This document discusses patterns of bone destruction in periodontal disease. It covers various causes of bone loss such as the extension of gingival inflammation, trauma from occlusion, and systemic disorders. Factors that determine bone destruction include normal bone variation, exostoses, buttressing bone formation, and food impaction. Common bone destruction patterns include horizontal loss, vertical defects, intrabony defects of one to three walls, furcation involvement, osseous craters, and ledges. Systemic conditions like osteoporosis and Paget's disease can also cause alveolar bone destruction.
Furcation involvement is a common sequela of severe chronic periodontal disease. Its effective management has a profound influence on the outcome of periodontal therapy.
This presentation describes the gingival recession, its classifications and theories of pathogenesis and different etiological factors in its progression.
In periodontology, classifications are widely used to categorize defects due to periodontitis according to their etiology, diagnosis, treatment and prognosis.
Several classifications have been proposed in the literature in order to facilitate the diagnosis of gingival recessions.
This presentation describes the occlusion evaluation, its role in periodontal disease and occlusal therapy. Various diagnostic options and treatment options opted for occlusal correction.
Furcation involvement is a common sequela of severe chronic periodontal disease. Its effective management has a profound influence on the outcome of periodontal therapy.
This presentation describes the gingival recession, its classifications and theories of pathogenesis and different etiological factors in its progression.
In periodontology, classifications are widely used to categorize defects due to periodontitis according to their etiology, diagnosis, treatment and prognosis.
Several classifications have been proposed in the literature in order to facilitate the diagnosis of gingival recessions.
This presentation describes the occlusion evaluation, its role in periodontal disease and occlusal therapy. Various diagnostic options and treatment options opted for occlusal correction.
Phase I periodontal therapy is the first in the chronologic sequence of procedures that constitute periodontal treatment. It is also referred to as cause related therapy or non-surgical periodontal therapy.
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
Phase I periodontal therapy is the first in the chronologic sequence of procedures that constitute periodontal treatment. It is also referred to as cause related therapy or non-surgical periodontal therapy.
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
explained here is bone loos and patterns of bone loos in alveolar bone to various insults . Dr Harshavardhan pawal also gives emphasis on rate on bone loss and radius of action .
this ppt depicts pattern of bone destruction. its a very good slide show showing the process of bone formation, bone destruction and their patterns in periodontal diseases.
BONE LOSS AND PATTERNS OF BONE DESTRUCTION ishu.pptxDr. Ishu SINGLA
Presentation on topic Bone Loss And Patterns of Bone Destruction.
This is for reading and knowledge purpose only. Text is taken from Standard books only.
The Art Pastor's Guide to Sabbath | Steve ThomasonSteve Thomason
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The map views are useful for providing a geographical representation of data. They allow users to visualize and analyze the data in a more intuitive manner.
Instructions for Submissions thorugh G- Classroom.pptxJheel Barad
This presentation provides a briefing on how to upload submissions and documents in Google Classroom. It was prepared as part of an orientation for new Sainik School in-service teacher trainees. As a training officer, my goal is to ensure that you are comfortable and proficient with this essential tool for managing assignments and fostering student engagement.
Ethnobotany and Ethnopharmacology:
Ethnobotany in herbal drug evaluation,
Impact of Ethnobotany in traditional medicine,
New development in herbals,
Bio-prospecting tools for drug discovery,
Role of Ethnopharmacology in drug evaluation,
Reverse Pharmacology.
The Roman Empire A Historical Colossus.pdfkaushalkr1407
The Roman Empire, a vast and enduring power, stands as one of history's most remarkable civilizations, leaving an indelible imprint on the world. It emerged from the Roman Republic, transitioning into an imperial powerhouse under the leadership of Augustus Caesar in 27 BCE. This transformation marked the beginning of an era defined by unprecedented territorial expansion, architectural marvels, and profound cultural influence.
The empire's roots lie in the city of Rome, founded, according to legend, by Romulus in 753 BCE. Over centuries, Rome evolved from a small settlement to a formidable republic, characterized by a complex political system with elected officials and checks on power. However, internal strife, class conflicts, and military ambitions paved the way for the end of the Republic. Julius Caesar’s dictatorship and subsequent assassination in 44 BCE created a power vacuum, leading to a civil war. Octavian, later Augustus, emerged victorious, heralding the Roman Empire’s birth.
Under Augustus, the empire experienced the Pax Romana, a 200-year period of relative peace and stability. Augustus reformed the military, established efficient administrative systems, and initiated grand construction projects. The empire's borders expanded, encompassing territories from Britain to Egypt and from Spain to the Euphrates. Roman legions, renowned for their discipline and engineering prowess, secured and maintained these vast territories, building roads, fortifications, and cities that facilitated control and integration.
The Roman Empire’s society was hierarchical, with a rigid class system. At the top were the patricians, wealthy elites who held significant political power. Below them were the plebeians, free citizens with limited political influence, and the vast numbers of slaves who formed the backbone of the economy. The family unit was central, governed by the paterfamilias, the male head who held absolute authority.
Culturally, the Romans were eclectic, absorbing and adapting elements from the civilizations they encountered, particularly the Greeks. Roman art, literature, and philosophy reflected this synthesis, creating a rich cultural tapestry. Latin, the Roman language, became the lingua franca of the Western world, influencing numerous modern languages.
Roman architecture and engineering achievements were monumental. They perfected the arch, vault, and dome, constructing enduring structures like the Colosseum, Pantheon, and aqueducts. These engineering marvels not only showcased Roman ingenuity but also served practical purposes, from public entertainment to water supply.
The Indian economy is classified into different sectors to simplify the analysis and understanding of economic activities. For Class 10, it's essential to grasp the sectors of the Indian economy, understand their characteristics, and recognize their importance. This guide will provide detailed notes on the Sectors of the Indian Economy Class 10, using specific long-tail keywords to enhance comprehension.
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We all have good and bad thoughts from time to time and situation to situation. We are bombarded daily with spiraling thoughts(both negative and positive) creating all-consuming feel , making us difficult to manage with associated suffering. Good thoughts are like our Mob Signal (Positive thought) amidst noise(negative thought) in the atmosphere. Negative thoughts like noise outweigh positive thoughts. These thoughts often create unwanted confusion, trouble, stress and frustration in our mind as well as chaos in our physical world. Negative thoughts are also known as “distorted thinking”.
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
4. Blood calcium
Receptors on chief cells of PTH
Release of PTH
Release calcium
Osteogenic substrates
BONE COUPLING
Osteoblasts
Monocytes
Osteoclasts
Bone
Introduction
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.
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.
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
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
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)
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
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
Editor's Notes
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
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.
