BONE LOSS PATTERN in periodontal diseasepptx

bone loss pattern in periodontal disease

1. BONE LOSS PATTERN IN PERIODONTAL DISEASES

2. Contents Introduction Causes of Bone Destruction In Periodontal Disease Factors Determining Bone Destruction In Periodontal Disease Bone Destruction Patterns In Periodontal Disease Conclusion References

3. Introduction Height and density of alveolar bone -- maintained by equilibrium, regulated by local and systemic influences between bone formation and resorption In health- amount of bone formation = amount of resorption , and is referred to as coupling . During inflammation, this coupling is broken. Inflammation from marginal gingiva extends into the supporting periodontal tissues and marks the transition from gingivitis  periodontitis.

4. Introduction Periodontal disease alters the morphologic features of the bone in addition to reducing bone height Hence level of bone is the consequence of past pathologic experiences and changes in soft tissues of pocket wall reflect the present inflammatory condition .

5. Periodontal Bone Architecture In Healthy Periodontium Alveolar bone roughly follows the cementoenamel junction (CEJ) on tooth surface. Interdental bone -- 1.0 mm from the CEJ Interdental bone -- placed coronally to the radicular bone  as scalloped bony outline known as ‘positive architecture’ . Posterior areas, the interdental bone is less coronally projected as compared to anterior areas

6. Bone Destruction Caused By Gingival Inflammation Extension of inflammation from marginal gingiva  periodontal tissues ------- main cause of bone destruction in periodontal diseases. Transition from Gingivitis  periodontitis----- associated with change composition of microbial plaque. Advanced stage— motile organisms, spirochetes coccoid rods or straight rods Periodontal destruction thus happened will be -- in an episodic, intermittent manner with periods of inactivity or quiescence.

7. Various Theories Related To Active And Inactive Periods Of Destruction Heijil et al., 1976 done experimental periodontitis ulceration of sulcular epithelium shift in connective tissue population; PMNs  plasma cells osteoclastic resorption of alveolar crest Acute destruction over time may be the cause of progressive bone loss in marginal periodontitis. Seymour et al ., 1978 postulated  a stage of contained gingivitis -- T lymphocytes are mainly present but as the lesion progress  there will be predominance of B-lymphocytes.

8. Various Theories Related To Active And Inactive Periods Of Destruction 3.Newman et al. , 1979 --- associated rapid bone loss with increased presence of loose, unattached and motile, Gram -ve bacterial species in pocket anaerobic flora. 4.Page and Schroeder 1981 - --- showed that bone resorption from the site of bacterial plaque accumulation is up to 2.5 mm  caused by bacterial invasion of gingival connective tissue  activate an inflammatory response  greater the number of osteoclasts formed  leading to greater amount of bone degradation. 5.Saglie et al. ,1987- -- postulated that connective tissue invasion by various bacterial species  elicit advanced host response  rapid bone resorption.

9. Histopathology Gingival inflammation extends  along collagen fiber bundles  follows course of blood vessels  loosely arranged tissues around them into the alveolar bone. Interproximally, inflammation spreads  loose connective tissue around the blood vessels via collagen fibers  through vessel channels  perforate the alveolar crest of the interdental septum.

10. Pathways of inflammation (A) Interproximally 1 - from the gingiva into bone 2 - From the bone into the periodontal ligament 3 -From the gingiva into the periodontal ligament . (B) Facially and lingually 1 - From gingiva along the outer periosteum 2 -From the periosteum into the bone 3 - From the gingiva into the periodontal ligament Pathways of inflammation from the gingiva into the supporting periodontal tissues during periodontitis

11. Extensive inflammatory infiltrate-- invaded marrow spaces from mesial and distal sides Fatty bone marrow – replaced by inflammatory cells and fibrous marrow. Resorption – takes place within marrow spaces  thinning of surrounding bone destruction of bone reduced bone height Interdental septum in a human autopsy section Amount of inflammatory infiltrate correlates with the degree of bone loss but not with no. of osteoclasts.

12. Classic study by Kronfeld 1935 demonstrated  bone destruction taking place in periodontitis is not bone necrosis . Because whole process is being executed by living cells along the viable bone . Findings were supported by Orban , 1939 . So, bone loss in periodontitis is not by necrosis of bone, but by resorption of bone . Available bone is not infected or necrotic and therefore it should be preserved if possible.

