4. 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.
In a study Heijl et al , were able to convert a
confined naturally occurring chronic gingivitis
into a progressive periodontitis in experimental
animals by placing a silk ligature into the
sulcus and tying it around the neck of the
tooth.
5. Pathways of Inflammation from the
gingiva into the supporting periodontal
tissues in periodontitis.
6. inflammation
Histopathological changes during
gingival inflammation
Gingival inflammation
extends along the
collagen fiber bundle and
follows the course of
blood vessels through
the loosely arranged
tissue around them into
the alveolar bone.
The inflammatory
infiltrate is concentrated
in the marginal
periodontium, the
reaction is a much more
diffuse one, often
reaching the bone and
eliciting a response
before evidence of
crestal resorption or loss
of attachment exists.
9. Less frequently,
the inflammation
spreads from the
gingiva in the
periodontal
ligament and from
there in the
interdental septum.
Facially and
Lingually,
inflammation from
the gingiva
spreads along the
outer periosteal
surface of the bone
and penetrates into
the marrow spaces
through vessel
channels in the
outer cortex.
10.
11. After inflammation reaches the bone, it spreads into
the marrow spaces and replaces the marrow with a
leukocytic and fluid exudate, new blood vessels and
proliferating fibroblasts.
Multinuclear osteoclasts and mononuclear
phagocytes increase in number, and the bone
surfaces appear, lined with Howship lacunae.
In the marrow spaces, resorption proceeds from
within, causing a thinning of the surrounding bony
trabeculae and enlargement of the marrow spaces,
followed by destruction of the bone and a reduction
in bone height .
12. Local Factors Involved In Bone
Destruction In Periodontal Disease
Plaque and its associated bacteria which populate the
periodontal pocket, release lipopolysaccharide and other
bacterial products into the sulcus, affecting both the immune
cells in the connective tissue as well as the osteoblasts.
These products induce local factor production including IL-1α,
IL-1β, IL-6, prostaglandin E2 and TNF-α.
13. These factors increase osteoclast formation and
activation as well as inhibit osteoblast function.
The bacterial products also affect the osteoblasts
directly, inhibiting their function and inducing factor
production and release, eventually inducing pre -
osteoclast differentiation and osteoblast activation.
14. 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 an human autopsy, postulated a
range of effectiveness of about 1.5 – 2.5 mm within which
bacterial plaque can induce loss of bone.
RADIUS OF ACTION
15. Beyond 2.5 mm there is
no effect.
Interproximal angular
defect can appear only in
spaces that are wider
than 2.5 mm because
narrower spaces would
be destroyed entirely.
Tal in 1984 corroborated
this with measurements
in human patients.
(Tal H. Relationship
between interproximal
distance of roots and the
prevalence of intrabony
pockets. J Periodontol
1984: 55: 604–607
16. Large defects greatly
exceeding a distance of 2.5 mm
from the tooth surfaces (as
described in aggressive types
of periodontitis) may be caused
by the presence of bacteria in
the tissues.
(Carranza FA Jr , Cabrini RL :
Histometric studies of
periodontal tissues
,Periodontics 5 :308 ,1967)
17. In a study of Sri lankan tea laborers with no oral
hygiene , Loe et al in 1986 , found rate of bone loss to
average about 0.2 mm a year for facial surfaces and
about 0.3 mm a year for proximal surfaces when
periodontal disease was allowed to progress
untreated .
(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)
RATE OF BONE LOSS
18. 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).
(Loe H, Anerud A , Boysen H : Natural history of periodontal
disease in man; the rate of periodontal destruction before 40 yrs of
age, J Periodontal 49:607;1978
Loe et al in 1978 identified the following three
subgroups of patients with periodontal disease
based on interproximal loss of attachment and
tooth mobility :
19. Periodontal destruction occurs in an episodic,
intermittent manner, with periods of inactivity or
quiescence .
The destructive periods leads to loss of collagen and
alveolar bone “ with deepening of the periodontal
pocket ’’.
PERIODS OF DESTRUCTION
20. 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)
21. 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)
25. Plaque products
induce the
differentiation of
bone progenitor cells
into osteoclasts and
stimulate gingival
cells to release
mediators that have
the same effect.
(Hausmann E, Raisz
LG , Miller WA ,1970)
They also act
directly on
osteoblasts or their
progenitors,
inhibiting their
action and
reducing their
numbers.
