The document discusses patterns of bone loss and destruction in periodontal disease. It states that while periodontitis is caused by bacterial plaque, bone loss is what leads to tooth loss. The most common type of bone loss is horizontal loss where bone height is reduced but the bone margin remains perpendicular to the tooth. Other patterns include intrabony (angular) defects, osseous craters in the interdental bone, bulbous bone contours, reversed architecture where facial/lingual plates are lost before root bone, and furcation involvement in multi-rooted teeth. Trauma from occlusion can also cause bone loss, especially when combined with inflammation.

1. Bone Loss and Patterns of
Bone Destruction
Chapter 28
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2. Bone Loss and Patterns of Bone
Destruction
• Although periodontitis is an infectious disease of the
gingival tissue, changes that occur in bone are crucial
because the destruction of bone is responsible for
tooth loss.
• The height and density of the alveolar bone are
normally maintained by an equilibrium, regulated by
local and systemic influences between bone
formation and bone resorption. When resorption
exceeds formation, bone height, density, or both are
reduced.
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3. BONE DESTRUCTION CAUSED BY EXTENSION
OF GINGIVAL INFLAMMATION
• The most common cause of bone destruction in periodontal
disease is the extension of inflammation from the marginal
gingiva into the supporting periodontal tissues.
• The inflammatory invasion of the bone surface and the initial
bone loss that follows mark the transition from gingivitis to
periodontitis.
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4. • Periodontitis is always preceded by gingivitis, but not all
gingivitis progresses to periodontitis. Some cases of
gingivitis apparently never become periodontitis, and others go
through a brief gingivitis phase and rapidly develop into
periodontitis. The factors that are responsible for the extension
of inflammation to the supporting structures and bring about
the conversion of gingivitis to periodontitis are not known at
this time.
• The extension of inflammation to the supporting structures of a
tooth may be modified by the pathogenic potential of plaque
or the resistance of the host.
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5. Rate of Bone Loss
the rate of bone loss may vary, depending on the type of disease
present. Löe and al identified three subgroups of patients with
periodontal disease based on interproximal loss of attachment
and tooth mortality:
1.Approximately 8% of persons had rapid progression of
periodontal disease, characterized by a yearly loss of
attachment of 0.1 to 1 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 to 0.09 mm yearly).
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6. Periods of Destruction
• The destructive periods result in loss of collagen and alveolar
bone with deepening of the periodontal pocket. The reasons
for the onset of destructive periods have not been totally
elucidated, although the following theories have been offered.
• Bursts of destructive activity are associated with subgingival
ulceration and an acute inflammatory reaction, resulting in
rapid loss of alveolar bone.
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7. Periods of Destruction con….
• Periods of exacerbation are associated with an
increase of the loose, unattached, motile, gram-
negative, anaerobic pocket flora, and periods of
remission coincide with the formation of a dense,
unattached, non motile, gram-positive flora with a
tendency to mineralize.
• Tissue invasion by one or several bacterial species is
followed by an advanced local host defense that
controls the attack.
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8. Mechanisms of Bone Destruction
The factors involved in bone destruction in periodontal
disease are bacterial and host mediated.
• 1- Bacterial plaque products induce the
differentiation of bone progenitor cells into
osteoclasts and stimulate gingival cells to release
mediators that have the same effect.
• 2- Plaque products and inflammatory mediators can
also act directly on osteoblasts or their progenitors,
inhibiting their action and reducing their numbers.
• 3- in rapidly progressing diseases such as localized
juvenile periodontitis, bacterial microcolonies or
single bacterial cells may be present between collagen
fibers and over the bone surface, suggesting a direct
effect.
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9. Mechanisms of Bone Destruction
4- Several host factors released by inflammatory cells are capable
of inducing bone resorption in vitro and can play a role in
periodontal disease. These include host-produced
prostaglandins, interleukin 1-α and -β, and tumor necrosis
factor (TNF)-α.
When injected intradermally, prostaglandin E2 induces the
vascular changes seen in inflammation; when injected over a
bone surface, it induces bone resorption in the absence of
inflammatory cells and with few multinucleated osteoclasts.
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10. Bone Formation in Periodontal Disease
• Areas of bone formation are also found
immediately adjacent to sites of active bone
resorption ,
• The response of alveolar bone to inflammation
includes bone formation and resorption;
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12. • but results from the predominance of resorption over
formation. New bone formation impairs the rate of
bone loss, compensating in some degree for the bone
destroyed by inflammation.
• These periods of remission and exacerbation
(or inactivity and activity, respectively)
appear to coincide with the quiescence or exacerbation of
gingival inflammation, manifested by changes in the
extent of bleeding, amount of exudate, and composition
of bacterial plaque.
