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- 1. BONE LOSS & PATTERNS OF BONE DESTRUCTION
- 2. CONTENTS INTRODUCTION CAUSES OF BONE DESTRUCTION IN PERIODONTAL DISEASE Extension of gingival inflammation Trauma from occlusion Systemic disorders FACTORS DETERMINING BONE DESTRUCTION IN PERIODONTAL DISEASE BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE LESIONS CAUSING ALVEOLAR BONE DESTRUCTION CONCLUSION REFERENCES
- 3. Introduction Periodontitis Bone loss past pathologic experience Bone formation Bone resorption
- 4. Blood calcium Receptors on chief cells of PTH Release of PTH Release calcium Osteogenic substrates BONE COUPLING Osteoblasts Monocytes Osteoclasts Bone Introduction
- 5. Introduction Mechanisms of bone destruction Osteolysis (Halisteresis) (Von Recklinghausen F 1910) Non-cellular resorption Vascular resorption (Jaffe HL 1930) Osteoclasis (Lacunar resorption) (McClean FC, Urist MR 1961)
- 6. Causes of bone destruction Gottlieb & Orban 1938 “senile atrophy” Male patient aged 67 years old. O/E: generalized class 1 gingival recession with generalized interdental bone loss. No periodontal pockets probed or tooth mobility observed.
- 7. Causes of bone destruction
- 8. BONE DESTRUCTION CAUSED BY EXTENSION OF GINGIVAL INFLAMMATION Gingivitis Periodontitis Bacterial composition (Lindhe J et al 1980) Cellular composition (Seymour & associates 1978, 1979) Immunologic activity (Ruben M 1981)
- 9. Bone destruction caused by extension of gingival inflammation Spread of inflammation Gingiva Blood vessels, collagen fibres Alveolar bone Marrow spaces
- 10. Bone destruction caused by extension of gingival inflammation Bone destruction = Bone necrosis (Kronfeld R 1935) Amount of infiltrate correlates with the degree of bone loss Distance from the apical border of the infiltrate correlates with number of osteoclasts (Rowe DJ 1981, Lindhe J 1978)
- 11. Bone destruction caused by extension of gingival inflammation Pathways of spread of inflammation A B A – Interproximally B – Facially& lingually
- 12. Bone destruction caused by extension of gingival inflammation Radius of action Garant and Cho 1979 Page and Schroeder 1982 (based on Waerhaug’s experiments 1980) Tal H 1984 – human patients 1.5 – 2.5 mm
- 13. Bone destruction caused by extension of gingival inflammation Rate of bone loss (Loe & associates 1986) ~ 0.2 mm a year for facial surfaces ~ 0.3 mm a year for proximal surfaces Rapid progression of periodontal disease (~ 8%) CAL = 0.1 to 1mm yearly Moderately progressive disease (~ 81%) CAL = 0.05 to 0.5mm yearly Minimal progression of periodontal disease (~ 11%) CAL = 0.05 to 0.09mm yearly
- 14. Bone destruction caused by extension of gingival inflammation Periods of bone destruction Page and Schroeder 1982 – inflammation Seymour GJ 1979 – B-lymphocytes Newman MG 1979 – microflora Saglie RF 1987 – bacterial invasion + host defense Periods of inactivity Periods of activity
- 15. Potential pathways for interaction between factors in plaque and alveolar bone resulting in alveolar bone loss Gingival tissue Release or activation of soluble mediators Bacterial plaque Soluble factor(s) Alveolar bone Bone progenitor cell Osteoclast 3 1 245 Bone destruction caused by extension of gingival inflammation Hausmann E 1974
- 16. Bone destruction caused by extension of gingival inflammation Bone formation in periodontal disease Retards the rate of bone loss Newly formed osteoid more resistant to resorption than mature bone (Irving JT 1969) Buttressing bone formation Affects the outcome of treatment
- 17. BONE DESTRUCTION CAUSED BY TRAUMA FROM OCCLUSION In the absence of inflammation When combined with inflammation Glickman’s concept (1965, 1967) Waerhaug’s concept (1979)
- 18. BONE DESTRUCTION CAUSED BY SYSTEMIC DISORDERS Bone factor concept (Glickman I 1951) The systemic regulatory influence upon the response of alveolar bone is termed the “bone factor” in periodontal disease. Systemic factors Local factors
- 19. Bone destruction caused by systemic disorders Role of “bone factor” in determining diagnosis and prognosis Positive bone factor Negative bone factor Patient’s age Gingival inflammation & occlusal disharmony Bone loss
- 20. Bone destruction caused by systemic disorders Clinical implications Positive bone factor in a 42-year old female with gingival inflammation and poor oral hygiene but minimal bone loss. Negative bone factor in a 41-year old female with gingival inflammation and poor oral hygiene but severe bone loss.
