2. CONTENTS
INTRODUCTION
CAUSES OF BONE DESTRUCTION IN PERIODONTAL DISEASE
Extension of gingival inflammation
Trauma from occlusion
Systemic disorders
FACTORS DETERMINING BONE DESTRUCTION IN PERIODONTAL DISEASE
BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE
LESIONS CAUSING ALVEOLAR BONE DESTRUCTION
CONCLUSION
REFERENCES
4. Receptors on chief cells of PTH
Release of PTH
Release calcium
Osteogenic substrates
BONE COUPLING
Osteoblasts
Monocytes
Osteoclasts
Bone
Introduction
Blood calcium
6. Causes of bone destruction
Gottlieb & Orban 1938 “senile atrophy”
Male patient aged 67 years old.
O/E: generalized class 1 gingival recession with
generalized interdental bone loss. No periodontal
pockets probed or tooth mobility observed.
8. BONE DESTRUCTION CAUSED BY EXTENSION OF GINGIVAL
INFLAMMATION
Gingivitis Periodontitis
Bacterial composition (Lindhe J et al 1980)
Cellular composition (Seymour & associates 1978, 1979)
Immunologic activity (Ruben M 1981)
9. Bone destruction caused by extension of gingival inflammation
Spread of inflammation
Gingiva
Blood vessels, collagen fibres
Alveolar bone
Marrow spaces
10. Bone destruction caused by extension of gingival inflammation
Bone destruction = Bone necrosis (Kronfeld R 1935)
Amount of infiltrate correlates with the degree of bone loss
Distance from the apical border of the infiltrate correlates
with number of osteoclasts (Rowe DJ 1981, Lindhe J 1978)
11. Bone destruction caused by extension of gingival inflammation
Pathways of spread of inflammation
A B
A – Interproximally
B – Facially& lingually
12. Bone destruction caused by extension of gingival inflammation
Radius of action
Garant and Cho 1979
Page and Schroeder 1982 (based on Waerhaug’s
experiments 1980)
1.5 – 2.5 mm
Tal H 1984 – human patients
13. Bone destruction caused by extension of gingival inflammation
Rate of bone loss (Loe & associates 1986)
~ 0.2 mm a year for facial surfaces
~ 0.3 mm a year for proximal surfaces
Rapid progression of
periodontal disease
(~ 8%)
CAL = 0.1 to 1mm
yearly
Moderately
progressive disease
(~ 81%)
CAL = 0.05 to 0.5mm
yearly
Minimal progression of
periodontal disease
(~ 11%)
CAL = 0.05 to 0.09mm
yearly
14. Bone destruction caused by extension of gingival inflammation
Periods of bone destruction
Page and Schroeder 1982 – inflammation
Seymour GJ 1979 – B-lymphocytes
Newman MG 1979 – microflora
Saglie RF 1987 – bacterial invasion + host defense
Periods of
inactivity
Periods of
activity
15. Gingival tissue
Release or
activation of
soluble mediators
Bacterial plaque
Soluble factor(s)
Alveolar bone
Bone
progenitor
cell
Osteoclast
3
1 2
4
5
Bone destruction caused by extension of gingival inflammation
Potential pathways for interaction between factors
in plaque and alveolar bone resulting in alveolar bone loss
Hausmann E 1974
16. Bone destruction caused by extension of gingival inflammation
Bone formation in periodontal disease
Retards the rate of bone loss
Newly formed osteoid more resistant to resorption than
mature bone (Irving JT 1969)
Buttressing bone formation
Affects the outcome of treatment
17. BONE DESTRUCTION CAUSED BY TRAUMA FROM OCCLUSION
In the absence of inflammation
When combined with inflammation
Glickman’s concept (1965, 1967)
Waerhaug’s concept (1979)
18. The systemic regulatory influence upon the respo
alveolar bone is termed
BONE DESTRUCTION CAUSED BY SYSTEMIC DISORDERS
Bone factor concept (Glickman I 1951)
nse of
the “bone factor” in periodontal
disease.
Local factors
Systemic factors
19. Bone destruction caused by systemic disorders
Role of “bone factor” in determining diagnosis and
prognosis
Positive bone factor
Negative bone factor
Patient’s age
Gingival
inflammation &
occlusal
disharmony
Bone loss
20. Bone destruction caused by systemic disorders
Clinical implications
Positive bone factor in a 42-year old
female with gingival inflammation
and poor oral hygiene but minimal
bone loss.
Negative bone factor in a 41-year
old female with gingival
inflammation and poor oral hygiene
but severe bone loss.
