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BONE LOSS AND
PATTERNS OF BONE
DESTRUCTION
Presented by:
Dr. ISHU SINGLA
MDS Student
Department of Periodontology
INTRODUCTION
 Periodontitis is an inflammatory condition of the teeth and their supporting structures.
 bacterial biofilm insult  inflammation  detrimental effects on the periodontal unit, which results in the
destruction of periodontal ligament fibres and bone loss.
 Bone loss is the ultimate and last consequence of the inflammatory process observed in periodontitis.
 Therefore the existing bone level is the result of past pathologic episodes, whereas changes present in the soft
tissue of the pocket wall reflect the presence of the inflammatory condition.
 Thus the degree of bone loss does not necessarily correlate with the depth of periodontal pockets, the severity of
ulceration of the pocket wall, or the presence or absence of suppuration
PHYSIOLOGICAL ALVEOLAR BONE EQUILIBRIUM
 Height of the alveolar bone is maintained by the constant equilibrium between bone formation and
bone resorption which is regulated by the local and systemic influences i.e., when resorption
exceeds formation bone height is reduced.
 Reduction in the height of alveolar bone occurs physiologically with age and is termed physiologic
or senile atrophy (Gottlieb & Orban 1938)
 So, bone loss in periodontal disease may result from any of following changes:
o Increased resorption in the presence of normal formation
o Decreased formation in the presence of normal resorption
o Increased resorption combined with decreased formation
BONE FACTOR CONCEPT
DEFINITION: when the alveolar bone responds to systemic regulatory influence is termed as the bone
factor in the periodontal disease.
This concept demonstrates :
1. The manner in which different systemic influences alter the response of alveolar bone to local
irritation.
2. The manner in which systemic influences cause destruction of periodontal tissues in the absence of
the local destructive factors.
3. The clinical procedure whereby the “bone factor” concept is applied in the diagnosis and
determination of prognosis of periodontal disease as follows:
a. Determine the patient’s age
b. Determine the distribution, severity and rate of bone loss.
CAUSES OF BONE DESTRUCTION
BONE DESTRUCTION CAUSED BY EXTENSION OF GINGIVAL INFLAMMATION
 This is Most common cause of bone destruction in periodontal disease
 Transition from gingivitis  periodontitis is associated with changes in composition of bacterial plaque
 Substances produced by the subgingival bacteria and the tissues during inflammation and immune reactions may
affect bone turnover, either by causing the differentiation and stimulation of osteoclasts or by inhibiting bone
formation by osteoblasts.
 In advanced stages of disease, the number of motile organisms and spirochetes increases, whereas the number of
coccoid rods and straight rods decreases. (Lindhe J, Liljenberg B, Listgarten MA 1980)
 The cellular composition of the infiltrated connective tissue also changes with increasing severity of the lesion.
 Fibroblasts and lymphocytes predominate in stage I gingivitis, whereas the number of plasma cells and blast cells
- increases gradually as the disease progresses.
 Seymour et al 1978 : stage of ‘Contained gingivitis’ – predominate T-lymphocyte seen,
but once B-lymphocyte comes it becomes progressively destructive.
A) Interproximally
1. from the gingiva into the bone
2. from the bone into the periodontal ligament
3. from the gingival into the periodontal ligament
B) Facially and Lingually
1.From the gingiva along the outer periosteum
2. From the periosteum to the bone
3. From the gingival into the periodontal ligament
Pathways of inflammation from the gingival into the supporting periodontal tissues in periodontitis
Histopathological changes during gingival inflammation
(Weinmann J.P. 1941)
 In the upper molar region, inflammation can extend to the maxillary sinus, resulting in thickening of the
sinus mucosa
 Interproximally, inflammation spreads to the loose connective tissue around the blood vessels, through
the fibers, and then into the bone through vessel channels that perforate the crest of the interdental
septum at the center of the crest.
 Less frequently, the inflammation spreads from gingiva directly into PDL and from there into interdental
septum (Akyoshi M, Mori K 1967)
 Bone destruction in periodontal disease is not a process of bone necrosis. It involves the activity of
living cells along viable bone. When tissue necrosis and pus are present in periodontal disease, they
occur in the soft tissue walls of periodontal pockets, not along the resorbing margin of the underlying
bone.