- 21. Factors determining bone destruction in periodontal disease Normal variation in alveolar bone
- 22. Interdental septa Alveolar plates Root & root trunk anatomy Root position Teeth alignment Root proximity Factors determining bone destruction in periodontal disease
- 23. Factors determining bone destruction in periodontal disease Exostoses Nery EB 1977 – palatal exostoses (40%) Buttressing bone formation (Lipping) Food impaction
- 24. Bone destruction patterns in periodontal disease Classification I. Goldman HM, Cohen DW (1958) II. Prichard JF (1965) III. Karn KW (1983) IV. Grant DA, Stern IB, Listgarten MA (1988) V. Papapanou NP, Tonetti MS (2000)
- 25. Bone destruction patterns in periodontal disease I. Goldman HM, Cohen DW (1958) Suprabony defect Intrabony defect • One-wall • Two-wall • Three-walls • Combined
- 26. Bone destruction patterns in periodontal disease II. Prichard JF (1965) 1. Thickened margin 2. Interdental crater 3. Hemiseptum 4. Infrabony defect with three osseous walls 5. Infrabony defect with two osseous walls 6. Infrabony defect with one osseous wall 7. Marginal gutter 8. Furcation involvement 9. Irregular bone margin 10. Dehiscence 11. Fenestration 12. Exostosis
- 27. Bone destruction patterns in periodontal disease III. Karn KW (1983) 1. Crater 2. Trench 3. Moat 4. Ramp 5. Plane 6. Cratered ramp 7. Ramp into crater or trench 8. Furcation invasions
- 28. Bone destruction patterns in periodontal disease IV. Grant DA, Stern IB, Listgarten MA (1988) A. Vestibular, lingual or palatal defects associated with: 1. Normal anatomic structures • External oblique ridge • Retromolar triangle • Mylohyoid ridge • Zygomatic process 2. Exostosis and tori • Mandibular lingual tori • Buccal and posterior palatal exostosis 3. Dehiscences 4. Fenestrations 5. Reverse osseous architecture B. Vertical defects: 1. Three walls 2. Two walls 3. One wall 4. Combination with a different number of walls at the various levels of the defect. C. Furcation defects: 1. Class I or incipient 2. Class II or partial 3. Class III or through and through
- 29. Bone destruction patterns in periodontal disease V. Papapanou NP, Tonetti MS (2000)
- 30. Bone destruction patterns in periodontal disease Horizontal bone loss Vertical or angular defects
- 31. Bone destruction patterns in periodontal disease Vertical or angular defects (Nielsen JI 1980) Prevalence rate: 60% of persons Commonly seen involving interproximal surfaces
- 32. Bone destruction patterns in periodontal disease Three – wall defect Sarati et al (1968), Larato DC (1970) – posterior segment
- 33. Bone destruction patterns in periodontal disease Two – wall defect Crater-like – most common Non-crater – like
- 34. Bone destruction patterns in periodontal disease One – wall defect Hemiseptal defect
- 35. Bone destruction patterns in periodontal disease Combined defect
- 36. Bone destruction patterns in periodontal disease Osseous craters Interproximal crater with heavy ledges. Pre-op & post-op.
