Intrabony Defects: Diagnosis and Treatment
by Dinh X. Bui, D.D.S., M.S.

Intrabony Defects: Diagnosis and Treatment
Studies of periodontal lesions have provided the classification of periodontal pocket: the suprabony or supracrestal and the infrabony or subcrestal. The suprabony pocket is defined as a pathological sulcus where the base of the pocket is coronal or occlusal to the alveolar crest, while the infrabony is defined as a pathological sulcus where the bottom of the pocket is apical to the alveolar crest. Recent publications has arrived at the correct term for the infrabony pocket as intrabony pocket. Classification of intrabony pocket was necessary for academic purposes but also to serve as a rational basis for the selection of a method of treatment. According to Henry Goldman ad Walter Cohen, intrabony pocket is classified base on morphology and is dependent on location and number of osseous walls remaining about the pocket. The intrabony pocket can be described as three osseous walls, of which can be proximal, buccal, and lingual walls; or buccal, mesial, and distal walls; or lingual, mesial, and distal walls. The three wall intrabony pockets are usually observed on the lingual surfaces of the maxillary and mandibular teeth where the lingual plate is intact as well as both proximal walls. The four osseous walls defects (buccal, lingual, mesial, and distal) usually involved circumferential pocket and involves the four surfaces of the tooth. Two wall infrabony pockets may be seen in the interdental areas. Two osseous walls defects usually consists of buccal and lingual walls; or the buccal and proximal walls, or the lingual and proximal walls. The two wall infrabony pocket in which the buccal and lingual walls remain while the proximal wall is destroyed is referred to as crater. Intrabony pocket with one osseous wall remaining is also usually seen in the interdental areas. Here it is most common to observe the proximal wall with the buccal and lingual walls destroyed. However, the remaining wall can be a proximal, buccal, or lingual wall. Goldman and Cohen also stressed the visualization of the topography of the infrabony pocket is essential for its clinical management, and also understanding the etiology is necessary to yield successful result. Etiology of the intrabony pocket involved tooth anatomy and tooth position. Tooth anatomy concerns with grooves or crevice or concavity on the root surface which facilitates accumulation of plaue and calculus formation, contact areas morphology, and also type of tooth. Tooth position which contributes to food impaction, plaque accumulation, angular position or position of the tooth in respect to the alveolar housing and buccal bone are the local environmental factors which can initiate the infrabony pocket process. Another important factor in the etiology of the intrabony pocket is the occlusal traumatic lesion. Even though occlusal traumatism cannot cause pocket formation alone; however, as the pocket formation began with the local factors (calculus, food impaction), the occlusal trauma can affect the attachment apparatus. Local factors and traumatic occlusion will inevitably lead to the formation of intrabony pocket. Another major cause for intrabony pocket formation is localized juvenile periodontitis, which predominantly affect the region of first molars and incisors. Goldman and Cohen also emphasized the necessity to eliminate causative factors in the therapy as followed:
1. Tooth anatomy-proximity of roots and width of the interdental septum.
2. Relative position of adjacent marginal ridges, cemento-enamel junctions and crest morphology.
3. Tilting of the tooth in group relationship.
4. Tilting of solitary tooth.
5. Position of the tooth in respect to alveolar housing and basal bone.
6. Contact points and resultant food impaction.
7. The occlusal relationships of the tooth.
8. Presence of calculus.
9. Causation by the disease process of Localized Juvenile Periodontitis.
Any attempt to treat the infrabony pocket without regard to the etiologic factor may result in failure. Temporary splinting of the mobile tooth can be used prior to operation, making sure that the splint is extended to strongly held tooth to assure rigid splint and the affected tooth cannot be moved by the occlusal force. According to Goldman and Cohen, two major methods of treatment have been developed for the infrabony pocket. The first consists of curettement of the portion below the bone crest, then gingivectomy is carried out for the portion above the alveolus to enhance the possibility of formation of new cementum, bone, and periodontal membrane. The second method involved osteoectomy, which the alveolus is reduced to a point coinciding the base of the pocket. When the pocket is shallow and not too much support is lost, osteoectomy is definitely indicated. There is a direct relationship between the prognosis of the therapy and the number of walls intact. Three wall defect has the best prognosis for new attachment, then the two walls. One or no wall defect demonstrated poor prognosis. When osteoectomy is used as part of the treatment, the length of the root must be considered. Two major procedures for osteoectomy-osteoplasty consist of 1) raising a flap and trimming the bone crest and 2) raising a flap and outline the contour of the bone for removals with small holes, then united the holes. The crater lesion (two wall defect) is usually treated by osteoectomy. Thus in short, the one and two wall lesions are treated with osseous surgery while the three wall lesions are treated with curettage-gingivectomy procedures. Inner wall of gingival flap should be debride prior to replacement. Scaling and root planing of the tooth surfaces to remove all local factors should be performed prior to the curettage-gingivectomy operation.