 Amount of infiltrate correlates with the degree of bone loss but not with the number of osteoclasts.
 Distance from the apical border of the infiltrate to the alveolar bone crest correlates with both the
number of osteoclasts on the alveolar crest and the total number of osteoclasts. (Rowe DJ 1981, Lindhe
J 1978)
As inflammation reaches Bone:-
• Spreads into marrow spaces
• Replaces marrow with a leucocytic and fluid exudate, new blood vessels & proliferating fibroblasts
• increase in number of Multinuclear osteoclasts & mononuclear phagocytes
• Bone surfaces appear lined with Howship lacunae
• In marrow spaces, resorption proceeds from within and causing thinning of surrounding bony trabeculae
& enlargement of marrow spaces
• Leads to destruction of bone & reduction in bone height
• Fatty bone marrow is partially or totally replaced by fibrous type
 Garant and Cho first to say that bone resorption stimulators produced by microbial plaque have a
finite RADIUS OF ACTION.
Also suggested that locally produced bone resorption factors may need to be present in the proximity of
the bone surface to-exert their action.
Large defects greatly exceeding a distance of 2.5 mm from the tooth surface (as described in aggressive
types of periodontitis) may be caused by the presence of bacteria in the tissues.
 Page & Schroeder postulated a range of effectiveness of about 1.5- 2.5 mm within which bacterial
plaque can cause bone destruction.
 Waerhaug applied this principle to human periodontium by making measurements on radiographs,
histologic sections & extracted teeth to determine the distance between microbial plaque and the bone
surface.
He showed that the bone margin is never located closer than 0.5mm to plaque and not farther than 1.5 to
2.5mm from plaque.
RADIUS OF ACTION
In a study, persons with NO ORAL HYGIENE & NO DENTAL CARE (Loe et al 1978), found the rate of
bone loss to average 0.2 mm/year-facial surfaces and about 0.3 mm/year-proximal surfaces when
periodontal disease was allowed to progress untreated.
Study conducted by loe et al in Srilankan tea workers identified the following 3 subgroups of patients with
periodontal disease (PD) based on interproximal loss of attachment and tooth mortality:
RATE OF BONE LOSS
• Periodontal destruction occurs in an episodic, intermittent manner, with periods of inactivity or
quiescence.
• destructive periods  loss of collagen and alveolar bone  deepening of the periodontal pocket.
• The reasons for the onset of destructive periods are not clear, although the following theories have been
offered:
1. destructive activity are associated with subgingival ulceration and an acute inflammatory Reaction,
resulting in rapid loss of alveolar bone.
2. conversion of a predominantly T-lymphocytes to predominantly B lymphocytes-plasma cell infiltrate.
3. Periods of exacerbation are associated with an increase in loose unattached, motile, gram negative,
anaerobic pocket flora, and periods of remission co-incide with the formation of a dense, unattached,
nonmotile, gram positive flora with a tendency to mineralize.
PERIODS OF DESTRUCTION
Role of cytokines and prostaglandins:
Many of the osteotropic cytokines such as IL -1, TNF, lymphotoxin and IL -6 are products of immune
cells and osteoblasts that are present in regions where bone resorption is actively occurring.
IL -1: stimulate bone resorption by direct action on osteoclasts
or by indirect action in terms of causing stimulation of PGE 2.
IL -6: leads to formation of cells with osteoclastic phenotype.
TNF and lymphotoxin ----- stimulate osteoclastic bone resorption
Gamma interferon ---- Has an effect opposite to IL -1 and TNF, it inhibits bone resorption.
MECHANISMS OF BONE RESORPTION
A. Lacunar Resorption (osteoclasts)-
The destruction of bone results from the action of osteoclasts, which are usually multinuclear. The
following explanation of the manner in which osteoclasts resorb bone have been offered:-
1. Initial local drop in PH  causes decalcification of the mineral salts of the bone
2. Proteolytic action upon the organic matrix, resulting in liberation of calcium salts.
3. Simultaneous destruction of the inorganic and organic components.
4. Phagocytosis of the organic matrix after the inorganic salts are removed as the result of alteration in
the local physio-chemical equilibrium.