26. In addition, 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.)
Host factors released
by inflammatory cells
capable of inducing
bone resorption
includes
prostaglandins and
their precursors,
interleukin 1-α and β
and TNF-α.
27. 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
multinucleated
osteoclasts.
( Goodson JM ,
Haffajee AD ,
Socransky SS :1984 )
In addition non
steroidal anti
inflammatory drugs,
flurbiprofen or
ibuprofen, inhibit
PGE2 production,
slowing bone
destruction in
naturally occurring
periodontal diseases.
( Jeffcoat MK , William
RC , Wachter WJ et al ,
1986)
28. HAUSMANN CONCEPTS OF BONE LOSS
Bone progenitor cells induces the differentiation of
the cells into osteoclasts
Destroying bone through a non-cellular mechanism
Stimulates gingival cells, causing them to release
mediators, which inturn induce bone progenitor cells
to differentiate into osteoclasts
Cause gingival cells to release agents that can act
as cofactors in bone resorption
Cause gingival cells to release agents tha destroy
bone by direct chemical action without osteoclasts
31. RECEPTOR ACTIVATOR OF NUCLEAR FACTOR-KAPPA B LIGAND
RANKL
RANK/OPG 3.33:1.89 1.8:4.0
Crotti T, Smith MD, Hirsch R, et al. Receptor activator NF kappaB ligand (RANKL) and osteoprotegerin (OPG) protein
expression in periodontitis. J Periodontal Res 2003;38:380-387.
32. The effect of occlusal forces on
periodontium
MAGNITUDEDURATION FREQUENCY DIRECTION
33. TFO in absence of inflammation
persistent trauma from occlusion
results in “funnel-shaped widening” of
the crestal portion of the periodontal
ligament
"cushioning"
When combined with inflammation,
trauma from occlusion aggravates the
bone destruction caused by the
inflammation and results in bizarre bone
patterns.
34. 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.
35. Based on this concept, the
periodontal structures can be
divided into two zones:
Zone of irritation
Zone of co-
destruction
36. 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.
ZONE OF IRRITATION
37. 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
38. 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
39. WAERHAUG’S CONCEPT ( 1979 )
Waerhaug (1979)
measured the distance
between the
subgingival plaque and
the periphery of the
associated
inflammatory cell
infiltrate in the gingiva
and the surface of the
adjacent alveolar bone.(
in addition to Glickman
concept.)
He concluded that
angular bony defects
and infrabony pockets
occur equally often at
periodontal sites of
teeth which are not
affected by TFO as in
traumatized teeth.
40. Loss of connective
tissue attachment and
the resorption of bone
around teeth are
exclusively the result
of inflammatory
lesions associated with
subgingival plaque.
Angular bony defects
and infrabony pockets
occur when the
subgingival plaque of
tooth has reached a
more apical level than
the microbiota of the
neighboring tooth and
the volume of the
alveolar bone
surrounding the roots
is comparatively large.
41. CLINICAL TRIALS
Several authors had conducted clinical trials in
human patients and arrived at the following
conclusions:
Rosling et al, 1976 : The infrabony pocket located at
hypermobile teeth exhibited the same degree of
healing as those adjacent to firm teeth. (Rosling, B.,
Nyman, S. & Lindhe, J. (1976). The effect of
systematic plaque control on bone regeneration in
infrabony pockets. Journal of Clinical
Periodontology 3, 38-53.)
42. Fleszar et al, 1980 : Pockets
of clinically mobile teeth do
not respond as well to
periodontal treatment as
those of firm teeth
exhibiting the same
disease activity.
(Fleszar, T.J., Knowles,
J.W., Morrison, E.C.,
Burgett, F.G., Nissle, R.R. &
Ramfjord, S.P. (1980). Tooth
mobility and periodontal
therapy. Journal of Clinical
Periodontology 7, 495-505.)
Pihlstrom et al, 1986 : teeth
with increased mobility and
widened PDL space had, in
fact, deeper pockets, more
attachment loss and less
bone support than teeth
without these symptoms.
(Pihlstrom , B.L., Anderson
K.A., Aeppli D. & Schaffer
E.M. (1986). Association
between signs of trauma
from occlusion and
periodontitis. Journal of
Periodontology 57, 1-6.)