John Prichard outlined the technique for treating infrabony pocket based on alveolar process morphology. The infrabony pocket is differ from the suprabony pocket in that the pattern of bone absorption is vertical rather than horizontal and the normal arrangement of the gingival and transeptal fibers of the periodontal ligament is altered. Again John Prichard stressed the coexistence of local environmental factors and the occlusal trauma as one of the two etiology of the intrabony pocket. The second cause is the degeneration of the periodontium. In Prichard analysis of wound healing in the intrabony pocket, he described the healing as similar to the fractured bone repair; healing is from the internal callus which forms from osteogenic cells that line the interior of bone and the nearby undifferentiated cells of the marrow. Cells for the genesis of periodontal ligament, cementum, and alveolar bone are available in the pocket, in addition to osteogenic cell from bone and marrow. Prichard stressed the important of the establishment of blood clot after therapy since it acts as the biological dressing, which indicates the absence of infection and greatly enhanced the chance of success by protecting the osteogenic cells from exposure and irritation, thus maintaining homeostasis. In described the anatomical factors, Prichard mentioned that the infrabony pockets with one osseous walls tend to occur where the dental arch is narrow as in the mandibular incisor, maxillary incisor, and the bicuspid regions. Infrabony pocket are most often found interproximal region. The mandibular molar region is the most common site of the infrabony pocket with three osseous walls. Diagnosis of bone topography involved the use of the periodontal probe, the roentgenogram, and definitive surgical exploration. Probing is to explored the buccal and lingual wall, whereas the roentgenogram is valuable assessing the proximal wall. Three osseous walls are mandatory for predictable success. Infrabony pocket involving the furcation area are difficult to treated. For the class II or class I lesion, regenerative therapy with barrier membrane are recommended. For class III furcation defects, the osseous resection as systematized by Schluger is indicated. Prichard emphasized the careful planing of the root surface and the complete surgical removal of all soft tissue between the tooth root and the bone in the intrabony therapy, with second stage procedure occasionally are necessary to complete the repair via osteoectomy.
Alan Polson and the Lars Heiji investigated the osseous repair process in infrabony periodontal defects and published their result in 1978. Fifteen defects were selected in nine patients and following the muco-periosteal flap reflection, the osseous defects were debrided. The flap were replaced at their original location and optimal plaque control regimen was instituted. Six to eight month after the therapy, all areas were reoperated and the osseous defects were remeasured at the same specific location. All osseous changes are quantitated in their study. There is the combination of coronal bone regeneration (mean 77%) and the marginal bone resorption (mean 18%). Intrabony defect may predictably remodel after surgical debridement and establishment of optimal plaque control.
According to William and Burton Becker reports of repair of intrabony defects by open debridement procedures. 36 three wall or circumferential intrabony defects were treated. Flap was raised using vertical relaxing incisions to provide access for debridement. The intrabony defects were thoroughly debrided of all visible granulation tissue and the presence of calculus on the root surfaces was recorded. After debridement, the defects were bathed in .2% chlorhexidine for three minutes and were then washed with water. The flaps were then sutured apically with 4.0 silk or gut sutures; however, an attempt was made to leave the margins of the flaps open adjacent to the treated site. Upon reentry at average of 14 month post operative, there is an average of 2.44 mm clinical attachment level gain from the initial clinical attachment level was 7.37 mm. There is also anaverage of 1.62 mm of recession and the average of .48mm crestal resorption. The net amount of defect repair was 2.55mm. The defect repaired by a combination of crestal resorption and fill from the defect base and surrounding osseous walls. Residual defects were found on all reentry sites of an average of 1.67mm. The majority of these defects were reduced with osseous surgery upon reentry. Compare to the other experiments such as that of Ellegaard, Karring, and Loe in 1974 which involved treatment of intrabony defect with autogenous cancellous bone graft and open debridement were used as control, the results were almost as favorable for debridement only sites as they were for the sites that received graft. Altiere, Reeve, and Sheridan in 1979 compared lyophilized bone allograft with debridement controls and the result is no difference between graft sites and control sites. Other studies such as those of Polson and Heiji and those of Froum et. al. and Prichard provided supportive evidence that the deeper the three wall defects, the greater the amount of bone fill following treatment.
