This document discusses bone destruction patterns seen in periodontal disease. It summarizes the different types of bone defects that can occur, including intrabony defects (1, 2, or 3 wall), angular defects, craters, dehiscences, and furcation involvement. Factors that can influence bone loss are also reviewed, such as the radius of effectiveness of bacterial plaque, rates of bone loss with/without treatment, trauma from occlusion, food impaction, and medical conditions. A variety of classification systems for bone defects are presented. Both clinical examinations and radiographs are important for diagnosis, though radiographs have limitations in depicting bone topography fully. Early diagnosis of risk factors can help prevent progression of periodontal disease and bone
4. Tissue necrosis & pus are present in periodontal disease,
Soft tissue wall of periodontal pockets
Not along the resorbing margin of the underlying bone.
4
5. RADIUS OF ACTION 5
Garant and Cho in 1979 locally produced bone
resorption factors may need to be present in proximity of
bone surface to exert their action.
Page and Schroeder in 1982 , on 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.
6. 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
6
7. RATE OF BONE LOSS
NO oral hygiene & NO dental care
Facial Surface : 0.2 mm a year
Proximal Surface : 0.3 mm a year
Rapid
progression
8 %
Loss of
attachment of
0.1- 1.0mm
Moderate
progression 81 %
Loss of
attachment of
0.05- 0.5mm
Minimal or
no
progression
11 %
0.05mm –
0.09mm
yearly 7
8. Mechanisms of Bone Destruction:
Several possible pathways by which products in plaque absorbed
by periodontal tissues could cause alveolar bone loss.
Hausman, 1974
8
Host factors:
• Prostaglandins
• IL-Iᵦ
• TNF-ᶛ
10. CHRONIC PERIODONTITIS:
Pocket depths are variable, and both horizontal and angular bone loss
can be found.
Tooth mobility often appears in advanced cases when bone loss has
been considerable.
Radiographically bone loss is usually horizontal.
10
11. Clinically, there is a small amount of plaque, which forms a
thin bio-film on the tooth and rarely mineralizes to become
calculus.
Mobility first molars & incisors
Distolabial migration of the incisors.
AGGRESSIVE PERIODONTITIS:
11
12. The progression of bone loss and attachment loss may be self-arresting.
Vertical loss of alveolar bone around first molars and incisors is seen. An
"arc-shaped" loss of alveolar bone extending from distal surface of second
premolar to mesial surface of second molar.
12
13. 13
GLICKMAN’S CONCEPT (1965, 1967)
Pathway of spread of plaque-associated gingival lesion can change if
forces of abnormal magnitude acting on teeth harboring subgingival
plaque.
This would imply the character of progressive tissue destruction of
periodontium at a "traumatized tooth" will be different from that a “non-
traumatized" tooth.
14. Based on this concept, the
periodontal structures can be
divided into two zones:
Zone of irritation
Zone of co-
destruction
14
15. In absence of inflammation, changes caused by TFO vary from
increased compression and tension of PDL and increased
osteoclasts of alveolar bone, necrosis of periodontal ligament,
resorption of bone and tooth structure.
TRAUMA FROM OCCLUSION:
15
16. Trauma from occlusion results in funnel-shaped widening of the
crestal portion of the periodontal ligament.
16
17. Interdental defects often occur where proximal contacts is abnormal or absent.
Pressure and irritation from food impaction contributes to inverse architecture.
FOOD IMPACTION:
Poor proximal relationship be result of shift in bone position because of
extensive bone destruction preceding food impaction.
In such cases food impaction is the complicating factor rather than the cause of
bone destruction.
17
20. INTRABONY DEFECT
Depending on number of walls present , angular defects
were classified by Goldman and Cohen (1958) as
(i) Three osseous walls
(ii) Two osseous walls
(iii) One osseous wall
(iv) Combination
20
21. z
Glickman (1964) :
1) Vertical or angular defects
2) Osseous craters
3) Bulbous bone contours
4) Reverse architecture
5) Ledges
6) Furcation involvement
21
23. 23
Concavities in the crest of alveolar
bone.
Confined to facial and lingual walls.
Reason for high frequency interdental
craters:
1. Interdentally area collects plaque and
is difficult to clean.
2. Normal flat or even concave
faciolingual shape of interdental
septum in lower molars favours
plaque formation.