B. Halisteresis (osteolysis)-
In this process the bone disintegrates into its separate components without the action of osteoclasts.
Theories offered in explanation of noncellular destruction of bone include:-
1. Softening and liquefaction of organic matrix following by leaching out of inorganic components.
2. Loss of the inorganic components by disturbances in normal physio-chemical equilibrium followed by
reversion of the organic components to connective tissue.
C. Increased Vascularity –
Increased osteoclastic resorption of bone due to pressure from hyperaemia.
According to Leriche and Policard, increased circulation within bone favours resorption whereas blood or
lymphatic stasis favours bone formation.
Japle describes a “vascular resorption” in which dilation and an increase in the number of blood vessel are
basic factors underlying the bone destruction. The vascular changes are made possible by decalcification of
bone matrix caused by alteration in the electrolytic balance by local and systemic factors.
• Activated osteoclasts initiates bone destruction.
 The activation signal is modulated by RANK L (Receptor activator of nuclear factor kappa-Β ligand),
RANK and OPG, three novel members of TNF ligand and receptor superfamilies.
 The formation of active osteoclast requires macrophage colony-stimulating factor (MCSF) and involves
cell to cell contact between precursors of monocyte/macrophage lineage and osteoblasts, marrow
stromal cells and T and B cells. These cells express the RANK L essential for this process. RANK L
attaches to RANK, a receptor on cell surface of osteoclasts and its precursors to stimulate proliferation
and differentiation of cells to form osteoclast phenotype.
 OPG (osteoprotegrin) a soluble receptor produced by osteoblast, marrow stromal cells and other cells
modify effect of RANK L by inhibiting RANK L/ RANK interaction.
MOLECULAR CONCEPT OF BONE DESTRUCTION
RANK L (Receptor activator of nuclear factor kappa-Β ligand)
OPG (osteoprotegrin)
MCSF (macrophage colony-stimulating factor)
PTH (parathyroid hormon)
Bone formation in periodontal disease
BONE DESTRUCTION CAUSED BY TRAUMA FROM OCCLUSION
 Trauma from occlusion can produce bone destruction in the absence or presence of inflammation.
 In the absence of inflammation, the changes caused by trauma from occlusion are
• increased compression and tension of the periodontal ligament
• increased osteoclasis of alveolar bone to necrosis of the periodontal ligament & bone
• resorption of bone and tooth structure
These changes are reversible in that they can be repaired if the offending forces are removed
 However, persistent trauma from occlusion results in funnel shaped widening of the crestal portion of the periodontal
ligament, and cause resorption of the adjacent alveolar bone. The modified bone shape may weaken tooth support and cause
mobility.
 When combined with inflammation, trauma from occlusion aggravates the bone destruction caused by the inflammation and
causes bizarre bone patterns.
BONE DESTRUCTION CAUSED BY SYSTEMIC DISORDERS
 Local and systemic factors regulate the physiologic equilibrium of bone.
 When a generalized tendency towards bone resorption exists, bone loss initiated by local
inflammatory processes may be magnified.
 Osteoporosis a physiologic condition of postmenopausal women, resulting in loss of bone mineral
content and structural bone changes. Periodontitis and osteoporosis share a number of risk factors
(e.g., aging, smoking, diseases, medications that interfere with healing).
 Periodontal bone loss may also occur in generalized skeletal disturbances (e.g.,
hyperparathyroidism, leukemia, Langerhans cell histiocytosis)
FACTORS DETERMINING BONE MORPHOLOGY IN PERIODONTAL DISEASE
anatomic features that substantially affect the bone destructive pattern in periodontal disease includes:
•thickness, width and crestal angulation of the interdental septa
•thickness of the facial and lingual alveolar plates
•presence of fenestrations and dehiscence.
•alignment of the teeth, Root and root trunk anatomy
•Root position within the alveolar process Proximity with another tooth surface
CLASSIFICATION OF BONE DESTRUCTION PATTERNS IN PERIODONTAL
DISEASE
According to Glickman (1964) :
 Osseous crater
 Infrabony defect
 Bulbous bone contour
 Hemisepta
 Inconsistent margins
Prichard (1965) classified defects into
 Interproximal crater
 inconsistent margins
 Hemisepta
 Furcation invasion
 Intrabony defects
• combination
According to Monson and Nicholson (1974)
 Thickened margins – a linear enlargement of buccal or
lingual marginal plate instead of thin , tapering or round
margins
 Interdental crater – concavity in the crest, confined within
lingual and buccal walls.
