulates
Monocytes
to migrate
to bone
LIF+monocy
tes
Resorb bone
Release of Ca
PTH
Breakdown
of collagen
Release of
osteogenic
substrates
Stim & diff
of
osteoblasts
Deposition
of bone
37

38. BONE REMODELLING
38

39. BONE DESTRUCTION CAUSED BY TRAUMA FROM OCCLUSION
Trauma from occlusion
An injury to the attachment apparatus as a result of excessive
occlusal force. (Glossary of periodontic terms,1992)
Primary TFO :
A tissue reaction, caused by excessive and non-physiological
forces exerted on teeth with a normal, healthy and non -
inflamed periodontium.
Secondary TFO :
It is related to situations in which occlusal forces cause
damage in a periodontium of reduced height (attachment loss
present).
39

40. 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.
BONE LOSS
TFO
ABSENCE OF
INFLAMMATION
PRESENCE OF
INFLAMMATION
40

41. TFO in absence of inflammation
 Persistent trauma from occlusion results in “funnel-shaped widening” of the crestal
portion of the periodontal ligament and "cushioning"
TFO in presence of inflammation
 When combined with inflammation, trauma from occlusion aggravates the bone
destruction caused by the inflammation and results in bizarre bone patterns.
GLICKMAN’S CONCEPT
(1965, 1967)
The pathway of the spread of a
plaque-associated gingival lesion
can change if forces of an
abnormal magnitude are acting on
teeth harboring subgingival
plaque.
This would imply that the
character of the progressive tissue
destruction of the periodontium at
a "traumatized tooth" will be
different from that characterizing
a “non-traumatized" tooth.
41

42. Based on this concept, the
periodontal structures can
be divided into two zones:
Zone of
irritation
Zone of co-
destruction
42

43. ZONE OF IRRITATION
It includes the marginal and
interdental gingiva.
The soft tissues of this zone
are bordered by hard tissue
only on side and this zone is
not affected by forces of
occlusion.
Therefore, gingival
inflammation is the result of
irritation from microbial
deposits, not from trauma
from occlusion.
This zone includes the PDL,
the root cementum and the
alveolar bone.
It is coronally demarcated
by the transseptal and the
dentoalveolar collagen
fiber bundles and is the
seat of a lesion caused by
trauma from occlusion.
ZONE OF CO-DESTRUCTION
43

44. The fiber bundles which separate the zone of co-destruction from the
zone of irritation can be affected from two different directions:
from the
inflammatory
lesion maintained
by plaque in the
zone of irritation.
from trauma
induced changes
in the zone of co-
destruction
44

45. BONE DESTRUCTION CAUSED BY SYSTEMIC DISEASES
 Local and systemic factors regulate the physiologic equilibrium of the bone.
 Generalized tendency for bone resorption exists- bone loss initiated by the local
inflammatory process is magnified.
 This is called “Bone Factor Concept”. Proposed by Glickman 1950 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, leukopenia
45

46. 46
DIABETES MELITUS

47. 47
STRESS

48. 48
OBESITY

49. 49
REACTIVE OXYGEN SPECIES

50. 50
RHEUMATOID ARTHRITIS

51. FACTORS DETERMINING BONE MORPHOLOGY IN PERIODONTAL DISEASE
 Normal variations in alveolar bone
 Exostoses
 Trauma from occlusion
 Buttressing bone formation
 Food impaction
 Aggressive periodontitis
51

52. NORMAL VARIATION OF 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
dehiscence.
The alignment of
the teeth.
Root and root
trunk anatomy.
Root position
within the
alveolar process.
Proximity with
another tooth
surface.
52

53. EXOSTOSES
 Overgrowths of bone
 They can occur as small or large nodules, sharp ridges, spike-like projections.
 Buccal exostoses : These are seen in about 25% of all teeth, and 77% of all individuals.
 Lingual Exostoses : This may be seen in 11% of all teeth, and in 50% of all individuals.
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54. BUTTRESSING BONE FORMATION
 Buttressing bone formation has been described as the development of
thickened or exostotic buccal alveolar bone in response to heavy occlusal
forces.
 Bone formation sometimes occurs in an attempt to buttress the 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.
 This may cause bulging of bone contours, termed as “Lipping”
54

55. FOOD IMPACTION :
a) interdental bone defects occur when there
is abnormal or absence of proximal contact.
b) food impaction here , results in inverted
bone architecture.
AGGRESSIVE PERIODONTITIS :
a) vertical or angular bone defects.
55

56. BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE
 Bone deformities (osseous defects)
 Horizontal bone loss
 Vertical / angular defect
 Osseous crater
 Bulbous bone contour
 Reverse architecture
 Ledge
 Furcation involvement
56

57. BONE DEFORMITIES (OSSEOUS DEFECTS)
 Different types of bone deformities can result
from periodontal disease.
 These usually occur in adults but have also been
reported in human skulls with deciduous
dentitions.
 Their presence may be identified in radiographs,
but careful probing and surgical exposure of the
areas are required to determine their exact
conformation
57

58. CLASSIFICATION
ACCORDING TO GLICKMAN - 1964
ACCORDING TO PRICHARD – 1967
He expanded Glickman’s classification by including furcation involvement,
anatomic aberrations of alveolar process, exostoses & tori, dehisence &
fenestrations.
1. Osseous craters
2. Hemiseptal defects
3. Infrabony defects
4. Bulbous bone contours
5. Inconsistent margins and Ledges
6. Reversed architecture
58

