BONE LOSS AND PATTERN

OF
BONE DESTRUCTION

Presented by :
Dr. Namita Adhikari
PG Resident
Department of Periodont ol ogy and Oral
Impl antology
 • Introduction
• Etiology of Bone destruction
• Mechanisms of bone
destruction
• Bone formation in
periodontal disease
• Bone destruction patterns in
periodontal disease
CONTENTS • Diagnosis
• Management
• Conclusion
• References
Click icon to add picture

INTRODUCTION

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
 Changes in the soft
Existing bone level –
tissue of the pocket
Past episodes of bone
wall reflects the
loss from the effects of
present inflammatory
periodontitis
condition

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BONE LOSS /
DESTRUCTION

1
Etiology of Bone Destruction

S
y
s
t
e
Extension of Gingival
Trauma From Occlusion
m Inflammation
i
c

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i
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 Extension of Gingival Inflammation

Gingivitis Periodontitis

“Periodontitis is always preceded by gingivitis, but not all gingivitis

progresses to periodontitis”

Inflammatory invasion of bone surface & initial bone loss - Marks

transition from gingivitis to periodontitis

Factors responsible for the extension of inflammation :

• Related to individual susceptibility to bacterial insult

• Microbiologic changes occuring in pocket environment and

surrounding tissues
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Heijl and coworkers (1976) - In experimental animals

Placed a silk ligature into the sulcus and tied

it around the neck of the teeth

Induced ulceration of the sulcular epithelium

• Shift in the inflammatory infiltrate from

predominantly plasma cells to PMNLs

• Osteoclastic resorption of the alveolar

crest

8
Seymour and colleagues (1978 and 1979) postulated a stage of
“contained” gingivitis
•TheTextension of inflammation is modified by :
lymphocytes - Preponderant
•Pathogenic potential
As the lesion becomesof plaque or
a B-lymphocytic, it becomes
Resistance of host
progressively destructive

Immunologic activity
Tissue-related mechanisms
 Degree of fibrosis of the gingiva
 Width of the attached gingiva
 Reactive fibrogenesis and osteogenesis that occur peripheral
to inflammatory lesion
 walling off by fibrin-fibrinolytic system
Histopathology

• Gingival inflammation extends along

the collagen fiber bundles
• Follows the course of blood vessels
through loosely arranged tissues
around them into alveolar bone

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Interproximally Facially and lingually
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• Along its course from gingiva to bone,
inflammation destroys gingival and
transeptal fibers, reducing them to
disorganized granular fragments interspersed
among inflammatory cells and edema

• Continuous tendency to recreate transeptal

fibers across the crest of interdental septum

12
In periodontitis, bone resorption may be related to the analogy of the
bone attempting to run away from the infectious/inflammatory process;
this may be seen as a host protection mechanism
 RADIUS OF ACTION

Garant and Cho in 1979 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 in 1982 , on the basis of Waerhaug’s

measurement made on human autopsy, postulated a range of
effectiveness of about 1.5 – 2.5 mm within which bacterial
plaque can induce loss of bone
1.5-
Interproximal angular defect can
appear only in spaces that are
2.5
wider than 2.5 mm because narrower spaces would be destroyed
entirely
Garant PR, Cho MJ: Histopathogenesis of spontaneous periodontal disease in
conventional rats. I. Histometric and histologic study, J Periodontal Res 14:297, 1979. 15
 RATE OF BONE LOSS

In a study of Sri Lankan tea laborers with no oral

hygiene, rate of bone loss averages about

Facial surface: 0.2 mm a year

Proximal surface: 0.3 mm a year

(Loe H, Anerud A , Boysen H : Natural history of periodontal disease in man; rapid, moderate, and no loss of attachment in
sri lankan laborers 14 to 46 yrs of age ,J Periodontal 13 :432,1986)

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On the basis of interproximal loss of attachment and tooth
mortality :

• Annual attachment loss of

8% - Rapid
attachment loss 0.1 to 1mm

• Annual attachment loss of

81%– Moderate
progression 0.05 to 0.5 mm

• Annual attachment loss of

11% - Minimum
or no progression 0.05 to 0.09 mm

Loe et al.
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Periods of Destruction

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 Period of destruction

Associated with subgingival ulceration & an acute

inflammatory reaction
Page RC,Schroeder 1982.