 Hemiseptum – the remaining half of interdental septum,
forming the proximal wall of an one wall intrabony defect
 Intrabony defect with 3 osseous walls
 Intrabony defect with 2 osseous walls
 Intrabony defect with one osseous wall other than
hemiseptum
 Marginal gutter
 Furcation involvement
 Irregular bony margins
 Dehiscence
 Fenestration
 Exostosis
Bone deformities (Osseous defects):
Vertical or angular defects: Bone loss occurs in an oblique direction.
It is usually accompanied by infrabony points
Horizontal bone defect: Bone is reduced in height
Bone margin is perpendicular to the tooth surface
EXOSTOSES
• These are outgrowths of bone of varied size and shape.
• Palatal exostoses found in 40% of human skulls. (Nery FB 1977)
• They can occur as small nodules, large nodules, sharp ridges, spike-like projections, or any combination
of these.
TRAUMA FROM OCCLUSION
• Important factor in determining the dimension and shape of bone deformities.
• May cause a thickening of the cervical margin of alveolar bone or a change in the morphology of the
bone (e.g., angular defects, buttressing bone) on which inflammatory changes will later be superimposed.
BUTTRESSING BONE FORMATION (LIPPING)
• Bone formation sometimes occurs in an attempt to buttress bony trabeculae weakened by resorption.
• When it occurs within the jaw, it is termed central buttressing bone formation .
• When occurs on the external surface it is referred to as peripheral buttressing bone formation. This may cause bulging of the
bone contour, termed lipping
FOOD IMPACTION:
• Interdental defects often occur where proximal contacts is abnormal or absent.
• Pressure and irritation from food impaction contributes to inverse architecture.
• In some instances the poor proximal relationship may be the result of shift in bone position because of extensive bone
destruction preceding food impaction.
• In such cases food impaction is the complicating factor rather than the cause of bone destruction.
AGGRESSIVE PERIODONTITIS
A vertical or angular pattern of alveolar bone destruction is found around the first molars in aggressive periodontitis.
The cause of the localized bone destruction in this type of periodontal disease is unknown.
OSSEOUS (CRATERS)
These are concavities in the asset of the interdental bone confined within the facial and lingual walls.
Craters have been classified as (Ochsenbein and Bohannan in 1964)
Class 1- have 2-3 mm osseous concavity with relatively thick buccal and lingual walls.
Treated with palatal ramping.
Class 2- have 4-5 mm osseous concavity with relatively thick buccal and lingual walls.
Treated with buccal and palatal ramping.
Class 3 - have 6-7 mm osseous concavity with relatively thick buccal and lingual walls.
Treated with buccal and palatal ramping.
Class 4- Lesions with variable depth and thin buccal and lingual walls.
BULBOUS BONE CONTOURS
There are bony enlargements caused by exostoses
•Due to Adaptation to function
•Maxilla > Mandible
REVERSED ARCHITECTURE
• Caused by loss of interdental bone
• Includes loss of facial or lingual plates without associated loss of
radicular bone, hence reversal of architecture.
LEDGES
These are plateaus – like bone margin caused by resorption of
thickened bony plates.
FURCATION INVOLVEMENT
•It is invasion of the bifurcation or trifurcation of multi rooted teeth by periodontal disease.
• Mandibular 1st molars are most common site and maxillary premolar are least common.
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 produced horizontal or angular , and very frequently crater develop
in interradicular area.
GLICKMAN`S CLASSIFICATION (1953)
Grade I
•Incipient.
•Just barely detectable with examination hand instruments.
•slight bone loss in the furcation area
Grade II
•Early bone loss.
•instrument goes partially into the furcation, but not all the way through.
•Furcation may be grade II on both sides of the tooth, but are not connected.
Grade III
•Advanced bone loss.
•Examination hand instrument goes all the way through furcation, to other side of tooth.
•Furcation is through-and-through.
Grade IV
•Through-and-through, plus furcation is clinically visible due to gingival recession.
