1. BONE LOSS AND PATTERNS OF
BONE DESTRUCTION IN
PERIODONTAL DISEASE
- Dr Aishwarya Pandey
- Department of Periodontology
- Banaras Hindu University

2. INTRODUCTION
■ Periodontium is composed of both soft and hard tissues in which alveolar bone
is the part that supports the teeth in both maxilla and mandible.
■ Alveolar bone formation occurs as the eruption of tooth takes place in order to
facilitate the osseous attachments to the periodontal ligament and disappears
once the tooth is lost.
 The height and density of the alveolar bone are normally maintained by an
equilibrium, which is regulated by local and systemic influences, between
bone formation and bone resorption.
 When resorption exceeds formation, both bone height and bone density may
be reduced.
 Bone loss is the ultimate and last consequence of the inflammatory
process observed in periodontitis.
• Therefore the existing bone level is the consequence of past pathologic
episodes, whereas changes present in the soft tissue of the pocket wall reflect
the presence of the inflammatory condition.

3. Causes of bone destruction

4. Bone Destruction Caused by the Extension of
Gingival Inflammation
• The most common cause of bone destruction in periodontitis is the extension of inflammation
from the marginal gingiva into the supporting periodontal tissues.
• The inflammatory migration of the bone surface and the initial bone loss that follows mark the
transition from gingivitis to periodontitis.
■ Periodontitis is always preceded by gingivitis, but not all gingivitis progresses to periodontitis.
Gingivitis Periodontitis Advanced Periodontitis

5. • The transition from gingivitis to periodontitis is associated with changes in the
composition of the bacterial biofilm.
• In advanced stages of disease, the number of motile organisms and spirochetes
increases, whereas the number of coccoid rods and straight rods decreases.
• The cellular composition of the infiltrated connective tissue also changes with
increasing severity of the lesion.
• Neutrophils predominate in stage 1 gingivitis, whereas the number of plasma cells and
blast cells increases gradually as the disease progresses.
• The extension of the inflammatory process into the supporting structures of a tooth
may be modified by the pathogenic potential of biofilm and the
susceptibility/resistance of the host

6.  Spread of inflammation
Gingiva
Blood vessels, collagen fibres
Alveolar bone
Marrow spaces
Enlargement of the marrow spaces
Thinning of the surrounding bony trabeculae
Destruction of the bone and a reduction in bone height
Bone destruction in periodontal disease is not a process of bone necrosis. It involves the activity
of living cells along viable bone.

7. Pathways of inflammation from the
gingiva into the supporting
periodontal tissues in a patient
with periodontitis
(A)
(1) Interproximally, from the gingiva
into the bone
(2) from the bone into the periodontal
ligament
(3) from the gingiva into the
periodontal ligament
(B)
(1) facially and lingually, from the
gingiva along the outer periosteum
(2) from the periosteum into the bone
(3) from the gingiva into the
periodontal
ligament

8.  Radius of Action
■ Locally produced bone resorption factors may need to be present in the
proximity of the bone surface to exert their action.
■ Page and Schroeder, postulated a range of effectiveness of about 1.5 mm to
2.5 mm in which bacterial biofilm can induce loss of bone.
■ Beyond 2.5 mm, there is little or no effect;
■ Large defects that greatly exceed a distance of 2.5 mm from the tooth surface
(as described in aggressive types of periodontitis) may be caused by the
presence of bacteria in the tissues itself.

9.  Periods of Destruction
■ Periodontal destruction occurs in an episodic, intermittent manner, with periods of
inactivity or quiescence that alternate with destructive periods that result in the loss of
collagen and alveolar bone and the deepening of the periodontal pocket.
■ Periods of destructive activity are associated with subgingival ulceration and an acute
inflammatory reaction that results in the rapid loss of alveolar bone.
■ It has been hypothesized that this coincides with the conversion of a predominantly T-
lymphocyte lesion to one with a predominantly B-lymphocyte–plasma cell infiltrate.
■ Microbiologically, these lesions are associated with an increase in 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.

10.  Mechanisms of Bone Destruction
■ The factors involved in bone destruction in periodontal disease are bacterial and host
mediated.
■ The bacterial biofilm products induce the differentiation of bone progenitor cells into
osteoclasts and stimulate gingival cells to release mediators that have the same effect.
■ Bacterial biofilm products and inflammatory mediators can also act directly on osteoblasts or
their progenitors, thereby inhibiting their action and reducing their numbers.
■ In addition, in patients with rapidly progressing diseases (e.g., 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 they play a role in periodontal disease. These include host-produced
prostaglandins and their precursors, interleukin-1α, interleukin-β, and tumor necrosis factor
alpha.
■ When injected intradermally, prostaglandin E2 induces the vascular changes that are seen
with inflammation and when injected over a bone surface, prostaglandin E2 induces bone
resorption.