13. Radius of Action Garant and Cho , 1979 ---pointed out that bone resorption stimulators produced by microbial plaque have a finite radius of action . Waerhaug's , 1979 – done study on human autopsy specimens. Postulated that range of 1.5 mm to 2.5 mm in which bacterial biofilm can induce bone loss. Beyond 2.5 mm--- little or no effect. Interproximal angular defects appear -- spaces wider than 2.5 mm , because narrower spaces would end up with horizontal bone loss. Bone resorption stimulated directly or indirectly by microbial plaque is only effective for a distance up to 1.5-2.5 mm .

14. Rate of Bone Loss Loe and colleagues, 1986- -- Study of Sri Lankan tea laborers with no oral hygiene and no dental care findings average rate of bone loss  about 0.2 mm per year for facial surfaces about 0.3 mm per year for proximal surfaces 8% of subjects  rapid progression of periodontal disease with yearly loss of attachment of 0.1 to 1 mm. 81%  had moderately progressive periodontal disease with yearly loss of attachment of 0.05 to 0.5 mm.   11% of persons  minimal or no progression of disease with a yearly loss of attachment of 0.05 mm to 0.09 mm.

15. Periods of Destruction Periodontal destruction --- occurs in an episodic, intermittent manner, Periods of inactivity or quiescence -- alternate with destructive periods  result in loss of collagen and alveolar bone  causing deepening of periodontal pocket. Destructive activity  associated with gingival ulceration ( acute inflammatory reaction)  resulting in rapid loss of alveolar bone.

16. Mechanisms of Bone Destruction Factors involved in bone destruction in periodontal disease :- 1.Bacterial 2.Host mediated 1. Influence of bacteria and their products on periodontal destruction Bacterial biofilm products induce  differentiation of bone progenitor cells osteoclasts ; also stimulate gingival cells  release mediators. Bacterial biofilm products + inflammatory mediators  act directly on osteoblasts or their progenitors  inhibit their action and reduce their numbers Rapidly progressing diseases ( Aggressive periodontitis ) -- bacterial microcolonies or single bacterial cells are found between collagen fibers and over the bone surface- ---- indicating direct effect.

17. Mechanisms of Bone Destruction Influence of Host factors in bone destruction Host produced  prostaglandins and their precursors such as IL- 1 α, IL- 1 β and TNF- α. Goodson,1974 - -- when injected intradermally PGE-2 induces vascular changes associated with inflammation and when injected over a bone surface , PGE-2  induces bone resorption in absence of inflammatory cells, with few multinucleated osteoclasts. Jeffcoat, 1986 -- NSAIDs (e.g., flurbiprofen, ibuprofen) inhibit PGE- 2 production  slows down bone loss naturally occuring periodontal disease in beagle dogs and humans. This effect disappears 6 months after the cessation of drug administration.

18.   Bone Formation In Periodontal Disease Areas of bone formation ( Buttressing bone formation) Found adjacent to the sites of active bone resorption Also seen along trabecular surfaces at a distance from the inflammation in an effort to reinforce the remaining bone ------------------ finding clearly found in experimental animals but less evident in humans

19.   Bone Formation In Periodontal Disease Human autopsy specimen of untreated periodontal disease show Areas of bone resorption ceased( stopped) and new bone being formed on previously eroded bone margins.  Periods of remission and exacerbation (or inactivity and activity, respectively) appear to coincide with the quiescence or exacerbation of gingival inflammation  manifested by changes in extent of bleeding , the amount of exudate , and the composition of bacterial biofilm .

20. Bone Destruction Caused By Trauma From Occlusion Another cause for periodontal destruction is trauma from occlusion that occur in the presence or absence of inflammation. Absence of inflammation Changes due to TFO  may be increased compression or tension of the periodontal ligament Increased osteoclasis of alveolar bone  necrosis of the periodontal ligament  r esorption of bone and tooth structure Changes are reversible if the offending forces-- removed.