23. Factors determining bone destruction in periodontal disease
Exostoses
Nery EB 1977 – palatal exostoses (40%)
Buttressing bone formation (Lipping)
Food impaction
24. Bone destruction patterns in
periodontal disease
Classification
I. Goldman HM, Cohen DW (1958)
II. Prichard JF (1965)
III. Karn KW (1983)
IV. Grant DA, Stern IB, Listgarten MA (1988)
V. Papapanou NP, Tonetti MS (2000)
25. Bone destruction patterns in periodontal disease
I. Goldman HM, Cohen DW (1958)
Suprabony defect
Intrabony defect
• One-wall
• Two-wall
• Three-walls
• Combined
26. Bone destruction patterns in periodontal disease
II. Prichard JF (1965)
1. Thickened margin
2. Interdental crater
3. Hemiseptum
4. Infrabony defect with three osseous walls
5. Infrabony defect with two osseous walls
6. Infrabony defect with one osseous wall
7. Marginal gutter
8. Furcation involvement
9. Irregular bone margin
10. Dehiscence
11. Fenestration
12. Exostosis
27. Bone destruction patterns in periodontal disease
III. Karn KW (1983)
1. Crater
2. Trench
3. Moat
4. Ramp
5. Plane
6. Cratered ramp
7. Ramp into crater or trench
8. Furcation invasions
28. Bone destruction patterns in periodontal disease
IV. Grant DA, Stern IB, Listgarten MA (1988)
defects
A. Vestibular, lingual or palatal
associated with:
1. Normal anatomic structures
• External oblique ridge
• Retromolar triangle
• Mylohyoid ridge
• Zygomatic process
2. Exostosis and tori
• Mandibular lingual tori
• Buccal and posterior palatal exostosis
3. Dehiscences
4. Fenestrations
5. Reverse osseous architecture
B. Vertical defects:
1. Three walls
2. Two walls
3. One wall
4. Combination with a different number of
walls at the various levels of the defect.
C. Furcation defects:
1. Class I or incipient
2. Class II or partial
3. Class III or through and through
30. Bone destruction patterns in periodontal disease
Horizontal bone loss
Vertical or angular defects
31. Bone destruction patterns in periodontal disease
Vertical or angular defects (Nielsen JI 1980)
Prevalence rate: 60% of persons
Commonly seen involving interproximal surfaces
32. Bone destruction patterns in periodontal disease
Three – wall defect
Sarati et al (1968), Larato DC (1970) – posterior segment
33. Bone destruction patterns in periodontal disease
Two – wall defect
Crater-like – most common
Non-crater – like
36. Bone destruction patterns in periodontal disease
Osseous craters
Interproximal crater
with heavy ledges.
Pre-op & post-op.
37. Bone destruction patterns in periodontal disease
Saari et al (1968) – most common defect
i. Vulnerability of the col (Cohen 1959)
ii. Plaque retentive
iii. Interdental bony configuration (Manson 1963)
a. Spread of inflammation (Weinmann 1941, Goldman 1957)
b. Cancellous trabeculation is more reactive (Amprino &
Marotti 1964)
39. Bone destruction patterns in periodontal disease
Bulbous bone contours
Pre-operative buccal
view
Pre-operative
occlusal view
Post-operative
buccal view
40. Bone destruction patterns in periodontal disease
Ledges
Blunted interdental
septa with bone
ledges
Small crater with
heavy ledges
Hemisepta with
heavy ledges
41. Bone destruction patterns in periodontal disease
Reversed architecture
Positive Flat Negative
Negative
architecture
42. Bone destruction patterns in periodontal disease
Fenestrations and dehiscences
Dehiscence
Fenestrations
43. Bone destruction patterns in periodontal disease
Furcation involvement
Stage in the progress of tissue destruction
Increases with age (Larato DC 1970, 1975)
Horizontal / angular bone loss evident
Factors contributing to furcation involvement
44. Bone destruction patterns in periodontal disease
Classification by Glickman (1953)
Grade I Grade II
Grade III Grade IV
48. References
Manson JD. Bone morphology and bone loss in periodontal
disease. J Clin Periodontol 1976; 3: 14-22.
Schwtarz Z et al. Mechanisms of alveolar bone destruction in
periodontitis. Periodontology 2000 1997; 14: 158.1 72.
Goldman HM, Cohen DW. The infrabony pocket: classification
and treatment. J Periodontol 1958; 10: 272-291.
Karn KW et al. Topographic classification of deformities of the
alveolar process. J Periodontol 1984; 5: 336-340.
Papapanou NP, Tonetti MS. Diagnosis and epidemiology of
periodontal osseous lesions. Periodontol 2000 2000; 22: 8–21.