- 37. Bone destruction patterns in periodontal disease Saari et al (1968) – most common defect i. Vulnerability of the col (Cohen 1959) ii. Plaque retentive iii. Interdental bony configuration (Manson 1963) a. Spread of inflammation (Weinmann 1941, Goldman 1957) b. Cancellous trabeculation is more reactive (Amprino & Marotti 1964)
- 38. Bone destruction patterns in periodontal disease Trench Moat Ramp Plane
- 39. Bone destruction patterns in periodontal disease Bulbous bone contours Pre-operative buccal view Pre-operative occlusal view Post-operative buccal view
- 40. Bone destruction patterns in periodontal disease Ledges Blunted interdental septa with bone ledges Small crater with heavy ledges Hemisepta with heavy ledges
- 41. Bone destruction patterns in periodontal disease Reversed architecture Positive Flat Negative Negative architecture
- 42. Bone destruction patterns in periodontal disease Fenestrations and dehiscences DehiscenceFenestrations
- 43. Bone destruction patterns in periodontal disease Furcation involvement Stage in the progress of tissue destruction Increases with age (Larato DC 1970, 1975) Horizontal / angular bone loss evident Factors contributing to furcation involvement
- 44. Bone destruction patterns in periodontal disease Classification by Glickman (1953) Grade I Grade II Grade III Grade IV
- 45. Lesions causing alveolar bone destruction Osteoporosis – ground glass appearance Paget’s disease – cotton-wool appearance Fibrous dysplasia – multilocular cystic pattern Cherubism Cysts & tumors – cortical thinning
- 46. Conclusion Alveolar bone destruction Characteristic sign of periodontal disease Main cause of tooth loss
- 47. References Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza’s Clinical Periodontology. 10th edition. Saunders Company. Glickman I. Clinical Periodontology. 4th Edition. WB Saunders Company. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry. 5th edition. Blackwell Munksgaard. Goldman HM, Cohen DW. Periodontal Therapy. 6th Edition. The CV Mosby Company. 1988. Genco RJ, Goldman HM, Cohen DW. Contemporary Periodontics. The CV Mosby Company. 1990.
- 48. Manson JD. Bone morphology and bone loss in periodontal disease. J Clin Periodontol 1976; 3: 14-22. Schwtarz Z et al. Mechanisms of alveolar bone destruction in periodontitis. Periodontology 2000 1997; 14: 158.1 72. Goldman HM, Cohen DW. The infrabony pocket: classification and treatment. J Periodontol 1958; 10: 272-291. Karn KW et al. Topographic classification of deformities of the alveolar process. J Periodontol 1984; 5: 336-340. Papapanou NP, Tonetti MS. Diagnosis and epidemiology of periodontal osseous lesions. Periodontol 2000 2000; 22: 8–21. References
Hinweis der Redaktion
- Periodontitis is defined as “an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both”. Changes in the soft tissue of the pocket wall reflect the present inflammatory condition, while the level of bone is the consequence of past pathologic experiences. Considerable variation occurs in the amount of bone loss, rate as well as pattern of bone loss between individuals and between different sites in the same mouth. The height and density of the alveolar bone is normally maintained by an equilibrium between bone formation and bone resorption, as regulated by local and systemic influences. This process which occurs throughout life is referred to as bone remodelling. When bone formation exceeds bone resorption, alveolar bone loss occurs.
- Receptor activator of nuclear factor kappa b
- 4th edition glickman
- Read host modn sem OAF is another name for???
- However, it is not a result of aging, but a cumulative effect of repeated injuries to the periodontium.