BONE LOSS AND PATTERNS OF BONE DESTRUCTION ishu.pptx
BONE LOSS AND PATTERNS OF BONE DESTRUCTION ishu.pptx

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BONE LOSS AND PATTERNS OF BONE DESTRUCTION ishu.pptx

  • 1. BONE LOSS AND PATTERNS OF BONE DESTRUCTION Presented by: Dr. ISHU SINGLA MDS Student Department of Periodontology
  • 2. INTRODUCTION  Periodontitis is an inflammatory condition of the teeth and their supporting structures.  bacterial biofilm insult  inflammation  detrimental effects on the periodontal unit, which results in the destruction of periodontal ligament fibres and bone loss.  Bone loss is the ultimate and last consequence of the inflammatory process observed in periodontitis.  Therefore the existing bone level is the result of past pathologic episodes, whereas changes present in the soft tissue of the pocket wall reflect the presence of the inflammatory condition.  Thus the degree of bone loss does not necessarily correlate with the depth of periodontal pockets, the severity of ulceration of the pocket wall, or the presence or absence of suppuration
  • 3. PHYSIOLOGICAL ALVEOLAR BONE EQUILIBRIUM  Height of the alveolar bone is maintained by the constant equilibrium between bone formation and bone resorption which is regulated by the local and systemic influences i.e., when resorption exceeds formation bone height is reduced.  Reduction in the height of alveolar bone occurs physiologically with age and is termed physiologic or senile atrophy (Gottlieb & Orban 1938)  So, bone loss in periodontal disease may result from any of following changes: o Increased resorption in the presence of normal formation o Decreased formation in the presence of normal resorption o Increased resorption combined with decreased formation
  • 4. BONE FACTOR CONCEPT DEFINITION: when the alveolar bone responds to systemic regulatory influence is termed as the bone factor in the periodontal disease. This concept demonstrates : 1. The manner in which different systemic influences alter the response of alveolar bone to local irritation. 2. The manner in which systemic influences cause destruction of periodontal tissues in the absence of the local destructive factors. 3. The clinical procedure whereby the “bone factor” concept is applied in the diagnosis and determination of prognosis of periodontal disease as follows: a. Determine the patient’s age b. Determine the distribution, severity and rate of bone loss.
  • 5. CAUSES OF BONE DESTRUCTION
  • 6. BONE DESTRUCTION CAUSED BY EXTENSION OF GINGIVAL INFLAMMATION  This is Most common cause of bone destruction in periodontal disease  Transition from gingivitis  periodontitis is associated with changes in composition of bacterial plaque  Substances produced by the subgingival bacteria and the tissues during inflammation and immune reactions may affect bone turnover, either by causing the differentiation and stimulation of osteoclasts or by inhibiting bone formation by osteoblasts.  In advanced stages of disease, the number of motile organisms and spirochetes increases, whereas the number of coccoid rods and straight rods decreases. (Lindhe J, Liljenberg B, Listgarten MA 1980)  The cellular composition of the infiltrated connective tissue also changes with increasing severity of the lesion.  Fibroblasts and lymphocytes predominate in stage I gingivitis, whereas the number of plasma cells and blast cells - increases gradually as the disease progresses.  Seymour et al 1978 : stage of ‘Contained gingivitis’ – predominate T-lymphocyte seen, but once B-lymphocyte comes it becomes progressively destructive.