11. Mechanisms of Bone Destruction

12.  Bone Formation in Periodontal Disease
■ Buttressing bone formation- Areas of bone formation are found immediately adjacent
to sites of active bone resorption and along trabecular surfaces at a distance from the
inflammation in an apparent effort to reinforce the remaining bone.
■ This confirms the intermittent character of bone resorption in periodontitis, and it is
consistent with the varied rates of progression observed clinically in individuals with
untreated periodontal disease.
■ The periods of remission and exacerbation (or inactivity and activity, respectively)
appear to coincide with the quiescence or exacerbation of gingival inflammation as
manifested by changes in the extent of bleeding, the amount of exudate, and the
composition of bacterial biofilm.
■ The presence of bone formation in response to inflammation, even in those with active
periodontal disease, has an effect on the outcome of treatment.
■ The basic aim of periodontal therapy is the elimination of inflammation to inhibit the
stimulus for bone resorption and therefore to allow the inherent constructive tendencies
to predominate.

13. Bone Destruction Caused by Trauma
From Occlusion
• Another cause of periodontal bone destruction is trauma from occlusion, which can occur in the
absence or presence of inflammation.
• In the absence of inflammation
• the changes caused by trauma from occlusion vary from increased compression and tension
of the periodontal ligament and increased osteoclasis of alveolar bone to necrosis of the
periodontal ligament and bone and the resorption of bone and tooth structure.
• These changes are reversible in that they can be repaired if the offending forces are
removed. However, persistent trauma from occlusion results in funnel-shaped widening of
the crestal portion of the periodontal ligament with resorption of the adjacent bone.
• These changes, which may cause the bony crest to have an angular shape, represent
adaptation of the periodontal tissues aimed at “cushioning” increased occlusal forces;
however, the modified bone shape may weaken tooth support and cause tooth mobility.
• When it is combined with inflammation, trauma from occlusion may aggravate the bone
destruction caused by the inflammation and results in bizarre bone patterns.

14. Bone Destruction Caused by
Systemic Disorders
• Local and systemic factors regulate the physiologic equilibrium of bone.
• When a generalized tendency toward bone resorption exists, bone loss
initiated by local inflammatory processes may be magnified. This systemic
influence on the response of alveolar bone, as envisioned by Glickman during
the early 1950s, considers a systemic regulatory influence in all cases of
periodontal disease.
• In addition to the virulence of biofilm bacteria, the nature of the systemic
component rather than its presence or absence influences the severity of the
periodontal destruction. This concept of a role played by systemic defense
mechanisms has been validated by the studies of immune deficiencies and host
modulation in severely destructive types of periodontitis.

15. • Osteoporosis is a physiologic condition of postmenopausal women that results in the
loss of bone mineral content as well as structural bone changes.
• Periodontitis and osteoporosis share a number of risk factors (e.g., aging, smoking,
certain diseases, medications that interfere with healing).
• Some studies show a relationship between skeletal density and oral bone density;
between crestal height and residual ridge resorption; and among osteopenia and
periodontitis, tooth mobility, and tooth loss.
• Periodontal bone loss may also occur with generalized skeletal disturbances (e.g.,
hyperparathyroidism, leukemia, histiocytosis X) via mechanisms that may be totally
unrelated to the more common biofilm-induced, inflammatory periodontal lesion.

16. Factors Determining Bone
Morphology in Periodontal Disease
# Normal Variation in Alveolar Bone
■ Considerable normal variation exists within the morphologic features of alveolar
bone, and this affects the osseous contours produced by periodontal disease.
■ The anatomic features that substantially affect the bone-destructive pattern of
periodontal disease include the following:
• Thickness, width, and crestal angulation of the interdental septa
• Thickness of the facial and lingual alveolar plates
• Presence of fenestrations and dehiscences
• Alignment of the teeth
• Root and root trunk anatomy
• Root position within the alveolar process
• Proximity with another tooth surface

17. Bone Destruction Patterns in
Periodontal Disease

18. I. Goldman HM, Cohen DW (1958)
Suprabony defect Intrabony defect
• One-walled
• Two-walled
• Three-walled
• Combined

19. Glickman (1964) :
1) Vertical or angular defects
2) Osseous craters
3) Bulbous bone contours
4) Reverse architecture
5) Ledges
6) Furcation involvement

20. • Horizontal Bone Loss
Horizontal bone loss in the
(A) Anterior region
(B) Posterior region
Horizontal bone loss is the most common pattern of bone loss in
periodontal disease.
- The bone is reduced in height, but the bone margin remains
approximately perpendicular to the tooth surface.
- The interdental septa and the facial and lingual plates are
affected but not necessarily to an equal degree around the same
tooth.

21. • Vertical or Angular Defects
 Vertical or angular defects are those that occur in an oblique direction, leaving a hollowed-out
trough in the bone alongside the root; the base of the defect is located apical to the surrounding
bone.
 Goldman and Cohen classified angular defects on the basis of the number of osseous walls.
Angular defects may have one, two, or three walls. Defects are identified by the number of
walls present.
 Continuous defects that involved more than one surface of a tooth, in a shape that is similar to a
trough, are called circumferential defects.
 If the number of walls in the apical portion of the defect is often greater than that in its occlusal
portion, the term combined osseous defect is used.

