Bone Loss and Patterns of Bone Destruction

Chapter 28
Dr. Amam Ali Amam PhD: Periodontal Disease

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Bone Loss and Patterns of Bone Destruction

Although periodontitis is an infectious disease of the gingival tissue, changes that occur in bone are crucial because the destruction of bone is responsible for tooth loss. The height and density of the alveolar bone are normally maintained by an equilibrium, regulated by local and systemic influences between bone formation and bone resorption. When resorption exceeds formation, bone height, density, or both are reduced.
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BONE DESTRUCTION CAUSED BY EXTENSION OF GINGIVAL INFLAMMATION

The most common cause of bone destruction in periodontal disease is the extension of inflammation from the marginal gingiva into the supporting periodontal tissues. The inflammatory invasion of the bone surface and the initial bone loss that follows mark the transition from gingivitis to periodontitis.

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 Periodontitis is always preceded by gingivitis, but not all gingivitis progresses to periodontitis. Some cases of gingivitis apparently never become periodontitis, and others go through a brief gingivitis phase and rapidly develop into periodontitis. The factors that are responsible for the extension of inflammation to the supporting structures and bring about the conversion of gingivitis to periodontitis are not known at this time. The extension of inflammation to the supporting structures of a tooth may be modified by the pathogenic potential of plaque or the resistance of the host.

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Rate of Bone Loss

the rate of bone loss may vary, depending on the type of disease present. Le and al identified three subgroups of patients with periodontal disease based on interproximal loss of attachment and tooth mortality: 1.Approximately 8% of persons had rapid progression of periodontal disease, characterized by a yearly loss of attachment of 0.1 to 1 mm. 2.Approximately 81% of individuals had moderately progressive periodontal disease, with a yearly loss of attachment of 0.05 to 0.5 mm. 3.The remaining 11% of persons had minimal or no progression of destructive disease (0.05 to 0.09 mm yearly).
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Periods of Destruction

The destructive periods result in loss of collagen and alveolar bone with deepening of the periodontal pocket. The reasons for the onset of destructive periods have not been totally elucidated, although the following theories have been offered. Bursts of destructive activity are associated with subgingival ulceration and an acute inflammatory reaction, resulting in rapid loss of alveolar bone.

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Periods of Destruction con.

Bursts of destructive activity coincide with the conversion of a predominately T-lymphocyte lesion to one with a predominance of B-lymphocyte-plasma cell infiltrate. Periods of exacerbation are associated with an increase of the loose, unattached, motile, gramnegative, anaerobic pocket flora, and periods of remission coincide with the formation of a dense, unattached, non motile, gram-positive flora with a tendency to mineralize. Tissue invasion by one or several bacterial species is followed by an advanced local host defense that controls the attack. DR AMAM

Mechanisms of Bone Destruction

The factors involved in bone destruction in periodontal disease are bacterial and host mediated. 1- Bacterial plaque products induce the differentiation of bone progenitor cells into osteoclasts and stimulate gingival cells to release mediators that have the same effect. 2- Plaque products and inflammatory mediators can also act directly on osteoblasts or their progenitors, inhibiting their action and reducing their numbers. 3- in rapidly progressing diseases such as localized juvenile periodontitis, bacterial microcolonies or single bacterial cells may be present between collagen fibers and over the bone surface, suggesting a direct effect.
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Mechanisms of Bone Destruction

4- Several host factors released by inflammatory cells are capable of inducing bone resorption in vitro and can play a role in periodontal disease. These include host-produced prostaglandins and their precursors, interleukin 1- and -, and tumor necrosis factor (TNF)-. When injected intradermally, prostaglandin E2 induces the vascular changes seen in inflammation; when injected over a bone surface, it induces bone resorption in the absence of inflammatory cells and with few multinucleated osteoclasts.

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Bone Formation in Periodontal Disease

Areas of bone formation are also found immediately adjacent to sites of active bone resorption , The response of alveolar bone to inflammation includes bone formation and resorption;

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 but results from the predominance of resorption over formation. New bone formation impairs the rate of bone loss, compensating in some degree for the bone destroyed by inflammation. These 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 the extent of bleeding, amount of exudate, and composition of bacterial plaque.

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 The presence of bone formation in response to inflammation, even in active periodontal disease, has an effect on the outcome of treatment. The basic aim of periodontal therapy is the elimination of inflammation to remove the stimulus for bone resorption and therefore allow the inherent constructive tendencies to predominate.