  • 7. A) Interproximally 1. from the gingiva into the bone 2. from the bone into the periodontal ligament 3. from the gingival into the periodontal ligament B) Facially and Lingually 1.From the gingiva along the outer periosteum 2. From the periosteum to the bone 3. From the gingival into the periodontal ligament Pathways of inflammation from the gingival into the supporting periodontal tissues in periodontitis
  • 8. Histopathological changes during gingival inflammation (Weinmann J.P. 1941)
  • 9.  In the upper molar region, inflammation can extend to the maxillary sinus, resulting in thickening of the sinus mucosa  Interproximally, inflammation spreads to the loose connective tissue around the blood vessels, through the fibers, and then into the bone through vessel channels that perforate the crest of the interdental septum at the center of the crest.  Less frequently, the inflammation spreads from gingiva directly into PDL and from there into interdental septum (Akyoshi M, Mori K 1967)  Bone destruction in periodontal disease is not a process of bone necrosis. It involves the activity of living cells along viable bone. When tissue necrosis and pus are present in periodontal disease, they occur in the soft tissue walls of periodontal pockets, not along the resorbing margin of the underlying bone.  Amount of infiltrate correlates with the degree of bone loss but not with the number of osteoclasts.  Distance from the apical border of the infiltrate to the alveolar bone crest correlates with both the number of osteoclasts on the alveolar crest and the total number of osteoclasts. (Rowe DJ 1981, Lindhe J 1978)
  • 10. As inflammation reaches Bone:- • Spreads into marrow spaces • Replaces marrow with a leucocytic and fluid exudate, new blood vessels & proliferating fibroblasts • increase in number of Multinuclear osteoclasts & mononuclear phagocytes • Bone surfaces appear lined with Howship lacunae • In marrow spaces, resorption proceeds from within and causing thinning of surrounding bony trabeculae & enlargement of marrow spaces • Leads to destruction of bone & reduction in bone height • Fatty bone marrow is partially or totally replaced by fibrous type
  • 11.  Garant and Cho first to say that bone resorption stimulators produced by microbial plaque have a finite RADIUS OF ACTION. Also suggested that locally produced bone resorption factors may need to be present in the proximity of the bone surface to-exert their action. Large defects greatly exceeding a distance of 2.5 mm from the tooth surface (as described in aggressive types of periodontitis) may be caused by the presence of bacteria in the tissues.  Page & Schroeder postulated a range of effectiveness of about 1.5- 2.5 mm within which bacterial plaque can cause bone destruction.  Waerhaug applied this principle to human periodontium by making measurements on radiographs, histologic sections & extracted teeth to determine the distance between microbial plaque and the bone surface. He showed that the bone margin is never located closer than 0.5mm to plaque and not farther than 1.5 to 2.5mm from plaque. RADIUS OF ACTION
  • 12. In a study, persons with NO ORAL HYGIENE & NO DENTAL CARE (Loe et al 1978), found the rate of bone loss to average 0.2 mm/year-facial surfaces and about 0.3 mm/year-proximal surfaces when periodontal disease was allowed to progress untreated. Study conducted by loe et al in Srilankan tea workers identified the following 3 subgroups of patients with periodontal disease (PD) based on interproximal loss of attachment and tooth mortality: RATE OF BONE LOSS
  • 13. • Periodontal destruction occurs in an episodic, intermittent manner, with periods of inactivity or quiescence. • destructive periods  loss of collagen and alveolar bone  deepening of the periodontal pocket. • The reasons for the onset of destructive periods are not clear, although the following theories have been offered: 1. destructive activity are associated with subgingival ulceration and an acute inflammatory Reaction, resulting in rapid loss of alveolar bone. 2. conversion of a predominantly T-lymphocytes to predominantly B lymphocytes-plasma cell infiltrate. 3. Periods of exacerbation are associated with an increase in loose unattached, motile, gram negative, anaerobic pocket flora, and periods of remission co-incide with the formation of a dense, unattached, nonmotile, gram positive flora with a tendency to mineralize. PERIODS OF DESTRUCTION
  • 14. Role of cytokines and prostaglandins: Many of the osteotropic cytokines such as IL -1, TNF, lymphotoxin and IL -6 are products of immune cells and osteoblasts that are present in regions where bone resorption is actively occurring. IL -1: stimulate bone resorption by direct action on osteoclasts or by indirect action in terms of causing stimulation of PGE 2. IL -6: leads to formation of cells with osteoclastic phenotype. TNF and lymphotoxin ----- stimulate osteoclastic bone resorption Gamma interferon ---- Has an effect opposite to IL -1 and TNF, it inhibits bone resorption.
  • 15. MECHANISMS OF BONE RESORPTION A. Lacunar Resorption (osteoclasts)- The destruction of bone results from the action of osteoclasts, which are usually multinuclear. The following explanation of the manner in which osteoclasts resorb bone have been offered:- 1. Initial local drop in PH  causes decalcification of the mineral salts of the bone 2. Proteolytic action upon the organic matrix, resulting in liberation of calcium salts. 3. Simultaneous destruction of the inorganic and organic components. 4. Phagocytosis of the organic matrix after the inorganic salts are removed as the result of alteration in the local physio-chemical equilibrium.