Conversion of a predominantly T-lymphocyte lesion to

predominantly B-lymphocyte–plasma cell infiltrate
Seymour 1979

Periods of exacerbation
Associated with an increase of the loose, unattached, motile,
gram –ve, anaerobic pocket flora Newman 1979

Periods of remission
Associated with formation of a dense, unattached, nonmotile,
gram-positive flora with a tendency to mineralize. Sagile
1987
Page RC, Kornman KS: The pathogenesis of human periodontitis:
Periodontology 2000 14:9–11, 1997

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MECHANISM OF BONE DESTRUCTION

Periodontology2000,Vol. 14, 1997

1. Bacterial plaque

Induce the differentiation of bone progenitor cells into

osteoclasts
Stimulate gingival cells to release mediators that have
the same effect
They also act directly on osteoblasts or their
progenitors, inhibiting their action and reducing their
numbers
 RANKL/ Hormones :
RANK/OPG PTH
2. Host mediated Calcitriol
Thyroxine

Host factors released by inflammatory cells capable of

inducing bone resorption includes prostaglandins
and their precursors, Interleukin 1-α and 1β and
TNF-α

ZVI Schwartz, Periodontology2000,Vol. 14, 1997

In rapidly progressing periodontitis, bacterial micro colonies
or single bacterial cells may be present between collagen
fibers and over the bone surface, suggesting a direct effect
(Schwartz Z , Goultschin J ,Dean DD et al : Mechanism of alveolar bone
destruction in periodontitis, Periodontal 2000,14: 158 ,1997)
In addition non steroidal anti inflammatory drugs,
flurbiprofen or ibuprofen, inhibit PGE2 production, slowing
bone destruction in naturally occurring periodontal diseases
When injected intradermally, PGE2 induces the vascular
changes seen in inflammation, when injected over bone
surface, it induces bone resorption in the absence of
inflammatory cell and within few
( Jeffcoat MKmultinucleated osteoclasts
, William RC , Wachter WJ et al , 1986)

( Goodson JM , Haffajee AD , Socransky SS :1984 )

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FACTORS REGULATING BONE RESORPTION

Interleuki
n-1

Gamma Sex
interferon steroids
Prostaglandins
and other
arachidonic
acid
metabolites
Colony Interleukin-
stimulating 6
factors
26
 Bone Formation in Periodontal Disease
Factorsregulatingboneformation

Platelet
derived
• Areas of bone formation - buttressing
growth factor bone formation

• Autopsy specimens show areas in which bone resorption

has ceased and new bone being formed on previously
Bone
eroded bone margins Insulin like Heparin
morphogen- growth binding
etic protein factor growth factor

Transforming
growth factor β
 Bone Destruction Caused by Trauma From
Occlusion

• In absence of inflammation

 Increased compression/tension of PDL  Necrosis in the

affected area

 Increased osteoclastic activity  Resorption of bone &

tooth structure

• These changes are reversible - Can be repaired if offending

forces removed
• Persistent TFO results in

Funnel-shaped widening of crestal

portion of PDL

Resorption of adjacent alveolar bone -

bony crest have an angular defect

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 When combined with inflammation ~
Bizzare bone pattern

Glickman’s concept (1965,

1967)

Waerhaug’s concept (1979)

Bone Destruction Caused by Systemic Disorders

• Systemic factors regulate the physiologic equilibrium of

• Peridontitis and osteoporosis share a number of risk factors
the bone
( aging, smoking, medication that interfere with healing )
• Generalized tendency for bone resorption exists- bone
• Generalized
loss initiatedskeletal disturbances-
by the local hyperparathyroidism,
inflammatory process is
leukemia,
magnifiedhistiocytosis X

Geurs NC; Relationship between periodontal bone loss and osteoporosis.

Periodontal 2000 ,44:29,2007 “Bone Factor Concept” Glickman (1950)
 Factors Determining Bone Morphology in Periodontal
Disease

Thickness, Width,
Presence of Proximity with
and crestal
fenestrations another tooth
angulation of the
and dehiscences surface
interdental septa

Root position
Alignment of Root and root
within alveolar
the teeth trunk anatomy
process

Thickness of
the facial and
lingual alveolar
plates
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• Angular osseous defects cannot form in thin facial or lingual
alveolar plates

• Entire crest of the plate gets destroyed, and height of bone is

reduced in a horizontal fashion

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PATTERN OF
BONE DESTRUCTION

2
 Classifications of bone destruction patterns
Prichard JF (1965)

1. Thickened margin
2. Interdental crater Karn KW (1983)
Glickman (1964) 3. Hemiseptum
1) Osseous craters 4. Infrabony defect 1. Crater
2) Infrabony defects with three, two or one 2. Trench
3) Bulbous bone osseous walls 3. Moat
contours 5. Marginal gutter 4. Ramp
4) Hemisepta 6. Furcation 5. Plane
5) Inconsistent margins involvement 6. Cratered ramp
6) Ledges 7. Irregular bone 7. Ramp into crater or
margin trench
8. Dehiscence 8. Furcation invasions
9. Fenestration
10. Exostosis
 EXOSTOSES