- chk
- Also refer 4th, 8th,10th edn of carranza 1974 May (338 - 343): Potential Pathways for Bone Resorption in Human Periodontal Disease Ernest Hausmann -------------------------------- 1. Absorbable products from plaque could stimulate bone progenitor cells in the periodontium to differentiate into osteoclasts which resorb alveolar bone (Figure 1, pathway 1 ) . 2. Absorbable products from plaque as, for example, complexing agents and hydrolytic enzymes could destroy alveolar bone through non-cellular mechanisms by dissolving bone mineral and hydrolyzing the organic matrix (Figure 1, pathway 2). 3. a) Absorbable products from plaque could stimulate cells within the gingiva to release mediators, which in turn could trigger bone progenitor cells to differentiate into bone resorbing osteoclasts (Figure 1, pathways 3 and 4). b) Gingival cells in response to plaque products could release agents which by themselves have no effect on bone, but could potentiate as co-factors other bone resorptive agents. c) Gingival cells could release agents which destroy bone by direct chemical action without osteoclasts (Figure 1, pathway 5).
- form of the defect is related to the occlusal stress on the related tooth or teeth (Glickman & Smulow 1962),
- The major difference between the maxilla and the mandible is a structural one. Sicher (1949) points out that the lower alveolar process in most areas is far stronger than that of the upper jaw. "Only in the incisor and cuspid area are the outer and inner plates of the (mandibular) alveolar process thin . . ." The maxilla is composed of predominantly cancellous trabeculation and thin cortical plates. It is more vascular and the intricate meshwork of trabeculation must make for a large variation in the patterns of inflammatory destruction.
- Goldman & Cohen (1958) Possible factors in the pathogenesis of the bone defects: tooth anatomy and position, the relationship of adjacent marginal ridges and cemento- enamel junctions, open contact points with resultant food impaction, and traumatic lesions affecting the attachment apparatus. Local dental factors which are related to bone defects, e.g. irregular teeth, teeth with roots in close contact, teeth with grooves down the roots, and enamel grooves are reported by Lee et al. (1968) to be associated with bone defects. No doubt any deviation in tooth morphology or tooth relationship can affect related bone morphology. form of the defect is related to the original anatomy of the alveolar process (Prichard 1965). Goldman & cohen 6th edition periodontal therapy Orthodontic alignment of dental arch wrt basal bone Tooth size irt arch size Shape of anatomic crown CEJ or enamel pearls Tooth prominence within dental arch (bucco-linguoversion) Root prominence (fr fenestrations/dehiscneces) Teeth angulation Partially erupted/impacted/extruded teeth Rotated teeth
- alternation in the balance between bone resorption and bone deposition as a result of chronic inflammation.
- The following descriptive classification (after Prichard) was used in deciding the gross morphology of any osseous defect present
- Vertical or angular defects are those that occur in an oblique direction, leaving a hollowed-out trough in the bone alongside the root; the base of the defect is located apical to the surrounding bone.
- These are classified as: class I, indicating minimal, but notable, loss of bone in a furcation; class II, displaying a variable degree of bone destruction in a furcation but not exceeding completely through the furcation; and class III, in which bone resorption extends completely through the furcation. Subclass A denotes furcation involvements with vertical bone loss of 3 mm or less, subclass B 4 to 6 mm, while subclass C presents with bone loss from the fornix of 7 mm or more (Tarnow & Fletcher 1984). Vertical or angular defects are those that occur in an oblique direction, leaving a hollowed-out trough in the bone alongside the root; the base of the defect is located apical to the surrounding bone.
- Horizontal bone loss is the most common pattern of bone loss in periodontal disease. The bone is reduced in height, but the bone margin remains roughly perpendicular to the tooth surface. The interdental septa and facial and lingual plates are affected, but not necessarily to an equal degree around the same tooth. Vertical or angular defects are those that occur in an oblique direction, leaving a hollowed-out trough in the bone alongside the root; the base of the defect is located apical to the surrounding bone.
- If we look at other intra-alveolar defects, one- two- and three-walled defects and hemisepta were found almost exclusively in the maxilla.