24. (Ochsenbein C :A Primer for osseous surgery, Int J Periodontics Restorative Dent 6(1):9,1986)
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
24
26. •PLANE: Both alveolar bone and supporting bone is lost to same degree
such that margins of deformity are at same level. Considered horizontal bone
loss about one tooth or portion of a tooth.
•HEMISEPTA: Associated with an inconsistent osseous margin. Hemisepta
occur between anterior as well as posterior teeth, and they are found in
combination with all other types of bony deformities.
26
27. These are outgrowths of
bone of varied size and
shape.
Palatal exostosis has
been found in 40% of
human skulls.
(Nery EB, Corn H,
Eisenstein IL, 1977)
EXOSTOSIS
27
28. z
BUTTRESSING BONE
FORMATION
Bone formation sometimes occurs
in an attempt to buttress the boy
trabeculae weakened by
resorption.
When it occurs on the external
surface, it is referred to as
“peripheral buttressing bone”
formation. may cause bulging of
the bone contour, which
sometimes accompanies the
production of osseous craters and
angular defects
28
(Glickman I ,Smulow J: Buttressing bone formation in the periodontium, J Periodontal 36 : 365,1965 )
29. z
This bulging of bone contours, termed as “Lipping”
Buttressing bone formation described as development of
thickened or exostotic buccal alveolar bone in response
to heavy occlusal forces.
29
30. 30
Defects produced by
loss of interdental
bone.
Includes facial plates
and lingual plates
without concomitant
loss of radicular bone.
Maxilla more common.
32. THICKENED MARGIN: An enlargement of facial
or lingual marginal alveolar plate, instead of a thin,
tapering, slightly rounded bony margin.
• MARGINAL GUTTER: A shallow
linear defect between marginal bone of
radical cortical plate or interdental crest,
extending the length of one or more root
surfaces.
32
33. 33
• Bony enlargements caused
by exostosis, adaptation to
function or buttressing bone
formation.
• Maxilla > Mandible
34. FENESTRATION :Isolated areas
in which root is denuded of bone &
root surface covered only by
Periosteum & overlying gingiva .
DEHISCENCE:
When the denuded areas extend
through marginal bone,
defect is called Dehiscence.
34
36. It is the invasion of bifurcations and trifurcations of
multirooted tooth by periodontal disease. (AAP 1992)
Furcation Defects
GRADE 1 GRADE 2
GRADE 3 GRADE 4
36
37. z
GOLDMAN’S & COHEN CLASSIFICATION(1958)
Grade I :
Incipient.
Grade II :
Cul-de-
sac
Grade III:
Through
and
through
37
38. 38
Most common pattern .
Bone is reduced in height .
Bone margins remain
perpendicular to tooth surface.
Interdental septa , facial and lingual
cortical plates are affected.
39. 39
Occur in oblique direction .
Leaves a hollowed out trough in
the bone alongside root .
Base of defect is apical to the
surrounding bone.
Angular defect and intrabony
periodontal defect.
41. Peri-implantitis : Infectious disease that causes inflammation of the surrounding gum
and bone of an already integrated dental implant, leading to the loss of supporting bone
Smoking definitely causes constriction of blood vessels which
leads to bone loss.
Medical issues such as diabetes, osteoporosis and poor
immune systems are more at risk for developing bone loss
around dental implants .
41
42. Careful probing reveals presence of pocket depth greater than that of
normal gingival sulcus.
Location of base of pocket in relative to mucogingival junction and
attachment level on adjacent teeth, the number of bony walls and
presence of furcation defects.
CLINICAL:
42
43. Transgingival probing, or sounding, under local anesthesia confirms
the extent and configuration of infrabony component of the pocket or
of furcation defects.
Probe should be "walked" along tissue-tooth interface, so as to feel the
bony topography.
Probe may also be passed horizontally through the tissue to provide
three-dimensional information regarding bony contours.
43
44. • Shows amount of remaining bone rather than amount lost.
• Amount of bone loss is estimated as-
Difference between the physiologic bone loss of the patient & the height of
the remaining bone.
• Distance from CEJ to the alveolar crest-
In adolescents- 2mm
May be greater in older patients
RADIOGRAPHIC DIAGNOSIS:
44
45. • Although radiographs cannot accurately reflect the bony morphology buccal
and lingual, they provide useful information on interproximal bone levels.
