BONE LOSS & PATTERNS IN PERIODONTAL DISEASE

INTRODUCTION:-

          The height and density of alveolar bone are normally maintained by equilibrium, regulated by local systemic influences between bone formation and bone resorption.  

When resorption exceeds formation, bone height, densities both are reduced.

REASONS FOR BONE LOSS:–

1) BONE DESTRUCTION CAUSED BY CHRONIC INFLAMMATION:-

         Chronic inflammation is the most common cause of bone destruction in periodontal disease.

          Inflammation reaches the bone by extension from gingival into the marrow spaces and replaces the marrow with a leukocyte and fluid exudate new blood vessels and proliferating fibroblasts.

          Multinuclear osteoclasis and mononuclear phagocytes are increased in number and the bone surfaces are lined with cave like resorption lacunae.

          In the marrow spaces resorption exceeds from within, causing first a thinning of the boney trabeculae and enlargement of the marrow spaces followed by destruction of bone and reduction in bone height.

MECHANISM OF BONE DESTRUCTION:-

        The following possible pathways by which plaque products could cause alveolar bone in periodontal disease have been listed by hausmann.

1. Direct action of plaque products on bone progenitor cells induces the differentiation of these cells into osteoclasts.
2. Plaque products act directly on bone, dstroying it through a non-cellular mechanism.
3. Plaque products cause gingival cells to release agents that can act as cofactors in bone resorption

4. Plaque products stimulate gingival cells, causing them to release mediators, which induce bone progenitor cells to differentiate into osteoclasts.
5. Plaque products cause gingival cells to release agents that destroy bone by direct chemical action without osteoclasts.

Radius of action:

Some of the authors suggested that, locally produced bone resorption factors may have to be present in the proximity of the bone surface to be able to exert their action. On the basis of Waerhaug’s measurements, it was postulated that there is a range of effectiveness of about 1.5-2.5 mm within which bacterial plaque can induce bone loss, beyond 2.5 mm there is no effect. Interproximal angular defects can appear only in spaces wider than 2.5 mm because narrower spaces are destroyed completely. Large defects far exceeding 2.5 mm can be seen in certain conditions, like localized juvenile periodontitis and papillon-lefevre syndrome, may be caused by the presence of bacteria within the tissues.

Rate of bone loss:

Loe and associates found the rates of bone loss on an average to be about 0.2 mm a year for facial surfaces and about o.3 mm a year for proximal surfaces, when periodontal disease is allowed to progress untreated. 

Periods of destruction

The reasons for the onset of destructive periods have not been totally elucidated, although the following theories have been offered:

1) Bursts of destructive activity are associated with subgingival ulceration and an acute inflammatory reaction, resulting in rapid loss of alveolar bone.

2) Bursts of destructive activity coincide with the conversion of a predominantly T-lymphocytes lesions to one with a predominantly B lymphocytes-plasma cell infiltrate.

3) Periods of exacerbation are associated with an increase of the loose, unattached, motile, gram negative, pocket flora, and periods of remission coincide with the formation of a dense, unattached, non motile, gram positive flora with a tendency to mineralize.

4) Tissue invasion by one or several bacterial species is followed by an advanced local host defence that controls the attack(antibody).

2) BONE DESTRUCTION CAUSED BY TRAUMA FROM OCCLUSION :-

             When occlusal forces exceed the adaptive capacity of the tissues, tissue injury results. This resultant injury is termed, trauma from occlusion.

         This term is generally used in connection to injury in the periodontiom.

            Trauma from occlusion can produce bone destruction in the absence or presence of information.

1. Trauma in the absence of inflammation:-

            In  the absence of inflammation, the change caused by trauma from occlusion vary from enhanced compression and tension of the periodontal ligament and increased   osteoclasis   of alveolar bone to necrosis of the periodontal ligament and bone resorption of   bone and structure.

           These changes are reversible only if the offending forces are removed otherwise persistent trauma from occlusion results in funnel shaped  widening of the crestal portion of the periodontal ligament, with resorption of adjacent bone.

           These changes which cause the bony crest to have angular shape represent adaptation of periodontal tissues aimed at cushioning increased occlusal forces but, the modified bone shape may weaken tooth support and cause mobility.

2. Trauma combined with inflammation:-

         Trauma combined with inflammation aggravates bone destruction and causes bizarre bone patterns.

3) BONE DESTRUCTION CAUSED BY SYSTEMIC DISORDERS:-

          Certain systemic components play a role in severely destructive types of periodontitis.