• Outgrowths of bone of varied size and

shape

• Occur as small to large nodules, sharp

ridges, spike like projection or
combination of these

• Both lingual tori and buccal exostoses

cause thicker bony masses which
provide conducive environment for
pocket formation and later funnel
shaped or trench like defect is formed
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 Buttressing bone formation (Lipping)

• When bone formation occurs in an attempt to

buttress bony trabeculae weakened by resorption

• Within jaw – Central

• External surface – Peripheral

• Sometimes accompanies production of osseous

craters & angular defects

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 Trauma From Occlusion

• It may cause a thickening of the cervical

margin of alveolar bone or a change in
bone morphology
(funnel-like crestal bone, buttressing bone)

• Inflammatory changes may later be

superimposed

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 Food Impaction

• Interdental bone defects may occur

• Interproximal resorption and

development of reverse bone
architecture

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 Aggressive Periodontitis

• Bone loss is usually horizontal in nature around incisors

• Vertical or angular pattern of bone destruction around first

molars

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 Bone Destruction Patterns In Periodontal Disease

Horizontal Bone Loss

• Most common pattern

• Bone - reduced in height, but bone margin

remains approximately perpendicular to the
tooth surface

• Interdental septa and the facial and lingual

plates affected but not necessarily to an equal
degree around the same tooth

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Vertical or Angular Defects

Those that occur in an oblique direction,

leaving a hollowed-out trough in bone
alongside the root

Base of defect located apical to

surrounding bone

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 Goldman and Cohen(1958)

On the basis of the number of osseous walls remaining

• One walled defect

• Two walled defect

• Three walled defect

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 • Vertical defects that occur interdentally can generally be seen
on the radiograph

• On facial and lingual or palatal surfaces, are more difficult to

visualize on radiographs

Vertical defects increase with age

Approximately 60% of people with interdental angular defects

have only a single defect (Nielsen and colleagues 1980)

Radiographically have been reported to appear most often on the

Three-wall defects are more frequently found on the mesial
distal and mesial surfaces
surfaces of the upper and lower molars
(Papapanou 2000)
(Larato DC 1970)
Circumferential osseous defect

Continuous defects that involved

more than one surface of a tooth, in
a shape that is similar to a trough

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 Combined defect

The number of walls in the apical portion of the defect is

often greater than that in its occlusal portion

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 OSSEOUS CRATERS

• Concavities in the crest of the interdental

bone that is confined within the facial
and lingual walls

• Make up about one third (35.2%) of all

defects & about two thirds (62%) of all
mandibular defects

• Occur twice as often in posterior

segments as in anterior segments

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The reasons for the high frequency of interdental craters :

 Interdental area collects biofilm and difficult to clean

Normal flat or even slightly concave bucco-lingual 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
Manson 1976, Saari 1968

Cancellous trabeculation is more reactive, i.e. has a more

rapid turnover than cortical bone (Amprino & Marotti 1964)
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 CLASSIFICATION OF CRATER

Class 1: 2-3 mm osseous concavity with relatively thick buccal

and lingual walls. Treated by palatal ramping

Class 2 : Osseous concavity 4-5 mm and thinner buccal and

lingual walls. Treated by buccal and palatal ramping

Class 3 : Concavities of 6- 7 mm with thin buccal and lingual

walls. Treated by both buccal and palatal ramping

Class 4 : Lesions with variable depth and thin buccal and lingual
walls

Ochsenbein and Bohannan (1964)

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• Walls of crater may be reduced at the
expense of buccal, lingual, or both walls

• Reduction should be made to remove the

least amount of alveolar bone required to
(a) Produce a satisfactory form
(b) Prevent the therapeutic invasion of
furcations
(c) Blend the contours with the adjacent
teeth

Selective reduction of bony defects by “ramping” the bone to

palatal or lingual to avoid involvement of the furcations
(Ochsenbein and Bohannan, 1964 and Tibbetts et al, 1976)
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Bulbous Bone Contours

Bony enlargements that are caused

by exostoses, adaptation to function
or buttressing bone formation

Found more frequently in the

maxilla than in the mandible

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Positive Architecture :
Interdental bone higher than the
radicular or facial bone

Reversed (Negative) Architecture:

Interdental bone is apical to the
radicular bone

Flat Architecture:
Interdental bone and radicular bone
are at the same level

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 Ledges

Plateau-like bone margins -caused

by the resorption of thickened bony
plates

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 Furcation Involvement

Invasion of bifurcation and trifurcation of multirooted teeth

by periodontitis

Glickman 1953

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The bone-destructive pattern may produce horizontal loss, but
angular osseous defects associated with intrabony pockets
may also exist and frequently crater develops in interradicular
area

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 Dehiscence and Fenestration

Fenestration: Isolated area in which the root is

denuded of bone and the root surface is covered only by
periosteum and overlying gingiva.