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BONE DESTRUCTION CAUSED BY TRAUMA FROM OCCLUSION

Another cause of periodontal destruction is 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 vary from increased compression and tension of the periodontal ligament and increased osteoclasis of alveolar bone to necrosis of the periodontal ligament and bone and resorption of bone and tooth structure. These changes are reversible in that they can be repaired if the offending forces are removed. When combined with inflammation, trauma from occlusion aggravates the bone destruction caused by the inflammation and causes bizarre bone patterns.
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Trauma from Occlusion:

Trauma from occlusion may be a factor in determining the dimension and shape of bone deformities. It may cause a thickening of the cervical margin of alveolar bone or a change in the morphology of the bone.

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BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE

Periodontal disease alters the morphologic features of the bone in addition to reducing bone height. An understanding of the nature and pathogenesis of these alterations is essential for effective diagnosis and treatment. Horizontal Bone Loss Bone Deformities (Osseous Defects) Vertical or Angular Defects Osseous Craters Bulbous Bone Contours Reversed Architecture Ledges Furcation Involvements
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Horizontal Bone Loss

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
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Bone Deformities (Osseous Defects)

Different types of bone deformities can result from periodontal disease. These usually occur in adults and have been reported in human skulls with deciduous dentitions. Their presence may be suggested on radiographs, but careful probing and surgical exposure of the areas is required to determine their exact conformation and dimensions.
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Vertical or Angular Defects

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. In most instances, angular defects have accompanying infrabony pockets; such pockets always have an underlying angular defect. Angular defects are classified on the basis of the number of osseous walls. The number of walls in the apical portion of the defect may be greater than that in its occlusal portion, in which case the term combined osseous defect is used
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Vertical or Angular Defects con

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Vertical defects occurring interdentally can generally be seen on the radiograph, although thick, bony plates sometimes may obscure them. Angular defects can also appear on facial and lingual or palatal surfaces, but these defects are not seen on radiographs. Surgical exposure is the only sure way to determine the presence and configuration of vertical osseous defects.
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Vertical or Angular Defects con

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vertical defects increase with age. Approximately 60% of persons with interdental angular defects have only a single defect. Vertical defects detected radiographically have been reported to appear most commonly on the distal surfaces and mesial surfaces. However, three-wall defects are more frequently found on the mesial surfaces of upper and lower molars. The three-wall vertical defect was originally called an intrabony defect. This defect appears most frequently on the mesial aspects of second and third maxillary and mandibular molars. The one-wall vertical defect is also called a hemiseptum.
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Osseous Craters
Osseous craters are concavities in the crest of the interdental bone confined within the facial and lingual walls. Craters have been found to make up about one third (35.2%) of all defects and about two thirds (62%) of all mandibular defects. They are twice as common in posterior segments as in anterior segments. The following reasons for the high frequency of interdental craters have been suggested: The interdental area collects plaque and is difficult to clean. The normal flat or even concave faciolingual shape of the interdental septum in lower molars may favor crater formation. Vascular patterns from the gingiva to the center of the crest may provide a pathway for inflammation

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Bulbous Bone Contours

Bulbous bone contours are bony enlargements caused by exostosis, adaptation to function, or buttressing bone formation. They are found more frequently in the maxilla than in the mandible.

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Reversed Architecture

Reversed architecture defects are produced by loss of interdental bone, including the facial plates, lingual plates, or both, without concomitant loss of radicular bone, thereby reversing the normal architecture. Such defects are more common in the maxilla.
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Ledges Ledges are plateau-like bone margins caused by resorption of thickened bony plates

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Furcation Involvements
The term furcation involvement refers to the invasion of the bifurcation and trifurcation of multirooted teeth by periodontal disease. The prevalence of furcation involved molars is not clear. Whereas some reports indicate that the mandibular first molars are the most common sites and the maxillary premolars are the least common, others have found higher prevalence in upper molars. The number of furcation involvements increases with age
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Furcation Involvements con

Furcation involvements have been classified as grades I, II, III, and IV according to the amount of tissue destruction. Grade I is incipient bone loss, Grade II is partial bone loss. Grade III is total bone loss with through-andthrough opening of the furcation. Grade IV is similar to grade III, but with gingival recession exposing the furcation to view.
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Any Questions?

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