Today, with the advance of guided tissue/bone regeneration technology, three wall and even two walls defect can be treated successfully with the used of membrane barrier to prevent the apical migration of soft tissue and allow true regeneration of alveolar bone to occur. Carlos Quinones, Markus Hurzeler, Raul G. Caffesse, Peter Schupbach, and Edith C. Morrison performed the treatment of interproximal intrabony defects in monkey with a synthetic bioresorbable guided tissue regeneration barrier. The control sites did not receive the barrier. Periodontal lesions were induced around the mandibular central incisor teeth using the orthodontic elastic. Resolut material was placed to cover the entire buccal and lingual extent of the interdental defect. The animal were sacrificed five month after surgery, and specimen were stained and sections for histologic and histometric analyses. Clinical observation of the results revealed uneventful healing in both experimental and control group with no soft tissue reaction nor inflammation. Histologic observation of control sites reveals long junctional epithelium extended apically along the entire length of the instrumented root surface, whereas the experimental specimens demonstrated new cellular cementum extended form the apical termination of root planing in a coronal direction, new lamellar-like bone almost completely filled the periodontal defect, and periodontal ligament attached the newly regenerate cementum to the bone. No remnants of the bioresorbable regenerative material were observed. In short, site receiving the bioresorbable regenerative material exhibit a significantly greater amount of periodontal regeneration than those sites treated by flap debridement alone.
Histologic evaluation of new attachment apparatus formation in humans are also investigated by G. Bowers, B. Chadroff, R. Carnevale, J. Mellonig, R. Corio, J. Emerson, M.Stevens, and E. Romberg. In their study, they compared the healing of intrabony defects with and without the placement of decalcified freeze-dried bone allograft in a submerged environment. 30 graft defects and 13 nongraft defects were analyzed. The result indicated that in a submerged environment significantly more new attachment apparatus and new bone formed in grafted than the nongrafted sites. Significantly greater loss of alveolar crest height occurred in nongrafted than graft defects; and regeneration of new attachment apparatus, new bone, and new cementum occurred more frequently in grafted than nongrafted defects. Finally, there was a greater chance for regeneration of a connective tissue attachment on the nongraft sites with no root resorption, ankylosis, or pulp death was observed in both grafted and nongrafted defects. Bone grafting materials will enhance regeneration of a new attachment apparatus with more cementum formation and bone formation. In their second study, they compared the healing of intrabony defects with and without the placement of DFDBA in a nonsubmerged environment. The result is also the same as before (with submerged environment). Significantly more new attachement apparatus, new cementum, new bone, new connective tissue will form in intrabony defects grafted with DFDBA than in nongrafted defect.
Intrabony defect repair has been always a challenge to the clinician. Goldman and Cohen classified intrabony defects according to the number of bony walls surrounding the lesion.
Prichard has presented impressive clinical documentation on treated three wall intrabony defects. Caranza and Patur and Glickman have presented the healing response of one, two, and three wall intrabony defects. Bowers, Schallhorn, and James Mellonig outlined the treatment of intrabony defect using DFDBA as the grafting material with regenerative success. Cafesse et. al. have reported the repair of intrabony defects using barrier membrane with new regeneration of the periodontal apparatus. The future is promising for the treatment of furcation defect using the GTR technology. Regardless of the treatment modality, understanding the etiology and visualization of the topography of the defect are the two most important elements in guarantee the good prognosis of the treatment therapy. Without elimination the causative factor, the treated site will fail or intrabony region will inevitably recur.



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