Dehiscence: Denuded areas extend through the

marginal bone

• Facial bone >Lingual bone

• Anterior teeth > posterior teeth

• Frequently bilateral

Prominent roots, labial protrusion of root, malposition

combined with thin bony plates (Elliot JR, Bowers GM)
 Trench

• When bone loss affects two or three confluent surfaces of

the same tooth
• Narrow ditch

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 Moat

Deformity totally encircling a tooth

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 Ramp

Deformity that results when both

alveolar bone and its supporting
bone lost to the degree in such a
manner that the margins of the
deformity at different levels

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 Cratered ramp

• When bone has been lost in the ramp

portion and the tooth interproximally,
may also be seen facial and lingual to
the teeth

• Usually seen in thick alveolar bone

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Ramp into crater or trench

Most coronal aspect of the deformity

is distinctly a ramp and the apical
portion is distinctly a crater or trench

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 Plane

• When both alveolar bone and supporting

bone is lost to the same degree such that
margins of deformity- at the same level

• It can be considered horizontal bone loss

about one tooth or portion of a tooth

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 Diagnosis

Radiographic diagnosis
• The height of interdental bone may be reduced, with the crest
perpendicular to the long axis of the adjacent teeth (horizontal bone
loss)

• or angular or arcuate defects (angular, or vertical, bone loss) could

form

• A reduction of only 0.5 to 1 mm in the thickness of the cortical plate is

sufficient to permit radiographic visualization of the destruction of the
inner cancellous trabeculae

• Radiographs do not indicate the internal morphology or depth of

crater-like defects

• Radiographs do not reveal the extent of involvement on the facial and

lingual surfaces
Surgical exposure
Management of osseous defects

Osseous
surgery

Additive Subtractive
 Rationale for osseous surgery

•  Most predictable pocket reduction technique

•Following
The majorsequential
rationale steps
for osseous resective
are suggested forsurgery is centered
resective osseous
to the view that discrepancies in level
surgery : and shapes of the bone
and gingiva predispose patientsgrooving
1.Vertical to the recurrence of pocket
postsurgically
2.Radicular blending
3.Flattening interproximal bone
• Reshape the marginal bone to resemble
4.Gradualizing that of the alveolar
marginal bone
process undamaged by periodontal disease

• Promote periodontal maintenance

 Regenerative surgery

Regeneration - Reproduction / reconstruction of a lost or

injured part in such a way that the architecture and function of
the lost or injured tissues are completely restored
(Glossary of Periodontal Terms, 1992)

Results from a
 Reconstructive study by Ellegaard
techniques and Löe (1971)
can be subdivided comprising
into three major 191
defects in 24approaches:
therapeutic patients with periodontal disease indicated that
complete
1) Non-bone regeneration, determined radiographically and by
graft-associated
periodontal probing, had occurred in around 70% of the three-wall
2) Graft-associated
defects, in 40%
3) Biologic of the combined new
mediator-associated two-wall and three-wall
attachment defects,
and regeneration
and in 45% of the two-wall defects.
The morphology of the osseous defect largely determines the
treatment technique to be used :

One-wall angular defects & Interdental crater - Recontoured

surgically (Ostectomy)

Two-wall angular defects can be treated with either method,

depending on their depth, width, and general configuration

Three-wall defects (narrow and deep) can be successfully

treated reconstructive surgery

Bony ledges, Exostoses: Osteoplasty

Osteoplasty and ostectomy – Done to patients with early to
moderate bone loss (2 to 3 mm) with moderate-length root
trunks that have bony defects with one or two walls
(Ochsenbein C- 1964)

Patients with deep, multiwalled defects - Treated with

regenerative therapies or by combining osteoplasty to reduce
bony ledges and to facilitate flap closure with new attachment
and regeneration procedures

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Correction of one-walled hemiseptal
defects -bone be reduced to level of
the most apical portion of defect

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 CONCLUSION

• Although periodontal disease is an infectious disease of

gingiva, changes that occur in bone are crucial because
destruction of bone is responsible for the tooth loss

• Patterns of bone destruction is caused by combination

of destructive and reparative process and is varied, so
the management should depend upon the type of bone
defect present.

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 REFERENCES

•Carranza’s Clinical Periodontology. 10th,13th edition. Lindhe’s, Clinical

Periodontology and Implant Dentistry. 5th edition.
•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.

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