43. Burgett et al (1992) :
Probing attachment
gain was on the
average about 0.5mm
larger in patients who
received scaling and
occlusal adjustment
than in patients in
whom the occlusal
adjustment was not
included.
(Burgett F, Ramfjord
S., Nissle R., Morrison
E., Charbeneau T.&
Caffesse R. (1992). A
randomized trial of
occlusal adjustment in
the treatment of
periodontitis patients.
Journal of Clinical
Periodontology 19,
381-387
44. Neiderud et al, 1992 : Tissue alterations which
occur at mobile teeth with clinically healthy gingiva
may reduce the resistance offered by the
periodontal tissues to probing.
Neiderud, A-M., Ericsson, I. & Lindhe, J. (1992).
Probing pocket depth at mobile/ nonmobile teeth.
Journal of Clinical Periodontology 19, 754-759.
45. These studies involved the placement of high
crowns or restorations on the teeth of dogs or
monkeys, resulting in a continuous or intermittent
force in one direction.
When a tooth is exposed to unilateral forces of a
magnitude , frequency or duration that its
periodontal tissues are unable to withstand and
distribute while maintaining stability of the tooth,
certain well-defined reactions develop in the
periodontal structures to the altered functional
demand.
ANIMAL EXPERIMENTS
(Orthodontic Type Trauma)
46. When horizontally
directed forces are
applied, the tooth tilts
in direction of the
force resulting in the
development of
pressure and tension
zones within the
marginal and apical
parts, the tooth
becomes
hypermobile
temporarily, moves to
a new position and
healing takes place.
There is no gingival
inflammation or loss
of connective tissue
attachment in a
healthy periodontium.
47. Radiographic signs of TFO may include the following:
Increased width of periodontal space, often with
thickening of the lamina dura along the lateral aspect
of the root, in the apical region and in bifurcation
areas.
These changes do not necessarily indicate
destructive changes because they may result from
thickening and strengthening of the periodontal
ligament and alveolar bone, constituting a favorable
response to increased occlusal forces.
48. A “vertical” rather than
“horizontal” destruction
of the interdental septum.
Radioluscence and
condensation of the
alveolar bone.
Root resorption
49. FACTORS DETERMINING BONE MORPHOLOGY IN
PERIODONTAL DISEASE
Normal Variation in
Alveolar Bone
morphologic feature
(which affects the
osseous contours
produced by
periodontal disease)
The anatomic features
that substantially affect
the bone destructive
pattern in periodontal
disease include the
following:
50. 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. CLASSIFICATIONS
Goldman & Cohen (1958) classified angular
defects as:-
Depending on number of walls present –
Three osseous walls
Proximal, buccal and lingual walls
Buccal, mesial and distal wall
Lingual, mesial and distal walls
53. Two osseous walls
Buccal and lingual walls (crater)
Buccal and proximal wall
Lingual and proximal walls
54. One osseous wall
Proximal wall (hemiseptum)
Buccal wall
Lingual wall
Combination
Three walls plus two walls
Three walls plus two walls plus one wall
63. According to the classification by Goldman &
Cohen ( Goldman HM , Cohen WD. The infrabony pocket :
classification and treatment .J Periodontal 1958 )
Suprabony defects are those where the base of
the pocket is located coronal to the alveolar crest.
Infrabony defects, on the other hand, are defined
by the apical location of the base of the pocket
with respect to the residual alveolar crest.
66. According to Goldman HM & Cohen DW in 1958, angular
defects are classified on the basis of number of osseous walls
into one, two or three walls.
67. Frequently, intrabony defects present a
complex anatomy consisting of a three-wall
component in the most apical portion of the
defect, and two- and / or one-wall
components in the more superficial portions.
Such defects are frequently referred to as
combination defects.
68. Hemiseptal defects, that is, vertical defects
in the presence of adjacent roots and where
half of a septum remains on one tooth,
represent a special case of one wall defects.
69. However, most intrabony
defects are of mixed types;
eg, the entrance is one wall
or two walls but the bottom
is three walls.
A defect that extends to the
tooth and surrounds the
tooth continuously to two or
more roots is called
circumferential defect.
70. Vertical defects detected radiographically have
been reported to appear most commonly on the
distal surface
(Neilson JI, Glavind L, Karring T: J Clin Periodontol; 1980)
And mesial surfaces.
