Dr. Harshavardhan Patwal

Introduction: Periodontitis is differentiated from gingivitis

by loss of attachment accompanied by bone loss.

The alveolar bone is never stable. A continuous process of resorption and

formation occurs in the alveolar bone

There is a balance between resorption and formation. But when resorption exceeds formation the bone density and height are reduced.

Bone level is an indication of the past pathologic changes.

Soft tissue changes are indicative of the present inflammatory changes.

Bone loss

Gingivitis Periodontitis. Periodontitis is always preceded by gingivitis,

but not all gingivitis progresses to periodontitis.

The transition from gingivitis to periodontitis – why should it happen?

1. Change in the composition of bacterial plaque- increase no of motile organisms and spirochetes and decrease in cocci.

2. Cellular composition of infiltrated connective – T cell lesion is a “contained gingivitis” lesion. When it become a lesion predominated by B cells it becomes a destructive lesion. (Seymour et al 1978,1979).

3. Recurrent episodes of acute destruction over time. (Heijl et al 1976). Experimental animal study by placing silk ligature in the sulcus.

4. Host resistance- includes immunologic activity, width of the attached gingiva, degree of fibrosis, reactive fibrogenesis and osteogenesis, fibrin-fibrinolytic system.

Pathway of spread of inflammation influences the “Pattern of bone destruction”.

Pathway of spread of inflammation has been studied primarily through “Histopathologic studies”.

Gingival inflammation connective tissue infiltrate spreads along the blood vessels and collagen fiber bundles towards the bone.

Transseptal fibers are destroyed during the spread of inflammation of towards bone.

But they are reformed at a lower level. After inflammation reaches bone it spreads

into the marrow spaces. Marrow changes- leukocyte and fluid

infiltrate, new blood vessels, osteoclastic cells increase in number and the bone surface is lined with Howship’s lacunae.

In the marrow, resorption occurs inside the spaces resulting in the reduction in bone height.

Bone destruction is not a process of necrosis. It is carried out by viable cells.

The amount of infiltrate co-relates with level of bone destruction.

The distance between the apical margin of infiltrate co-relates with no of osteoclasts at the alveolar crest.

Garant and Cho: reported that locally produced factors induce bone destruction.

Page and Schroeder: range of effectiveness is 1.5 to 2.5 mm- bacterial plaque can cause damage.

For angular defect to form the width of the inter-dental bone should be more than 2.5 mm (Tal 1984).

Large defects exceeding 2.5 mm may be produced by the presence of bacteria in the tissues.

Loe et al 1986- untreated periodontitis in Sri Lankan tea laborers: annual rate of bone loss is 0.2 mm in the facial aspect and 0.3 mm in the inter-proximal aspect.

Loe et al identified three sub-groups of patients with periodontal disease:

8%- rapid attachment loss- annual attachment loss of 0.1 to 1mm.

81% of individuals –moderate progression of periodontal disease, annual attachment loss of 0.05 to 0.5 mm.

11% of individuals- minimum or no progression of Periodontal disease, annual attachment loss of 0.05 to 0.09 mm.

Chronic periodontitis is characterized by “periods of destruction and inactivity or quiescence”.

During periods of destruction- there is a loss of collagen and alveolar bone.Theories proposed for onset of destructive periods:

Subgingival ulceration and acute inflammation (Schroeder and Lindhe, 1980).

T cell to B Cell Lesion shift.(Seymour et al 1979). Increase number of unattached, motile , gram negative

pocket flora. (Newman MG, 1979). Tissue invasion by one or more of the following bacteria.

(Saglie et al 1987).

Areas of bone formation: adjacent to resorption areas, and a little away – Buttressing bone formation.

Intermittent pattern of resorption is seen in periodontal disease.

The basic aim in periodontal therapy- to remove the stimulus for resorption.

Changes can be produced in the presence or absence of inflammation:

In absence of inflammation: Angular bone loss pattern- as a result of an attempt by the periodontal ligament to adapt to the excessive occlusal forces.

In presence of inflammation: TFO aggravates the bone destruction caused by the periodontal disease.

Local and systemic factors regulate the physiologic equilibrium of the bone.

Generalized tendency for bone resorption exists- bone loss initiated by the local inflammatory process is magnified.

This is called “Bone Factor Concept”. Proposed by Glickman (1950).

Osteoporosis, skeletal deformities (Hyperparathyroidsm, leukemia).

Normal variations in alveolar bone:thickness, width, crestal angulation, thickness of the facial and lingual plates, presence of fenestration and dehiscence, alignment of the teeth, root position in the alveolar complex.

Exostoses: small nodules, large nodules, spike like projections.

Trauma from occlusion. Buttressing bone formation. Food impaction. Localized aggressive periodontitis.

Two broad patterns of bone loss: Horizontal and Vertical/ angular.

Horizontal bone loss: most common pattern of bone loss, bone is reduced in height and is roughly perpendicular to the root surface. The inter-dental septa and the facial and lingual plates are affected.

Bone deformities / Osseous defects: Vertical or angular defects. Osseous craters. Bulbous bone contours. Reversed architecture. Ledges. Furcation involvement.

Defn: 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.

Usually associated with an intrabony pocket.

Goldman and Cohen ,1958: classified the vertical defects based on the number of osseous walls present.

One wall defect/ hemiseptum. Two wall defect. Three wall defect. Combined osseous defects.

Vertical defects can be seen when present; in the inter-dental area in a radiograph.

Three wall defects have been noted particularly in the mesial surfaces of upper and lower molars.

Combined osseous defects: the number of walls in the apical portion of the defect are more than in the coronal portion of the defect.

Osseous craters: Defn: are concavities in the crest of the inter-

dental bone confined within the facial and lingual walls.

They constitute one third of all defects (35.2%) and two thirds (62%) of all mandibular defects.

They are twice as common in the posterior than anterior region.

Facial and the lingual plates are:Equal in height- 85% of the cases, remaining 15 % of cases – higher buccal or lingual plates.

High frequency of the inter-dental craters: The inter-dental area collects plaque and is

difficult to clean. Normal flat or concave shape of the inter-

dental septum in lower molars may favor crater formation.

Vascular patterns from gingiva to center of the inter-dental crest.

Bulbous bone contours: Exostoses, buttressing bone formation.Reversed architecture: Loss of inter-dental bone including the facial and

lingual plates without a concomitant loss of the radicular bone.

Ledges: Plateau like bone margins caused by resorption of

the thickened bony plates.

Furcation Involvement: Defn: invasion of the bi- furcation and the

tri- furcation areas of multi-rooted teeth by periodontal disease.

Mandibular first molars are the most common sites affected.

Four gradings are there for the horizontal component.

H/P: Early stage- widening of the PDL space,

cellular and inflammatory fluid exudate. Epithelial proliferation into furcation area. Extension of inflammation to the bone-

resorption of the bone and reduction of the bone height.

Factors influencing furcation involvement: TFO. Root trunk length. Cervical enamel projections. Enamel pearls.

Extension of inflammation from gingiva to bone- bone loss ( periodontitis onset).

Pathway of spread influences pattern of bone loss. Influence of systemic states on locally induced

alveolar bone loss- Glickman’s bone factor concept. Bone loss patterns- horizontal and vertical. Osseous defects- vertical defects, craters etc.