Physiologic equilibrium b/w bone formation & resorption maintains height & density The level of bone is the result of past pathologic experiences soft tissue wall represents the present infly condition
ETIOLOGY :- EXTENSION OF GINGIVAL INFLAMMATION TRAUMA FROM OCCLUSION SYSTEMIC DISORDERS
EXTENSION OF GINGIVAL INFLAMMATION The most common cause of bone destruction in periodontal disease is extension of inflammation from the marginal gingiva into the supporting PD tissue. Periodontitis is always preceded by gingivitis, but not all gingivitis progresses to periodontitis The transition from gingivitis to periodontitis is associated with changes in composition of bacterial plaque.
The recurrence of episode of acute destruction over time may be one mechanism leading to progressive bone loss in marginal gingivitis. The extension of inflammation is modified by pathogenic potential of plaque or resistance of host
Degree of fibrosis of gingiva
Width of attached gingiva
Peripheral reactive fibrogenesis and osteogenesis .
“ walling off “ by fibrin-fibrinolytic system.
After inflammation reaches the bone by extension from the gingiva,it spreads into the marrow spaces And replaces the marrow with leukocytic and fluid exudate,new blood vessel, & proliferating fibroblasts. Multinuclear osteoclasts and mononuclear phagocytes increase in number ,the bone surfaces appear ,lined with howship’s lacunae.
In marrow spaces ,resorption proceeds, causing a thinning of surrounding bony trabeculae and enlargement of marrow spaces Destruction of bone and reduction in height
Radius of action 1.5 to 2.5 mm within which bacterial plaque induce loss of bone. Interproximal angular defect can appear in spaces that are wider than 2.5 mm because bone marrow spaces would be destroyed entirely.
Rate of bone loss Range of bone loss varies depending on the type of disease present. Periods of destruction
bursts of destructive activity associated with sub gingival ulceration and acute inflammatory reaction, resulting in rapid bone loss.
Bursts of destructive activity coincide with the conversion of T-lymphocyte lesion to B-lymphocyte
Exacerbation are associated with loose , unattached ,motile gram negative ,anaerobic pocket flora and period of remission coincide with the formation of dense ,unattached ,nonmotile, grame positive flora with tendency to mineralize.
Tissue invasion by one or several bacterial species is followed by an advanced local host defense that controls the attack.
Mechanisms of bone destruction The factors involved in bone destruction in periodontal disease are bacteria and host mediated Plaque products induce osteoclast differentiation and also stimulate gingival cells to release mediators (direct effect by bacterial colonies) Plaque products & infly mediators can inhibit action of osteoblasts & reduce their number Several host factors released by inflammatory cells are prostaglandins , interleukin 1-alpha and beta ,and tumor necrosis factor
Bone formation in periodontal disease Areas of bone formation are found adjacent to areas of bone resorption and along trabecular surfaces at a distance from the inflammation – BUTTRESSING BONE FORMATION Intermittent bone formation and destruction. Periods of remission & exacerbation occur
Bone destruction caused by trauma from occlusion Trauma from occlusion can produce bone destruction in absence or presence of inflammation In the absence of inflammation the changes are caused by increased compression and tension of pdl and increased osteoclasis of alveolar bone to necrosis of pdl and bone and resorption of bone. This changes are reversible which may cause angular shape bone loss. In the presence of inflammation the changes cause bizarre patterns.
Bone destruction caused by systemic disorders Systemic influence on the response of alveolar bone has been termed as BONE FACTOR IN PERIODONTAL DISEASE ( IRVING GLICKMAN IN 1950 ) Relationship between periodontal bone loss and osteoporosis. Osteoporosis is physiological condition of post menopausal women ,resulting in loss of bone mineral content and structrual bone changes. Bone loss may also occur in generalized skeletal disturbances like hyperparathyroidism ,leukemia.
FACTORS AFFECTING BONE MORPHOLOGY IN PERIODONTAL DISEASE Normal variation in alveolar bone Exostoses Trauma from occlusion Buttressing bone formation Food impaction Juvenile periodontitis
Exostoses are outgrowths of bone of varied size & shape.Can occur as nodules, ridges, spike-like projections. Buttressing bone formation on the external surface cause bulging of bone contour (lipping) Food impaction abnormal or absent proximal contact causes pressure & irritation from F.I leading to inverted bone architecture. It may be a complication of bone defect Juvenile periodontitis vertical or angular bone destruction around 1 st molars
BONE DESTRUCTION PATTERN :- Horizontal bone loss
Most common pattern It occurs when the path of inflammation is to the crest bone. The crest of the bone is perpendicular to the tooth surface. This type of bone loss produce suprabony pocket.
Vertical bone loss Less common pattern It occurs when the pathway of inflammation travels directly into the pdl space. This type of bone loss produce infrabony pocket. It occurs intradentally which can see on radiograrh. It increases with age.
Osseous craters Osseous craters are concavities in the crest of the interdental bone confined within the facial and lingual walls Reasons for high frequency : The interdental area collects Plaque and is difficult to clean. Normal flat or even concave faciolingual shape of interdental septum in lower molar Vascular pattern
Bulbous bone contours They are bony enlargements caused by exostoses,adaptation to function or butteresting bone They are more in maxilla than mandible. Reversed architecture They are produced by loss of interdental bone including the facial plates, lingual plates Or both without concomitant loss of radicularbone. More in maxilla
ledges Ledges are plateau like bone margins caused by resorption of thickened bony plates. Furcation involvement Furcation refers to the invasion of the bifurcatoin and trifurcation of multirooted teeth by periodontal disease. Mandibular 1 st molars are most common site and maxillary premolar are least common. Grade 1 – incipient bone loss Grade 2 – partial bone loss Grade 3 – total bone loss ( through & through opening of furcation
Grade 4 – similar to grade 3 but with gingival recession Microscopically – It is simply a phase of rootward extension of periodontal pocket In its early stage , widening of the periodontal space with cellular and fluid exudates Extension of the inflammation into the bone leads to bone resorption and reduction in height. Bone destruction pattern may produce horizontal or angular , and very frequently craters in interradicular area.