- three-wall defects are more frequently found on the mesial surfaces of second and third upper and lower molars . Larato DC 1970 Saari et al. (1968) and Larato (1970) found three-walled defects to be most common in posterior segments. They suggest that where there is a greater thickness of supporting alveolar bone, three-walled defects are likely to occur. If this were the case, one would expect the greatest incidence of three-walled defects to be in the lower posterior segment; but in the present study this was found to be the most common site of the interdental crater. These trough-like defects are commonly observed in the interdental areas where one finds an intact proximal wall as well as the buccal and lingual walls of the alveolar process. Some of these lesions may be shallow with a broad orifice to the osseous part of the pocket while others may be narrow and deep. Three wall infrabony pockets are occasionally observed on the lingual surfaces of maxillary and mandibular teeth where the lingual plate is intact as well as both proximal walls. Less frequently noted are infrabony pockets located on the buccal surfaces of maxillary and mandibular posterior teeth.
- most common two-walled defects, craters bone resorption has occurred between two adjacent teeth, with the greatest loss under the contact area and facial and lingual cortical plates that extend more coronally remain
- bone loss is greater on one teeth than on the other (adjacent) one one walled osseous defect is also called a hemiseptum The one osseous wall of such a defect always supports the adjacent tooth; therefore the interproximal pocket depth on the affected tooth is several millimeters deeper than that on the adjacent tooth. Source: Journal of Periodontology on CD-ROM (Copyrights © 1998, AAP), 1958 Oct (272 - 291): The Infrabony Pocket: Classification and Treatment by Henry M. Goldman, d.m.d and D. Walter Cohen, d.d.s. -------------------------------- The infrabony pocket which has one osseous wall remaining is usually seen in the interdental area. Here it is most common to observe the presence of a proximal wall with the buccal and lingual walls destroyed. This can be detected clinically by probing or passing a needle through the soft tissue; radiographic examination may also be helpful. It is much less common to find the buccal wall intact with loss of the proximal and lingual walls or to have a lingual wall intact with the loss of the proximal and buccal.
- Manson 1976 Crater is defined as, cup or bowl shaped defect in the interdental alveolar bone with bone loss nearly equal on the roots of two contiguous teeth and more coronal position of the buccal and lingual alveolar crest; the facial and lingual / palatal walls may be of unequal height – American Academy of Periodontology.
- The normal bucco-lingual shape of the interdental alveolar septum between lower molars is usually flat and occasionally concave; the crest of the septum is not composed of cortical bone; and there is a marked structural contrast between the cortical bone of the facial and lingual plates and the interdental trabeculation (Manson 1963). Inflammation travels on vascular pathways (Weinmann 1941), i.e. most rapidly through vascular cancellous trabeculation (Goldman 1957).
- Trench – bone loss affects 2-3 confluent surfaces of the same tooth Moat – bone loss affects all 4 surfaces of the same tooth Ramp – bone deformity that results when both alveolar bone and its supporting bone are lost to the same degree in such a manner that the margins of the deformity are at different levels Plane – bone deformity that results when both alveolar bone and its supporting bone are lost to the same degree in such a manner that the margins of the deformity are at the same level Horizontal bone loss - bone deformity that results when both interdental septa and cortical (facial and lingual) plates are not lost to the same degree
- Thickened alveolar margins were found much more frequently in the maxilla than in the mandible and most frequently in the maxillary posterior segments. Irregular margins were found exclusively in the maxilla and mostly in the maxillary anterior segments. In the dry skull study of Saari et al. (1968), irregular margins were found to occur most frequently in the maxilla. It is possible that both thickened and irregular alveolar margins are related to the rate of remodelling possible in the vascular maxilla; in the former defect, osteoblastic activity predominates; in the latter, resorption. Gutters were found much more frequently in the maxilla, and it is suggested that this phenomenon is also related to the greater reactivity of the thin plates of maxillary bone.
- Chk goldman
- Loss of alveolar bone support is one of the characteristic signs of destructive periodontal disease. Osseous lesions may represent site-specific risk factors or indicators for disease progression and are also one of the main causes of tooth loss. The extent and the severity of alveolar bone loss is important for diagnosis, treatment planning, and assessment of prognosis of the periodontal patient.