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CONTENTS
INTRODUCTION HISTOPATHOLOGY RADIUS OF ACTION PERIODS OF DESTRUCTION MECHANISMS OF BONE DESTRUCTION BONE FORMATION IN PERIODONTAL DISEASE
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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 6/26/12 wall=present inflammatory condition
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Sequence
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Histopathology
Interproximally,inflammation spreads to
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
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Bone
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Contd
Note:
Fatty bone marrow-partial or total replacement by fibrous type of marrow Bone destruction bone necrosis
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According to Loe et als study of untreated periodontal disease avg. rate of bone loss is -0.2mm/yr for facial surfaces -0.3mm/yr for proximal surfaces
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 reaction ii)Conversion of T-lymphocyte lesion 6/26/12 into B-lymphocyte-plasma cell infiltrate
iii)Periods of exacerbation- of loose,unattached,motile,gram negative anaerobic pocket flora and Periods of remissiondense,unattached,nonmotile,grampositive flora with tendency to mineralise. iv)Tissue invasion by several bacterial species.
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i)Bone progenitor cells osteoclasts ii)Gingival cells mediators Note:Both cause bone resorption + act on osteoblasts/progenitors; thus inhibit action and reduce no.
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Host factors(PGE2,IL-,IL-,TNF-):
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
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