21. Bone Destruction Caused By Trauma From Occlusion Persistent trauma from occlusion  “ funnel-shaped widening ” of crestal portion of the periodontal ligament with resorption of adjacent bone.  Can lead bony crest to have an angular shape--- which represent adaptation of the periodontal tissues aimed at “cushioning” increased occlusal forces But in real, modified bone shape  weaken tooth support  cause tooth mobility . Presence of inflammation Combined with inflammation---- trauma from occlusion  aggravate bone destruction  results in bizarre bone patterns

22. Bone Destruction Caused By Systemic Disorders Irwing Glickman , 1949s -- in addition to the virulence of biofilm bacteria, the nature of the systemic component rather than its presence or absence influences the severity of the periodontal destruction--- “Bone factor concept” According to this concept-- dynamic relationship between the local and systemic factors  maintenance of normal physiology of the bone. Individual has a generalized tendency for bone resorption, aggravated bone destruction can be seen in local inflammation. Concept helps – in determination of prognosis

23. Bone Destruction Caused By Systemic Disorders Osteoporosis is a physiologic condition of postmenopausal women Results  in loss of bone mineral content and structural bone changes Periodontitis and osteoporosis share a number of risk factors (e.g., aging, smoking, certain diseases, medications that interfere with healing) Periodontal bone loss – occur in generalized skeletal disturbances such as hyperparathyroidism, leukaemia, histiocytosis X  via mechanisms that is unrelated to biofilm-induced, inflammatory periodontal lesion.

24.   Factors Determining Bone Morphology In Periodontal Disease Bone thickness Anatomical factors:  Presence of lingual tori and buccal Exostosis:  Crater formation: Presence of thick or thin periodontium:  Presence of trauma from occlusion (TFO):  Role of systemic factors in bone destruction 

25. Bone Thickness Bone Thickness: Pattern of bone resorption -- respect to variability in blood supply to alveolar bone. Resorption follows inflammation pathway. Angular osseous defects -- cannot form in thin facial or lingual alveolar p lates (little or no cancellous bone)  entire crest of the plate gets destroyed,; height of the bone  reduced in a horizontal fashion.  

26. Bone Thickness A)Lower incisor with thin labial bone B) Upper molars with thin facial bone C)Upper molar with a thick facial bone that allows for vertical bone loss. Angular osseous defects ---- cannot form in thin facial or lingual alveolar plates– as it have little or no cancellous bone between the outer and inner cortical layers. Entire crest of the plate get destroyed  reduction in height of bone in a horizontal fashion.

27. Bone Thickness Dehiscence -- seen in areas with a thin labial plate , where inflammation extends from marginal gingiva to apical direction. If the investing bone is thick  marginal inflammation  extends apically causing pattern of bone resorption like a trench or well .

28. Anatomic Features Anatomic features that affect the bone-destructive pattern Thickness, width, crestal angulation of interdental septa Alignment of the teeth Root and root trunk anatomy Root position within the alveolar process Proximity with another tooth surface

29. Anatomic Features Tooth location and tooth anatomy also play a major role in bone loss Tooth location Lateral incisor– thick bone and canine– thin bone  insufficient contact between two teeth  favourable environment for pocket formation deep interdental craters.

30. Exostoses   Are outgrowths of bone of varied size and shape. Incidence of palatal exostoses--- around 40%. Occur as:- Small nodules Large nodules Sharp ridges Spike like projections, or any combination of these

31.   Osseous Craters Specific type of two-wall defect present as concavities in the crest of the interdental bone Confined within the facial and lingual walls. Craters present – about 35.2% of all defects and 62% of all mandibular defects Occur twice as in posterior segments than anterior segments

32. Classification of Osseous Craters Ochsenbein and Bohannan in 1964 Class 1 craters- -- 2-3 mm osseous concavity with relatively thick buccal and lingual walls Class 2 craters- -- 4-5 mm osseous concavity and thinner buccal and lingual walls. Class 3 craters- --- 6-7 mm with thin buccal and lingual walls Class 4 craters- --- lesions with variable depth and thin buccal and lingual walls

33. Reasons for high frequency of interdental craters • Interdental area collects biofilm -- difficult to clean. • Normal flat or even slightly concave buccolingual shape of interdental septum in lower molars  favour crater formation. • Vascular patterns from the gingiva to the centre of the crest  pathway for inflammation

34. Ledges   Ledges are plateau-like bone margins that are caused by the resorption of thickened bony plates

35. Food Impaction  Interdental bone defects occur-- proximal contact is light or absent. Physical pressure and additional collection of bacteria from food impaction  interproximal resorption and reverse bone architecture. Poor proximal relationship  shift in tooth position due to extensive bone destruction that precedes food impaction.