• However, even at this level, the exact topography of defects cannot be
assessed accurately from radiographs.
45
46. CBCT
Cone beam CT (CBCT) is still underused for periodontal diagnosis.
Research comparing use of three-dimensional (3D) volumetric images and 2D images in
artificial bone defects have shown that CBCT has a sensitivity of 80–100% in detection and
classification of bone defects.
While intraoral radiographs present a sensitivity of 63–67%.
When compared with periapical and panoramic images, CBCT has also shown an
absence of distortion ,overlapping and dimensions it presents are compatible with the
actual size.
Vandenberghe B 2007
46
47. • So there is a need for early diagnosis and identification of these factors
such as local factors, TFO, Smoking, Stress, Systemic Disorders,
prevention of which would further prevent progression of the disease”.
Conclusion
Prevention is
better than
cure”
47
49. THANK YOU
49
Dr. Soundarya Singh
Lecturer
Department of Periodontology
Subharti Dental College and Hospital
Meerut
Hinweis der Redaktion
Pathways of spread of inflammation from the gingiva into the supporting periodontal tissues in periodontitis.
A=1- interproximally from gingiva into bone
2- from bone into periodontal ligament
3- from gingiva into periodontal ligament
B =1- facially & lingually from gingiva along the outer periosteum.
2- from periosteum into bone
3- from gingiva into periodontal ligam.
Histopathology
After inflammation reaches the bone via extension from the gingiva (Fig. 19.6), it spreads into the marrow spaces and replaces the marrow with a leukocytic and fluid exudate, new blood vessels, and proliferating fibroblasts (Fig. 19.7). Multinuclear osteoclasts and mononuclear phagocytes increase in number, and the bone surfaces appear to be lined with Howship lacunae
In the marrow spaces, resorption proceeds from within and causes a thinning of the surrounding bony trabeculae and an enlargement of the marrow spaces; this is followed by the destruction of the bone and a reduction in bone height. Normally, fatty bone marrow is partially or totally replaced by a fibrous type of marrow in the vicinity of the resorption.
Bone destruction in periodontal disease is not a process of bone necrosis . It involves the activity of living cells along viable bone.
When tissue necrosis and pus are present in periodontal disease, they occur in the soft tissue wall of periodontal pockets, not along the resorbing margin of the underlying bone.
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.
Plaque can induce bone loss within 1.5-2.5mm Page and Schroeder (1982), on the basis of Waerhaug's (1980) measurements made on human autopsy specimens, postulated that there is a range of effectiveness of about 1.5 to 2.5 mm within which bacteria/ plaque can induce loss of bone.
Beyond 2.5 mm, there is no effect; interproximal angular defects can appear only in spaces that are wider than 2.5 mm because narrower spaces would be destroyed entirely. Tal corroborated this with measurements in human patients.
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 tissues.
(Carranza FA Jr , Cabrini RL : Histometric studies of periodontal tissues Periodontics 5 :308 ,1967)
In a study of Sri Lankan tea laborers with no oral hygiene and no dental care, Löe et al. found the rate of bone loss to average about 0.2 mm/year for facial surfaces and about 0.3 mm/year for proximal surfaces when periodontal disease was allowed to progress untreated.
Löe et al. also identified the following three subgroups of patients with periodontal disease on the basis of the interproximal loss of attachment and tooth mortality Approximately 8% of persons had a rapid progression of periodontal disease that was characterized by a yearly loss of attachment of 0.1–1.0 mm.
Approximately 81% of individuals had moderately progressive periodontal disease with a yearly loss of attachment of 0.05–0.5 mm.
3. The remaining 11% of persons had minimal or no progression of destructive disease with a yearly loss of attachment of 0.05– 0.09 mm.
(loss of attachment can be equated with loss of bone although attachment loss precedes bone loss by about 6–8 months):
Many investigations have been conducted but the mechanism by which inflammation and/or plaque-derived products destroy bone in inflammatory periodontal disease have not yet been determined.
There are ………..
Mechanisms of bone destruction
The factors involved in bone destruction in periodontal disease are bacterial and host mediated
1.Absorbable products from plaque as, for example, complexing agents…………… could stimulate bone progenitor cells in the periodontium to differentiate into osteoclasts, which resorb alveolar bone.