(Papapanou, Wennstrom , Grondahl ; Journal of clinical
periodontology.1988; 15(7):469-78. Radiographic and clinical
assessments of destructive periodontal disease.)
However three wall defects are more frequently
found on the mesial surfaces of upper and lower
molar.
(Larato DC in 1970)
71. OSSEOUS CRATERS
(Manson JD ,Nicholson K, The distribution of bone defects in chronic periodontitis ,
J Periodontal 1976)
72. Manson and Nicholson in 1974 reported that the
interdental crater was found to represent one third (
35.2 % ) of all maxillary defects and about two-thirds
(62 %) of all mandibular defects.
Early to moderate interproximal craters often do not
cause loss in papillary height.
They are seen as irregular areas of reduced
radiopacity in the alveolar bone crest.
( Manson JD ,Nicholson K : The distribution of bone defects in chronic
periodontitis, J Periodontal 54 : 88-92,1974.)
73. 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
(Ochsenbein C :A Primer for osseous surgery, Int J
Periodontics Restorative Dent 6(1):9,1986)
74. The heights of the facial and lingual crests
of a crater have been found to be identical in
85% of cases, with the remaining 15% being
almost equally divided between higher facial
crests and higher lingual crests.
75. 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
77. These are outgrowths
of bone of varied size
and shape.
Palatal exostoses has
been found in 40% of
human skulls.
(Nery EB, Corn H,
Eisenstein IL, 1977)
78. Buccal exostoses : These are seen in about 25% of
all teeth, and 77% of all individuals. They may be
expressed as alveolar margin lippings(18 % of all
teeth ) or as larger and more globular buccal
exostoses (7% of all teeth).
Lingual Exostoses : this may be seen in 11% of all
teeth, and in 50% of all individuals.
(Horning GM, Cohen ME, Neils TA, Buccal alveolar exostoses : prevalence
,characteristics and evidence for buttressing bone formation. J Periodontal
2000 ;71;1032 – 1042)
Several bony overgrowth occur on the vestibular
alveolar bone and are called multiple exostoses.
79. A definitive female sex predilection is characteristic
of this condition, which usually presents in the
canine – premolar area of the mandible or maxilla.
EXOSTOSES IN THE FACIAL
ASPECT OF SECOND
PREMOLAR AND MOLARS
80. They can occur as small nodules, large nodules,
sharp ridges, spike-like projections, or any
combination of these.
They have been described in rare cases as
developing after the placement of free gingival
grafts. (Pack ARC, Gaudie WM, Jennings AM: Bony exostoses as a
sequele of free gingival grafting : two case reports , J Periodontal 62 :
269,1991)
EXOSTOSES IN THE PALATAL ASPECT OF
FIRST AND SECOND MOLARS.
81. FENESTRATIONS AND DEHISCENCES
Isolated areas in which the root is denuded of
bone and the root surface is covered only by
periosteum and overlying gingiva is termed
Fenestrations.
When the denuded area extends through the
marginal bone, the defect is called Dehiscence.
82. They occur more often on the facial bone than on
the lingual and more common in anterior teeth
and frequently bilateral. These are important
because they may complicate the outcome of
periodontal surgery.
Approximately occurs on 20% of teeth.
83. Prominent root contours ,malposition and
labial protrusion of the root combined with
thin bony plate are predisposing factors.
( Elliot JR ,Bowers GM : Alveolar
Dehiscence and fenestrations. Periodontics 1 : 245 ,1963
)
84. BUTTRESSING BONE FORMATION
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”
85. 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”
Buttressing bone formation in response to trauma
from occlusion is a popular concept first proposed
by Glickman and Smulow more than 35 yrs ago.
(Glickman I ,Smulow J: Buttressing bone formation in
the periodontium, J Periodontal 36 : 365,1965 )
86. Buttressing bone formation has been described as
the development of thickened or exostotic buccal
alveolar bone in response to heavy occlusal forces.
In a study conducted by Horning GM ,Cohen, Neil's
- Buccal alveolar bone enlargements were found in
25% of all teeth examined :
18% were expressed as marginal bony lippings and
7% as buccal exostoses.
