Bone Destruction Caused by Gingival Inflammtion

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.