  • 16. B. Halisteresis (osteolysis)- In this process the bone disintegrates into its separate components without the action of osteoclasts. Theories offered in explanation of noncellular destruction of bone include:- 1. Softening and liquefaction of organic matrix following by leaching out of inorganic components. 2. Loss of the inorganic components by disturbances in normal physio-chemical equilibrium followed by reversion of the organic components to connective tissue. C. Increased Vascularity – Increased osteoclastic resorption of bone due to pressure from hyperaemia. According to Leriche and Policard, increased circulation within bone favours resorption whereas blood or lymphatic stasis favours bone formation. Japle describes a “vascular resorption” in which dilation and an increase in the number of blood vessel are basic factors underlying the bone destruction. The vascular changes are made possible by decalcification of bone matrix caused by alteration in the electrolytic balance by local and systemic factors.
  • 17. • Activated osteoclasts initiates bone destruction.  The activation signal is modulated by RANK L (Receptor activator of nuclear factor kappa-Β ligand), RANK and OPG, three novel members of TNF ligand and receptor superfamilies.  The formation of active osteoclast requires macrophage colony-stimulating factor (MCSF) and involves cell to cell contact between precursors of monocyte/macrophage lineage and osteoblasts, marrow stromal cells and T and B cells. These cells express the RANK L essential for this process. RANK L attaches to RANK, a receptor on cell surface of osteoclasts and its precursors to stimulate proliferation and differentiation of cells to form osteoclast phenotype.  OPG (osteoprotegrin) a soluble receptor produced by osteoblast, marrow stromal cells and other cells modify effect of RANK L by inhibiting RANK L/ RANK interaction. MOLECULAR CONCEPT OF BONE DESTRUCTION
  • 18. RANK L (Receptor activator of nuclear factor kappa-Β ligand) OPG (osteoprotegrin) MCSF (macrophage colony-stimulating factor) PTH (parathyroid hormon)
  • 19. Bone formation in periodontal disease
  • 20. BONE DESTRUCTION CAUSED BY TRAUMA FROM OCCLUSION  Trauma from occlusion can produce bone destruction in the absence or presence of inflammation.  In the absence of inflammation, the changes caused by trauma from occlusion are • increased compression and tension of the periodontal ligament • increased osteoclasis of alveolar bone to necrosis of the periodontal ligament & bone • resorption of bone and tooth structure These changes are reversible in that they can be repaired if the offending forces are removed  However, persistent trauma from occlusion results in funnel shaped widening of the crestal portion of the periodontal ligament, and cause resorption of the adjacent alveolar bone. The modified bone shape may weaken tooth support and cause mobility.  When combined with inflammation, trauma from occlusion aggravates the bone destruction caused by the inflammation and causes bizarre bone patterns.
  • 21. BONE DESTRUCTION CAUSED BY SYSTEMIC DISORDERS  Local and systemic factors regulate the physiologic equilibrium of bone.  When a generalized tendency towards bone resorption exists, bone loss initiated by local inflammatory processes may be magnified.  Osteoporosis a physiologic condition of postmenopausal women, resulting in loss of bone mineral content and structural bone changes. Periodontitis and osteoporosis share a number of risk factors (e.g., aging, smoking, diseases, medications that interfere with healing).  Periodontal bone loss may also occur in generalized skeletal disturbances (e.g., hyperparathyroidism, leukemia, Langerhans cell histiocytosis)
  • 22. FACTORS DETERMINING BONE MORPHOLOGY IN PERIODONTAL DISEASE anatomic features that substantially affect the bone destructive pattern in periodontal disease includes: •thickness, width and crestal angulation of the interdental septa •thickness of the facial and lingual alveolar plates •presence of fenestrations and dehiscence. •alignment of the teeth, Root and root trunk anatomy •Root position within the alveolar process Proximity with another tooth surface
  • 23. CLASSIFICATION OF BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE
  • 24. According to Glickman (1964) :  Osseous crater  Infrabony defect  Bulbous bone contour  Hemisepta  Inconsistent margins Prichard (1965) classified defects into  Interproximal crater  inconsistent margins  Hemisepta  Furcation invasion  Intrabony defects • combination According to Monson and Nicholson (1974)  Thickened margins – a linear enlargement of buccal or lingual marginal plate instead of thin , tapering or round margins  Interdental crater – concavity in the crest, confined within lingual and buccal walls.  Hemiseptum – the remaining half of interdental septum, forming the proximal wall of an one wall intrabony defect  Intrabony defect with 3 osseous walls  Intrabony defect with 2 osseous walls  Intrabony defect with one osseous wall other than hemiseptum  Marginal gutter  Furcation involvement  Irregular bony margins  Dehiscence  Fenestration  Exostosis
  • 25. Bone deformities (Osseous defects): Vertical or angular defects: Bone loss occurs in an oblique direction. It is usually accompanied by infrabony points Horizontal bone defect: Bone is reduced in height Bone margin is perpendicular to the tooth surface
  • 26. EXOSTOSES • These are outgrowths of bone of varied size and shape. • Palatal exostoses found in 40% of human skulls. (Nery FB 1977) • They can occur as small nodules, large nodules, sharp ridges, spike-like projections, or any combination of these. TRAUMA FROM OCCLUSION • Important factor in determining the dimension and shape of bone deformities. • May cause a thickening of the cervical margin of alveolar bone or a change in the morphology of the bone (e.g., angular defects, buttressing bone) on which inflammatory changes will later be superimposed.
  • 27. BUTTRESSING BONE FORMATION (LIPPING) • Bone formation sometimes occurs in an attempt to buttress bony trabeculae weakened by resorption. • When it occurs within the jaw, it is termed central buttressing bone formation . • When occurs on the external surface it is referred to as peripheral buttressing bone formation. This may cause bulging of the bone contour, termed lipping FOOD IMPACTION: • Interdental defects often occur where proximal contacts is abnormal or absent. • Pressure and irritation from food impaction contributes to inverse architecture. • In some instances the poor proximal relationship may be the result of shift in bone position because of extensive bone destruction preceding food impaction. • In such cases food impaction is the complicating factor rather than the cause of bone destruction. AGGRESSIVE PERIODONTITIS A vertical or angular pattern of alveolar bone destruction is found around the first molars in aggressive periodontitis. The cause of the localized bone destruction in this type of periodontal disease is unknown.
  • 28. OSSEOUS (CRATERS) These are concavities in the asset of the interdental bone confined within the facial and lingual walls. Craters have been classified as (Ochsenbein and Bohannan in 1964) Class 1- have 2-3 mm osseous concavity with relatively thick buccal and lingual walls. Treated with palatal ramping. Class 2- have 4-5 mm osseous concavity with relatively thick buccal and lingual walls. Treated with buccal and palatal ramping. Class 3 - have 6-7 mm osseous concavity with relatively thick buccal and lingual walls. Treated with buccal and palatal ramping. Class 4- Lesions with variable depth and thin buccal and lingual walls.
  • 29. BULBOUS BONE CONTOURS There are bony enlargements caused by exostoses •Due to Adaptation to function •Maxilla > Mandible REVERSED ARCHITECTURE • Caused by loss of interdental bone • Includes loss of facial or lingual plates without associated loss of radicular bone, hence reversal of architecture.
  • 30. LEDGES These are plateaus – like bone margin caused by resorption of thickened bony plates. FURCATION INVOLVEMENT •It is invasion of the bifurcation or trifurcation of multi rooted teeth by periodontal disease. • Mandibular 1st molars are most common site and maxillary premolar are least common. 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 produced horizontal or angular , and very frequently crater develop in interradicular area.
  • 31. GLICKMAN`S CLASSIFICATION (1953) Grade I •Incipient. •Just barely detectable with examination hand instruments. •slight bone loss in the furcation area Grade II •Early bone loss. •instrument goes partially into the furcation, but not all the way through. •Furcation may be grade II on both sides of the tooth, but are not connected. Grade III •Advanced bone loss. •Examination hand instrument goes all the way through furcation, to other side of tooth. •Furcation is through-and-through. Grade IV •Through-and-through, plus furcation is clinically visible due to gingival recession.