(J Periodontal Jun 2000 ; Vol 71 (issue 6) : pg
1032-42 )
87. BULBOUS BONE CONTOUR :
( Manson JD ,Bone morphology and bone loss in periodontal disease ,
JCP ,1976)
90. FURCATION INVOLVEMENT :
It refers to the invasion of the bifurcation and trifurcation of
multirooted teeth by periodontal disease.
(Larato DC , J Periodontal ,1975)
Mandibular first molar are the most common site and
maxillary premolar are the least common site.
91. CLASSIFICATION
One of the most widely used furcation
classification systems was developed by
Glickman (1958 ) .
In this system, furcation involvement is
divided into four categories, primarily on the
basis of the horizontal component of
destruction
92. GRADE I
Incipient bone loss or
early bone loss.
The pocket is suprabony
and primarily affects the
soft tissues.
Early furcation
involvement just into the
furcation is present.
93. GRADE II
Partial bone loss .
Distinct horizontal destruction
of the furcation area is present.
This lesion has been called a
"cul de sac" because destruction
may extend to any depth within
the furcation, but does not
extend all the way through the
furcation to its other side.
94. The extent of horizontal probing determines whether
the Grade II furcation is shallow or deep.
Vertical bone loss may or may not be present.
It can affect one or more furcations of the same
tooth.
95. GRADE III
Total bone loss with through
and through opening .
Bone is not attached to dome
of furcation.
In early lesion, opening may
be filled with soft tissue and
may not be visible.
R/G found as a radiolucent
area in the crotch of the tooth.
96. Destruction of bone and connective tissue all the
way through the furcation such that an instrument
can be passed from its opening to its exit.
The furcation defect is not visible to the eye
because the gingival tissues cover the furcation
entrance.
97. GRADE IV
Destruction of bone and
connective tissue all
the way through the
furcation.
Gingival recession has
occurred to the point that the
entire furcation invasion can
be seen on visual
examination.
98.
99. PREVALENCE OF OSSEOUS DEFECTS
Nielsen et al conducted a study on 209 adult
patients, osseous morphology was recorded in
radiographs, the lesions with a depth and width of
>= 2 mm were considered to be ‘‘periodontal
intrabony defects”.
(Nielsen IM, Glavind L, Karring T. Interproximal periodontal
intrabony defects. Prevalence, localization and etiological factors. J Clin
Periodontol 1980: 7: 187–198.)
18% of the subjects displayed >= 1 defects;
higher prevalence was noted in older age groups;
100. Defects occurred equally frequently with respect to
tooth type but more often at distal than mesial
surfaces.
The presence of intrabony defects correlated with
loss of attachment, increased tooth mobility, a wide
interproximal space and open interdental mesiodistal
contact relationships .
101. In a study by Papapanou et al - 531 dentate
individuals aged 25–75 years angular defects were
assessed in periapical or bite-wing radiographs.
(Papapanou PN, Wennstrom JL, Grondahl K. Periodontal status in
relation to age and tooth type. A cross-sectional radiographic study. J Clin
Periodontol 1988: 15: 469–478)
A defect was considered present if the ‘‘bottom of
the oblique radiolucency was located >= 2 mm
apical to the most coronal level of the
interproximal alveolar bone and radiographic signs
of bone resorption in the lateral boundary of the
defect was evident.
102. Angular defects were registered at 8% of all teeth .
The frequency increased with age.
It was higher at mesial than distal tooth surfaces
(ratio 1.6 : 1)
Defects occurred most frequently adjacent to
maxillary first premolars (14%) followed by
mandibular second molars (12%) and second
premolars (11%).
103. Wouters et al. studied 733 randomly selected dentate
individuals aged > =20 years; presence of ‘‘intrabony’’
defects was recorded in x5-magnified periapical
radiographs, defects were required to be >=1 mm
wide and >=2 mm deep.
Defects were recorded in 32% of the subjects.
104. The number of defects per subject ranged from 1
to 15.
Prevalence increased with age and was higher in
men than women and on mesial than distal tooth.
( Wouters FR, Salonen LE, Hellden LB, Frithiof L. Prevalence of
interproximal periodontal intrabony defects in an adult population in Sweden. A
radiographic study. J Clin Periodontol 1989: 16: 144–149.)
106. REFERENCES
Michael G. Newman, Henry H. Takei, Fermin A. Carranza;
Clinical periodontology,9th 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
107. 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