59. ACCORDING TO GOLDMAN AND COHEN (1958)
Supra bony pocket
Infra bony pocket
Infra bony defect
1. one walled defect
2. two walled defect
3. three walled defect
4.combined defect
Craters
Inter radicular defects
Horizontal defects (Glickman’s)
1. Class I
2. Class II
3. Class III
Vertical defects (Tarnow & Fletcher)
1. Sub-class A
2. Sub-class B
3. Sub-class C
59

60. BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE
HORIZONTAL BONE LOSS
 Most common pattern of bone loss
 Bone is reduced in such a way that the bone margin
is approximately perpendicular to the teeth surface
 Interdental septa and facial and lingual plates of
bone are affected, but necessarily to an equal degree
around the same tooth.
 Zone of Irritation – Gingival tissues – alveolar bone
60

61. VERTICAL OR ANGULAR DEFECTS
 Vertical/ Angular defects occur in a oblique direction.
 This creates a hollowed-out trough in the bone alongside the root.
 The base of the defect is located apical to the surrounding bone.
 In most instances, angular defects have an accompanying
intrabony periodontal pockets.
 Zone of co- destruction – Transeptal fibers – Pdl – Angular bone
loss
61

62. TYPES OF ANGULAR DEFECTS
Classified based on the number of osseous wall…. (Goldman & Cohen)
1.ONE WALLED DEFECTS
2.TWO WALLED DEFECTS
3.THREE WALLED DEFECTS
4.COMBINED OSSEOUS DEFECTS
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63. A. THREE WALLED DEFECT - INTRABONY DEFECT
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64. B. TWO WALLED DEFECT
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65. C. ONE WALLED DEFECT - HEMISEPTUM
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66. D. COMBINED OSSEOUS DEFECT
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67. 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 make up about one-third of all defects
and about two-thirds of all mandibular defects.
 They occur twice as often in posterior segments as in anterior
segments.
Ochsenbein divided bony craters into three basic types :
Crater type Dimension
Shallow crater 1 -2 mm
Medium crater 3 -4 mm
Deep crater 5 mm or more
67

68. Heights of facial and lingual crests of the crater
- Equal in 85% cases
- Facial > Lingual in 6.5%
- Lingual > Facial in 6.5%
Several authors have also used descriptive terms to define special
morphological characteristics: funnel shaped defects, moat-like
defects, trenches
The high frequency of interdental craters have been attributed to
 The interdental area collects plaque and is difficult to clean
 The normal flat or even slightly concave faciolingual shape of the
interdental septum in lower molars may favor crater formation.
 Vascular patterns from the gingiva to the centre of the crest may
provide a pathway for inflammation. 68

69. BULBOUS BONE CONTOURS
 Bulbous bone contours are bony enlargements caused by
exostoses, adaptation to function, or buttressing bone
formation.
 They are found more frequently in the maxilla than in the
mandible.
REVERSED ARCHITECTURE
 They are produced by loss of interdental bone, including the
facial plates, without concomitant loss of radicular bone.
 The normal architecture of bone is thus reversed
 These defects are more commonly seen in the maxilla
69

70. LEDGES
- Ledges are plateau like bone margins
caused by resorption of thickened bony
plates
70

71. FURCATION INVOLVEMENT
 The term Furcation involvement refers to the
invasion of the bifurcation and trifurcation of
multi-rooted teeth by periodontal disease.
 Denuded furcation may be visible clinically or
covered by the wall of pocket.
 Extend of involvement is determined by
exploration with a blunt probe, along with a
simultaneous blast of warm air to facilitate
visualization.
--
71

72. CLASSIFICATION BY GLICKMAN -1958 (Horizontal)
Grade I - Incipient bone loss
Grade II - Partial bone loss (cul-de-sac)
Grade III - Total bone loss - through-and through
Grade IV - Bone loss similar to grade III with gingival recession
exposing the furcation area.
CLASSIFICATION BY TARNOW & FLETCHER-1984 (vertical)
1. Sub-class A (0-3mm)
2. Sub-class B (4-6mm)
3. Sub-class C (>7mm)
72

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74. POTENTIAL THERAPEUTIC STRATEGIES TO TREAT BONE RESORPTION
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76. CONCLUSION
76

77. REFERENCE
 Michael G. Newman, Henry H. Takei, Fermin A. Carranza; Clinical
periodontology,10th - edition.
 Jan Lindhe, Clinical Periodontology and Implant dentistry.
 Panos n. Papapanou & Maurizio S. Tonetti ; Diagnosis and epidemiology of
periodontal osseous lesions ; Periodontology 2000, Vol. 22, 2000, 8–21.
 Rose, Mealey, Genco, Cohen – Periodontics Medicine, Surgery and
Implants
 Marcello Cattabriga, Vinicio Pedrazzoli & Thomas G. Wilson Jr ; The
conservative approach in the treatment of furcation lesions ; Periodontology
2000, Vol. 22, 2000, 133–153
77

78.  KV ARUN. Molecular biology of periodontium
Molecular and cellular biology of alveolar bone- Jaro Sodek & Marc D.
Mckee - Perio 2000, vol.24 , 99 -126 .
 Grant and Lisgarten, Periodontics
 Buccal Alveolar Exostoses : Prevalence, Characteristics ,and Evidence for
Buttressing Bone Formation - Gregory M. Horning ,Mark E. Cohen and
Todd A. Neils, J Periodontal ,Vol- 71,Jun 2000
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