22. Clinical view of a vertical (angular)
defect mesial of the upper right central
incisor. The periodontal probe in a more
apical position than the surrounding walls
of the bony defect. Radiographic view of a
vertical (angular) defect
mesial of the upper right
central incisor.

23. Three Walled Defects
A. Clinical Picture of a
Three-wall defect mesial of
the maxillary first bicuspid
(mesial wall is missing)
(A) Three bony walls:
(1) distal
(2) lingual
(3) facial

24. Two Walled Defects
(B) Two-wall defect:
(1) distal
(2) lingual
B. Clinical Picture of a Two-
wall defect mesial of the
lower central incisor (labial
and mesial wall is missing)

25. One Walled Defects
(C) one-wall defect:
(1) distal wall only
C. Clinical Picture of a One-
wall defect mesial of the first
molar (buccal, lingual and
mesial walls are missing)

26. Combined Osseous Defects
Combined type of osseous defect.
Because the facial wall is half the
height of the distal (1) and lingual (2)
walls, this is an osseous defect with
three walls in its apical half and two
walls in its occlusal half.
Clinical Picture of a Combined type of
osseous defect.
Because the facial wall is half the
height of the distal (1) and palatal (2)
walls, this is an osseous defect with
three walls in its apical half and two
walls in its occlusal half.

27. ■ Osseous Craters
 Osseous craters are a specific type of two-wall defect; they present as concavities in the crest of the interdental bone that
is confined within the facial and lingual walls.
 Craters have been found to make up about one-third (35.2%) of all defects and about two-thirds (62%) of all mandibular
defects.
 They occur twice as often in posterior segments as in anterior segments.
 The following reasons for the high frequency of interdental craters have been suggested -
• The interdental area collects biofilm and is difficult to clean.
• The normal flat or even slightly concave buccolingual
shape of the interdental septum in the lower molars
may favor crater formation.
• Vascular patterns from the gingiva to the center of
the crest may provide a pathway for inflammation.
Diagrammatic representation of an osseous crater in a
buccolingual section between two lower teeth.
(A) Normal bone contour. (B) osseous crater.

28. ■ Bulbous Bone Contours
 Bulbous bone contours are bony enlargements that are caused by
exostoses, adaptation to function, or buttressing bone formation.
• Exostoses are outgrowths of bone of varied size
and shape.
• They can occur as small nodules, large nodules,
sharp ridges, spike like projections, or any
combination of these examples
 They are found more frequently in the maxilla than in the
mandible.
Palatal view of exostoses on the first and second molars.

29. ■ Reversed Architecture
 Reverse (or negative) alveolar bone architecture is the result of a loss of
interdental bone, without a concomitant loss of radicular (buccal or
lingual/palatal) bone, thereby reversing the normal (or positive) architecture.
 Negative architecture is more common in the maxilla of patients with
periodontitis.
Peaks of bone typically remain at the
facial and lingual/palatal line angles of
the teeth are known as Widow’s Peaks.

30. ■ Ledges
 Ledges are plateau-like bone margins that are caused by the resorption of thickened
bony plates.
Example of bone ledge on the lingual aspect of the bicuspid
and molar.

31.  Fenestration and Dehiscence
■ Fenestration is a localized defect in the alveolar bone that exposed the root
surface usually in the apical or middle third but did involve the alveolar
margin. The marginal bone is intact.
■ Dehiscence is a localized defect when the root is denuded of bone and extends
through the marginal bone.
■ These defects are more prevalent in the buccal aspect.
■ Anterior regions are frequently involved.

32. ■ Furcation Involvement
 The term furcation involvement refers to the invasion of the bifurcation and
trifurcation of multirooted teeth by periodontal disease.
 The mandibular first molars are the most common sites and that the maxillary
premolars are the least common.
 The number of furcation involvements increases with age.
 The denuded furcation may be visible clinically or covered by the wall of the
pocket.
 The extent of the involvement is determined by exploration with a periodontal
or Nabers probe.

33.  Glickman Classification (1953)
 Furcation involvements have been classified as grades I through IV according to
the amount of tissue destruction.
 Grade I involves incipient bone loss;
 Grade II involves partial bone loss (cul-de-sac);
 Grade III involves total bone loss with a through-and-through opening of the
furcation, but the opening of the furcation is not visible due to the gingiva,
which covers the orifice.
 Grade IV is similar to grade III but includes gingival recession that exposes the
furcation to view.

34. Grade I Grade II
Grade IV
Grade III

35. References
• Carranza’s clinical periodontology, 12th edition
• Lindhe J, ed. Textbook of Clinical Periodontology & implant dentistry, 6th ed.
• Glickman I. Clinical Periodontology. 4th Edition. WB Saunders Company.
• Goldman HM, Cohen DW. Periodontal Therapy. 6th Edition. The CV Mosby Company.
1988.
• Schwtarz Z et al. Mechanisms of alveolar bone destruction in periodontitis.
Periodontology 2000 1997; 14: 158.1 72.

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