BONE DESTRUCTION CAUSED BY GINGIVAL
INFLAMMTION
CONTENTS
• INTRODUCTION• HISTOPATHOLOGY• RADIUS OF ACTION• PERIODS OF DESTRUCTION• MECHANISMS OF BONE DESTRUCTION• BONE FORMATION IN PERIODONTAL DISEASE
Introduction
• Equilibrium between bone formation and bone resorption
• Bone resorption >> Bone formation
Bone destruction• Level of bone loss = past pathologic experiences• Soft tissue changes of pocket wall=present
inflammatory condition
Causes of bone destruction
1) Extension of gingival inflammation2) Trauma from occlusion3) Systemic diseases
SequenceInflammation of marginal gingiva
Bone loss/destruction
Histopathology• Gingival inflammation extends along:i)collagaen fiber bundles ii)course of blood vessels into alveolar bone• Interproximally,inflammation spreads toi) loose connective tissue ii) bone through vessel channels• Facially and lingually,inflammation spreads fromGingiva outer periosteal surface marrow
spaces
Effects Gingival and trans septal fibers
Destruction Granular fragments(interspersed among inflammatory cells and
edema)Note:transseptal fibers are recreated across
crest of the interdental septum
Bone
Inflammation reaches bone
Replacement with leukocytic
and fluid exudate,new blood vessels
and proliferating fibroblasts Resorption
Reduction in height
Contd… Note:• Fatty bone marrow-partial or total
replacement by fibrous type of marrow• Bone destruction bone necrosis
Rate of bone loss• According to Loe et al’s study of untreated
periodontal disease avg. rate of bone loss is -0.2mm/yr for facial surfaces -0.3mm/yr for proximal surfaces• 3 subgroups of patients with periodontal dis i)approx. 8%=rapid progression of pdl dis + loss of
attachment of 0.1-1mm/yr ii)approx. 81%=moderate progression of pdl dis +
loss of attachment of 0.05-0.5mm/yr iii)approx. 11%=minimal/no progression of pdl dis +
loss of attachment of 0.05-0.09mm/yr
Periods of destruction• Episodic,intermittent manner with periods of
inactivity or quiescence• Result in- loss of collagen and alveolar bone
thus deepening of pocket• Reasons:i)Subgingival ulceration + acute inflammatory
reactionii)Conversion of T-lymphocyte lesion into B-
lymphocyte-plasma cell infiltrate
iii)Periods of exacerbation- of
loose,unattached,motile,gram negative anaerobic pocket flora and
Periods of remission-dense,unattached,nonmotile,gram-positive flora with tendency to mineralise.
iv)Tissue invasion by several bacterial species.
Mechanisms of Bone Destruction
• Two factors:bacterial and host mediated• Bacterial plaque products i)Bone progenitor cells → osteoclastsii)Gingival cells → mediatorsNote:Both cause bone resorption + act on
osteoblasts/progenitors; thus inhibit action and reduce no.
• Rapidly progressing disease:bacterial micro colonies/single bacterial cells present between collagen fibers and over bone surface,direct effect.
• Host factors(PGE2,IL-α,IL-β,TNF-α): Inflammatory cells → host factors → bone
resorption in vitro -PGE2(intradermal)→vascular changes -PGE2(bone surface)→bone resorption
without inflammatory cells and with few osteoclasts.
Note:NSAIDS(flurbiprofen and ibuprofen) inhibit PGE2 production → slows bone loss
Bone Formation in Periodontal Disease• Found near:i)sites adjacent to active bone resorptionii)Trabecular surfaces• Alveolar bone’s response to inflammation: - bone resorption and formation -Thus in bone destruction,bone resorption is more
than bone formation -new bone forms on previously eroded bone margins
on ceasation of resorption -periods of remission and exacerbation appear to
coincide with quiescense or exacerbation of gingival inflammation.