           According to recent studies there’s a relationship between periodontal bone loss and osteoporosis, periodontitis and osteoporoses share a number of common risk factors such as aging, smoking, diseases and medications that interfere with healing.

Periodontal bone loss may also occur in generalized skeletal disturbances e.g., hyperparathyroidism, leukemia, langerhans cell histiocytosis.

Pharmacological agents and bone resorption:

These include prostaglandin and their precursors and osteoclast activating factors, all of which are present in inflamed gingiva. Complement can also induce bone resorption by enhancing the synthesis of prostaglandins. Pg are synthesized by fatty acid precursorssuch as arachidonic acid and is controlled by cyclo-oxygenase pathway. Flurbiprofen (NSAID) is a potent inhibitor of cyclo-oxygenase pathway of arachidonic acid metabolism which retards the rate of bone loss.

FACTORS DETERMINING BONE MORPHOLOGY IN PERIODONTAL DISEASE

Normal variation in alveolar bone:

• The anatomic features that substantially affect the bone destructive pattern in periodontal disease include the following:
• The thickness, width, and crestal angulation of the interdental septa.
• The thickness of the facial and liongual alveolar plates.
• The presence of fenestration and dehiscences.
• The alignment of the teeth.
• Root and root trunk anatomy.
• Root position within the alveoalar process.
• Proximity with the another tooth surface.

EXOSTOSES

They are outgrowths of bone.

They can occur as small or large nodules, sharp ridges, spike like projections, or any combination of these.

TFO(Trauma from Occlusion)

It may cause a thickening of the cervical margins of alveolar bone or change in the morphology of the alveolar bone i.e. angular defects, buttressing bone formation.

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 as central BBF. When it occurs on the external surface it is termed as peripheral BBF. The latter which may cause bulging of the bone contour, termed lipping, which sometimes accompanies the  production of osseous craters and angular defects.

FOOD IMPACTION

Interdental bone defects often occur where proximal contact is abnormal or absent.pressure and irritation from food impaction contribute to the inverted bone architecture.

 BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE

Periodontal disease alters the morphologic features of bone in addition to reducing height.

Different patterns of bone loss are:-

1. HORIZONTAL BONE LOSS:-

• Most common pattern of bone loss in periodontal disease.
  • Bone is reduced in height but the bone margin remains roughly perpendicular to tooth surface.
  • Interdental septa and lingual plates are affected, but not necessarily to on equal degree around the same tooth.
  • Seen in case of suprabony pockets.
    
    2. VERTICAL/ANGULAR DEFECTS:-
    

• Occur in an oblique direction, leaving a hollowed out trough in one alongside the root, base of the defect is located apical to the surrounding bone.
  • Vertical defects can occur interdentally which are generally seen on the radiograph.

                        These also occur on the facial, lingual / palatal surfaces which can be best

                        determined only by surgical exposure.

• Vertical defects increase with age.
  • Vertical / angular defects are classified on the basis of number of osseous

                         walls as:-

1. One wall defects also called hemiseptum – one wall is present.
2. Two wall defects-2 walls are present.
3. Three wall defects also called intraboney defect most frequently seen on mesial aspects of second and third maxillary and mandibular molars- 3 walls are present.

 3. OSSEOUS CRATERS:-

• Osseous craters are concavities in the crest of the interdental bone confined to facial and lingual walls..
  • Craters have been found to make up about 1/3 of all defects and 2/3 of all   mandibular defects.
  • Twice as common in posterior segments as in anterior segments.

REASONS FOR INTERDENTAL CRATERS ARE:-

1. Interdental areas collect plaque and are difficult to clean.
2. Normal flat /even concave faciolingual shape of the interdental septum in lower molars may favor crater formation.
3. Vascular patterns from the gingiva to the center of the crest may provide a pathway for inflammation.

4) REVERSED ARCHITECTURE:-

             This defect is produced by loss of interdental bone, including the facial and / or lingual plates without concomitant loss of reticular bone, thereby reversing the normal architecture such defects are more common in maxilla.

5) LEDGES:-

              Ledges are plateau like bone margin caused by resoption of thickened boney plates.

6)  FURCATION  INVOLVENMENT:-

• Stage of progressive periodontal disease which refers to the invasion of the bifurcation and trifurcation of multirooted teeth by periodontal disease.
  • Most commonly seen in mandibular 1^st molars.
  • Denuded furcation may be visible clinically or determined by exploration with a blunt probe.

Contributor- Dr. Priyanka Jairaj Dalvi