Bone loss in the alveolar process can occur due to periodontitis or aging. Periodontitis is caused by bacterial plaque that leads to gingival inflammation and bone destruction. As inflammation spreads from the gingiva into the bone marrow spaces, it causes an increase in osteoclasts and bone resorption. Over time this can cause reductions in bone height and width. Trauma from occlusion can also contribute to bone loss, especially when combined with inflammation. The pattern of bone loss varies and can be horizontal, angular defects, or furcation involvement of multi-rooted teeth.

1. BONE LOSS
Pattern of bone Destruction

2. BONE DESTRUCTION
• Bone destruction due to periodontitis is responsible for tooth
loss .
• Senile ( physiologic ) atrophy is reduction of alveolar bone
height that occurs with aging
• Bone destruction in periodontal disease is caused by local
factors :
1. Gingival inflammation (responsible for reduction in alveolar
bone height )
2. trauma from occlusion (cause bone loss lateral to the root
surface)
• The degree of bone loss is not necessarily correlated with the
depth of periodontal pocket.

3. Bone destruction caused by
gingival inflammation
• Chronic inflammation results in the extension of the
inflammatory process to the bone
• Transition from gingivitis to periodontitis is associated
with changes in composition of bacterial plaque ( >
spirochetes and motile organism , < coccids and straight
rods )
• Cellular composition of infiltrated CT ( > fibroblast and
lymphocytes +T- lymphocytes in gingivitis , > plasma
and blast cells +B - lymphocytes as the disease
progress )
• Changes in tissue – related mechanism , degree of
gingival fibrosis , attached gingival width , reactive
fibrogenesis and osteogenesis peripheral to the
inflammatory lesion.

4. Histopathology :
• Gingival inflammation extend along the collagen fiber
bundles and follow the course of the blood vessels
through the loosely arranged tissue around them into
the alveolar bone.
• After inflammation reaches the bone , it spreads into
the marrow spaces replaces the marrow with a
leukocytic and fluid exudates
• Multinuclear osteoclasts and mononuclear phagocytes
are increased in number
• In the marrow spaces resorption proceeds from within
causing :
1. Thinning of surrounding bony trabeculae
2. Enlargement of marrow spaces
3. Destruction of bone , reduction of bone height
4. Replacement of fatty bone marrow by a fibrous type

5. Bone Destruction in Periodontal
Disease
1. Bone destruction in periodontal disease is not a
process of bone necrosis.
2. It involves the activity of living cells along viable bone.
3. When tissue necrosis and pus are present in
periodontal disease , they occur in the soft tissue walls
of periodontal pocket , not along the resorbing margin
of the underlying bone
Rate of bone loss :
• About 0.2 mm a year for facial surfaces
• About 0 .3 mm a year for proximal surfaces ( when
periodontal disease was allowed to progress untreated
) study of Sri Lanka laborers.

6. Mechanism of bone destruction :
possible pathways for alveolar bone loss by plaque
products:
1. Direct action on bone progenitor cells into osteoclasts
2. Destroying the bone directly by plaque products through a
noncellular mechanism.
3. Gingival cells mediators induce bone progenitor cells to
differentiate into osteoclasts.
4. Plaque products cause gingival cells to release agents that can
act as cofactors in bone resorption.
5. Agents released by gingival cells to destroy bone by direct
chemical action , without osteoclasts.
• Bone destruction caused by trauma from occlusion :
1. Trauma in the absence of inflammation
2. Trauma combined with inflammation

7. 1. Trauma in the absence of inflammation:
• ligament + increased osteoclasis of alveolar bone to
necrosis of PL and resorption of bone and tooth
structure.
• These changes are reversible Vary from increased
compression and tension of the periodontal
• If persist it results in funnel-shaped widening of crestal
portion of PL
+ resorption of adjacent bone.
• These changes cause the bony crest to have an
angular shape.
2. Trauma combined with inflammation :
• When combined with inflammation it aggravates the
bone destruction caused by the inflammation
• It causes bizarre bone patterns

8. Factors determining bone morphology in
periodontal disease ( normal variation in
alveolar bone ) :
1. The thickness , width ,and crestal angulations of the
interdental septa
2. The thickness of the facial and lingual alveolar plates.
3. The presence of fenestration and, or dehiscence.
Exostosis : out growth of bone of varied size and shape
Buttressing bone formation (lipping ): bone formation
sometimes occur in an attempt to buttress bony
trabeculae weakened by resorption
Bone destruction patterns in periodontal disease :
1. Horizontal bone loss: the most common pattern , the bone is
reduced in height ,but the bone margin remains roughly
perpendicular to the tooth surface.

9. Bone deformities ( osseous defects ): occur in adults and reported in
deciduous dentition , suggested in radiograph.
2. Vertical or angular defect :
• Occur in oblique direction leaving a hollowed – out
trough in the bone alongside the root
• Angular defect are classified on the basis of the
number of osseous walls. It may have one , two or
three walls ( combined osseous defect)
• Vertical defects increase with age , they are found
radiographically most commonly on the distal surfaces
of molar teeth
• Three- wall defects ( intrabony defect ) are more
common on the mesial surfaces of upper and lower
molars.
• The one-wall vertical defect is called ( hemi septum )

10. •Osseous craters ; concavities in the crest of the
interdental bone confined within the facial and lingual
walls .
• Bulbous bone contours ; bony enlargement caused by
exostosis, adaptation to function or buttressing bone
formation. Found more frequently in maxilla.
• Reversed architecture ; defects produced by loss of
interdental bone
• Ledge : plateau- like bone margin caused by resorption
of thickened bony plates
• Furcation involvement : invasion of the bifurcation and
trifurcation of multirooted teeth by periodontal disease.
Most common in mandibular first molars , > with age .