36. Trauma From Occlusion (TFO) TFO has been defined as structural and functional changes in the periodontal tissues caused by excessive occlusal forces factor in determining the dimension and shape of bone deformities. Occlusal trauma is the overall process by which traumatic occlusion (occlusion that produces forces that cause injury) produces injury to the attachment apparatus. Cause thickening of cervical margin of alveolar bone Change in bone morphology (e.g., funnel-like crestal bone, buttressing bone) on which inflammatory changes may later be superimposed.

37. Bone Destruction Patterns In Periodontal Disease Periodontal disease – alters morphologic features of bone in addition to reduced bone height. Horizontal Bone Loss Most common pattern of bone loss in periodontal disease Reduced bone height Bone margin remains perpendicular to the tooth surface. Interdental septa, facial and lingual plates are affected

38. Vertical or Angular Defects Defects occur in an oblique direction  leaving a hollowed-out trough in the bone along side the root. Base of the defect -- located apical to the surrounding bone. Vertical defects increase with age Presence of vertical defect—can be evident in radiographs Probing and surgical exposure of areas -- determine exact dimensions.

39. Classification of angular defects Based on number of osseous walls, Goldman and Cohen, 1958 angular defects having one wall angular defects having two walls angular defects having three walls Continuous defects --more than one surface of a tooth involved. Shape of the defect is similar to a trough, therefore called circumferential defects . Combined osseous defect- - Number of walls in the apical portion of the defect is greater than that in its occlusal portion

40. Classification Of Bone Defects Vertical or angular defects Osseous craters Bulbous bone contours Reverse architecture Ledges Furcation involvement Glickman (1964) :

41. Bulbous Bone Contours Bony enlargements --- caused by exostoses As an adaptation to function or buttressing bone formation Found more frequently in the maxilla than in the mandible. Reversed Architecture Reverse (or negative) alveolar bone architecture  loss of interdental bone, without loss of radicular (buccal or lingual / palatal) bone, thereby reversing the normal (or positive) architecture.

42. Furcation Involvement   Refers– to invasion of bifurcation and trifurcation of multirooted teeth by periodontitis. Some studies report  furcation involvement mostly seen in mandibular first and least in maxillary premolars . No. of furcation involvements increases with age. Denuded furcation ---- visible clinically or may be covered by pocket wall Extent of the involvement  determined by exploration with a periodontal or Nabers probe

43. Classification Of Furcation Involvement Grade I --- incipient bone loss Grade II ---- partial bone loss (cul-de-sac) Grade III ---- through-and-through opening of the furcation, but the opening of the furcation is not visible due to the gingiva, which covers the orifice. Grade IV ---- similar to grade III but gingival recession that exposes the furcation to view.

44. Etiopathogenesis of Furcation Involvement Difficulty in controlling biofilm in furcation area  extensive lesion Trauma from occlusion --- etiology is controversial Enamel projections into the furcation—occurs in 13% of multirooted teeth, and the proximity of the furcation to the CEJ --- occurs in about 75% of cases of furcation involvement. Accessory pulpal canals in the furcation area  extension of pulpal inflammation to the furcation.

45. Diagnosis of Furcation Involvement Either by Clinical examination – involving careful probing with a specially designed probe Radiographic examination of the area ---lesions can be obscured by the angulation of the beam and the radiopacity of neighbouring structures.

46. conclusion Understanding of anatomy, histology, and pattern of bone loss for the diagnosis of and prognosis for periodontal disease is of major importance in determining the therapy that must be rendered. In the final analysis, it is the loss of bone that will determine the retention, maintenance, or loss of the dentition in periodontal disease.

47. references 1.M Michael G. Newman, Henry H. Takei, Fermin A. Carranza; Clinical periodontology,9 th edition. 2. Jan Lindhe, Clinical Periodontology and Implant dentistry ichael G. Newman, Henry H. Takei, Fermin A. Carranza; Clinical periodontology,9 th edition. 3) Irving Glickman, The experimental basis for the "bone factor “concept in periodontal disease,JOP,1949 4) Loe H, Anerud A, Boysen H and Morrison E: Natural history of periodontal disease in man. Rapid, moderate and no loss of attachment in Sri Lankan laborers 14 to 46 years of age. J Clin Periodontol 1986; 13: 431-440.

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