2. Complexing agents & hydrolytic enzymes could destroy alveolar bone through non-cellular mechanism by dissolving bone mineral and hydrolyzing the organic matrix.
CHRONIC PERIODONTITIS:
The characteristic findings in slowly progressive periodontitis are gingival inflammation, which results from the accumulation of plaque, and loss of periodontal attachment and alveolar bone, which results in formation of a pocket.
Pocket depths are variable, and both horizontal and angular bone loss can be found.
Tooth mobility often appears in advanced cases when bone loss has been considerable.
Radiographically bone loss is usually horizontal
AGGRESSIVE PERIODONTITS:
Localized:
Clinically, there is a small amount of plaque, which forms a thin bio-film on the tooth and rarely mineralizes to become calculus.
The most common initial symptoms are mobility of the first molars and incisors, distolabial migration of the incisors.
Bone loss is about 3-4 times faster than in chronic periodontitis.
The progression of bone loss and attachment loss may be self-arresting.
Vertical loss of alveolar bone around the first molars and incisors is seen. An "arc-shaped" loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface of the second molar.
Generalized:
Bone loss occurring around more than three permanent teeth.
.
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.
ZONE OF IRRITATION
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 CO-DESTRUCTION
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.
1. Trauma from occlusion can produce bone destruction in the absence or presence of inflammation.
In absence of inflammation, changes caused by TFO vary from increased compression & tension of PDL & increased osteoclasts of alveolar bone, necrosis of PDL & bone, & resorption of bone & tooth structure.
Persistent trauma from occlusion results in funnel-shaped widening of the crestal portion of the periodontal ligament with resorption of the adjacent bone.
When combined with inflammation, trauma from occlusion aggravates the bone destruction caused by the inflammation and results in bizarre bone patterns.
,
FOOD IMPACTION:
Interdental defects often occur where proximal contact is abnormal or absent.
Pressure & irritation from food impaction contributes to inverse architecture.
In some instances poor proximal relationship may be the result of shift in bone position because of extensive bone destruction preceding food impaction.
In such cases food impaction is complicating factor rather than cause of bone destruction.
Food impaction can be vertical—due to occlusal forces or lateral—due to pressure from the lips, cheeks, and
Classifications are generally based upon specific morphological criteria and are aimed at guiding clinicians with their diagnosis, treatment and prognosis.
A first level of classification differentiates between suprabony defects, infrabony defects, and interradicular or furcation defects.
.. 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.
.
Goldman and Cohen classified angular defects on the basis of the number of osseous walls.
The continuous defects that involve more than one surface of a tooth, in a shape that is similar to trough, are called circumferential defects.
Three osseous walls
Proximal, buccal and lingual walls
Buccal, mesial and distal wall
Lingual, mesial and distal walls
Two osseous walls
Buccal and lingual walls (crater)
Buccal and proximal wall
Lingual and proximal walls
One osseous wall
Proximal wall (hemiseptum)
Buccal wall
Lingual wall
Combination The number of walls in the apical portion of the defect is often greater than that in its occlusal portion, in which case the term combined osseous defect is used
Three walls plus two walls
Three walls plus two walls plus one wall
Osseous craters are concavities in the crest of the interdental bone that is confined within the facial and lingual walls
3. Craters are one of the most commonly found bone defects which make around one third (35.2%) of all the defects and about two third (62%) of all the mandibular defects & Occur twice as often in posterior as in anterior defects.
TRENCH: When bone loss affects two or more three confluent surfaces of the same tooth.
PLANE: This term is applied when Both alveolar bone and supporting bone is lost to same degree such that margins of deformity are at same level. It can be considered horizontal bone loss about one tooth or portion of a tooth.
HEMISEPTA: A hemiseptum often is associated with an inconsistent osseous margin. Hemisepta occur between anterior as well as posterior teeth, & they are found in combination with all other types of bony deformities. Represents a one wall defects
) Overgrowths of bone
b) They can occur as small or large nodules, sharp ridges , spike-like projections.