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13. • The presence of bone formation in response
to inflammation, even in active periodontal
disease, has an effect on the outcome of
treatment. The basic aim of periodontal
therapy is the elimination of inflammation to
remove the stimulus for bone resorption and
therefore allow the inherent constructive
tendencies to predominate.
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14. BONE DESTRUCTION CAUSED BY TRAUMA
FROM OCCLUSION
• Another cause of periodontal destruction is trauma from
occlusion.
• Trauma from occlusion can produce bone destruction 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 resorption of bone and tooth structure. These changes are
reversible in that they can be repaired if the offending forces
are removed.
• When combined with inflammation, trauma from occlusion
aggravates the bone destruction caused by the inflammation
and causes bizarre bone patterns.
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15. Trauma from Occlusion:
• Trauma from occlusion may be a factor in
determining the dimension and shape of bone
deformities. It may cause a thickening of the
cervical margin of alveolar bone or a change in
the morphology of the bone.
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16. BONE DESTRUCTION PATTERNS IN
PERIODONTAL DISEASE
• Periodontal 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.
• Horizontal Bone Loss
• Bone Deformities (Osseous Defects)
• Vertical or Angular Defects
• Osseous Craters
• Bulbous Bone Contours
• Reversed Architecture
• Ledges
• Furcation Involvements
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17. Horizontal Bone Loss
• 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 roughly
perpendicular to the tooth surface. The
interdental septa and facial and lingual
plates are affected, but not necessarily to
an equal degree around the same tooth
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19. Bone Deformities (Osseous Defects)
• Different types of bone deformities can result
from periodontal disease. These usually occur in
adults and have been reported in human skulls
with deciduous dentitions. Their presence may
be suggested on radiographs, but careful
probing and surgical exposure of the areas is
required to determine their exact conformation
and dimensions.
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20. 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.
• In most instances, angular defects have accompanying
infrabony pockets; such pockets always have an
underlying angular defect.
• Angular defects are classified on the basis of the number
of osseous walls.
• The number of walls in the apical portion of the defect
may be greater than that in its occlusal portion, in which
case the term combined osseous defect is used
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21. Vertical or Angular Defects con…..
• Vertical defects occurring interdentally can
generally be seen on the radiograph,
although thick, bony plates sometimes
may obscure them. Angular defects can
also appear on facial and lingual or palatal
surfaces, but these defects are not seen
on radiographs. Surgical exposure is the
only sure way to determine the presence
and configuration of vertical osseous
defects.
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22. Vertical or Angular Defects con…..
• vertical defects increase with age. Approximately 60% of
persons with interdental angular defects have only a
single defect. Vertical defects detected radiographically
have been reported to appear most commonly on the
distal surfaces and mesial surfaces.
• However, three-wall defects are more frequently found
on the mesial surfaces of upper and lower molars.
• The three-wall vertical defect was originally called an
intrabony defect. This defect appears most frequently on
the mesial aspects of second and third maxillary and
mandibular molars. The one-wall vertical defect is also
called a hemiseptum.
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30. 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 (35.2%) of all defects and about two
thirds (62%) of all mandibular defects. They are twice as common in
posterior segments as in anterior segments.
• The following reasons for the high frequency of interdental craters
have been suggested:
 The interdental area collects plaque and is difficult to clean.
 The normal flat or even concave faciolingual shape of the interdental
septum in lower molars may favor crater formation.
 Vascular patterns from the gingiva to the center of the crest may
provide a pathway for inflammation
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32. Bulbous Bone Contours
• Bulbous bone contours are bony
enlargements caused by exostosis,
adaptation to function, or buttressing bone
formation. They are found more frequently
in the maxilla than in the mandible.
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34. Reversed Architecture
• Reversed architecture defects are
produced by loss of interdental bone,
including the facial plates, lingual plates,
or both, without concomitant loss of
radicular bone, thereby reversing the
normal architecture. Such defects are
more common in the maxilla.
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36. Ledges
• Ledges are plateau-like bone margins
caused by resorption of thickened bony
plates
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37. Furcation Involvements
• The term furcation involvement refers to the
invasion of the bifurcation and trifurcation of
multirooted teeth by periodontal disease.
• The prevalence of furcation involved molars is
not clear. Whereas some reports indicate that
the mandibular first molars are the most
common sites and the maxillary premolars are
the least common, others have found higher
prevalence in upper molars.
• The number of furcation involvements increases
with age
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38. Furcation Involvements con….
Furcation involvements have been classified as
grades I, II, III, and IV according to the amount
of tissue destruction.
• Grade I is incipient bone loss,
• Grade II is partial bone loss.
• Grade III is total bone loss with through-and-
through opening of the furcation.
• Grade IV is similar to grade III, but with gingival
recession exposing the furcation to view.
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41. Any Questions?
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