The Buttressing Bone (Lipping) formation: Alveolar bone formation at some instances occurs to buttress the bony trabeculae which are weakened due to bone resorption and if it occurs within the jaw, termed as central buttressing bone formation
When it occurs on the external surface, it is referred to as “peripheral buttressing bone” formation. may cause bulging of the bone contour, which sometimes accompanies the production of osseous craters and angular defects
This causes bulging of the contour of bone, termed as lipping,
Buttressing bone formation in response to TFO is a popular concept first proposed by Glickman and Smulow more than 35 yrs ago.
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.
These defects are produced by loss of interdental bone.
Including the facial and/or lingual plates, without concomitant loss of radicular bone, thereby reversing the normal architecture.
Such defects are more common in the maxilla.
Also called as inconsistent bony margins , results when the interproximal crest is more apical than the buccal or palatal/ lingual radicular bone height , producing a reverse pattern in comparison to the normal scalloped alveolar process.
Ledges are plateau-like bone margins caused by resorption of thickened bony plates.
The width of the alveolar housing around a tooth is often greater in a more apical location.
As the bone resorbs because of periodontitis, the osseous margin in the new apical position may be considerably thicker than in the normal periodontium, giving the appearance of a bony ledge.
THICKENED MARGIN: An enlargement of facial or lingual marginal alveolar plate, instead of a thin, tapering, slightly rounded bony margin. Irregular bone margin is seen where there are abrupt irregularities in the scalloped level of marginal bone and interdental septa.
MARGINAL GUTTER: A shallow linear defect between marginal bone of the radical cortical plate or interdental crest, extending the length of one or more root surfaces, usually formed by resorption of the socket side of the plate and deposition on the facial surface.
1. These 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.
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.
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.
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 )
Glickman 1953, goldman 1958, hamp et al 1975, ramford and ash 1979,linde and Nyman 1983, tarnow fletcher 1984
Grade I It is the incipient or early stage of furcation involvement . The pocket is suprabony and primarily affects the soft tissues. Early bone loss may have occurred with an increase in probing depth, but radiographic changes are not usually found.
Grade II The furcation lesion is essentially a cul-de-sac with a definite horizontal component. If multiple defects are present, they do not communicate with each other because a portion of the alveolar bone remains attached to the tooth. The extent of the horizontal probing of the furcation determines whether the defect is early or advanced. Vertical bone loss may be present and represents a therapeutic complication. Radiographs may or may not depict the furcation involvement, particularly with maxillary molars because of the radiographic overlap of the roots.
Grade III In grade III furcations, the bone is not attached to the dome of the furcation. In early grade III involvement, the opening may be filled with soft tissue and may not be visible. The clinician may not even be able to pass a periodontal probe completely through the furcation because of interference with the bifurcational ridges or facial-lingual bony margins. Properly exposed and angled radiographs of early class III furcations display the defect as a radiolucent area in the crotch of the tooth .
Grade IV In grade IV furcations, the interdental bone is destroyed, and the soft tissues have receded apically so that the furcation opening is clinically visible. A tunnel therefore exists between the roots of such an affected tooth. Thus the periodontal probe passes readily from one aspect of the tooth to another
This 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.
Vertical or angular defects are those that occur in an oblique direction, leaving a hollowed-out through in the bone along side the root;
the base of the defect is located apical to the surrounding bone.
Classified on the basis of number of walls:
1 wall defect
2 wall defect
3 wall defect
Combined osseous defect
There are several risk factors. Smoking definitely causes constriction of blood vessels which leads to bone loss.
Periodontal probing and exploration are key aspects of clinical examination.
Careful probing reveals the presence of pocket depth greater than that of a normal gingival sulcus.
The location of the base of the pocket in relative to the mucogingival junction and attachment level on adjacent teeth, the number of bony walls and the presence of furcation defects.
Transgingival probing, or sounding, under local anesthesia confirms the extent and configuration of the infrabony component of the pocket or of furcation defects.
The probe should be "walked" along the tissue-tooth interface, so as to feel the bony topography.
The probe may also be passed horizontally through the tissue to provide three-dimensional information regarding bony contours.
It is a indirect method for determining the amount of bone loss in periodontal disease
Also it is a traditional method used to assess the destruction of alveolar bone associated with periodontitis.
In the experience of the author, cone beam CT (CBCT) is still underused for periodontal diagnosis.
Research comparing the use of three-dimensional (3D) volumetric images and 2D images in artificial bone defects have shown that CBCT has a sensitivity of 80–100% in the detection and classification of bone defects,