Periodontal Regeneration: Myth or Reality

One of the goals of periodontal therapy is regeneration. During the past 20 years, several materials and techniques have been developed and tested for enhancing periodontal regeneration. This paper evaluates flap debridement, allogenic and alloplastic grafting, and the use of nonresorbable and resorbable barrier membranes as regenerative techniques. One of the most predictable regenerative therapies is treatment of the three-walled intrabony defect. This defect can be repaired with 2 to 2.5 mm of bone fill and results in significant gains in clinical probing attachment and decreases in probing depths. There is a slightly greater improvement in periodontal measures with barrier membranes. Commercial preparations of allogenic bone and alloplastic fillers have a long, safe history of use and are primarily osteoconductive. They decrease probing depths and provide short-term gains in clinical attachment levels. Barrier membranes provide short-term evidence of improving Class II furcation invasions, however there is insufficient evidence that these improvements are sustained long-term. Class III furcations are not predictably treated by regenerative therapies. To date, there is an absence of clinical evidence that regenerative therapy increases the long-term life span of teeth.

Regeneration is one of the primary goals of periodontal therapy. During the past 20 years, there has been an explosion of techniques and materials designed to increase the predictability of periodontal regeneration. Regeneration is defined as restoration of lost parts.¹ Periodontal regeneration requires the restitution of cementum with inserting fibers and bone. Repair implies healing by long junctional epithelium. Unfortunately, regeneration can only be ascertained by histologic evaluation, hence most of the procedures designed for regeneration probably result in repair. Studies using filler materials have demonstrated improved periodontal measures. To date, none of these studies has provided evidence that filler materials increase the life span of the treated teeth. The purpose of this paper is to evaluate periodontal regenerative procedures and determine their patient benefits.

Defect Anatomy

Prichard described the classic intrabony defect as having three bony walls, with the root forming the fourth wall. The defect has definite limits and does not extend into the furcation.² Saari³ and Tal⁴ examined dry skulls and described the frequency and location of intrabony defects. These defects were frequently found distal to mandibular second molars. Alveolar bone in this location has thick cortical plates with varying quantities of cancellous bone. In the presence of inflammation, cancellous bone resorbs, leaving a bony crypt surrounded by a varying number of bony walls.

Open Flap Debridement

Carranza⁵ and Prichard² are credited with presenting successful treatment of classic three-wall intrabony defects. These defects are surrounded by bone on three sides, with the root forming the fourth wall. Prichard followed successfully treated patients for more than 30 years. Examination of case reports demonstrated clinical evidence of bone fill. These defects appeared to be deep and were primarily located distal to mandibular second molars. Polson and Heijl⁶ reported an average gain of 2.5 mm of bone after treatment of deep two- and two-to-three-wall intrabony defects. Becker and colleagues^7,8 reported clinical findings after treatment of 36 consecutive three-wall defects. These defects were deeper than 5 mm and were wide. The average gain of bone fill was 2.5 mm, with significant decreases in clinical probing depth.

Treatment of these defects by flap debridement requires an understanding of anatomy, a thorough clinical examination, and identification of etiologic factors. The diagnosis and treatment depends upon evaluation of probing depths, clinical attachment levels, and good periapical radiographs. Defect depth can frequently be estimated from radiographs. In defects greater than 5 mm, the presence of subgingival calculus and positive tooth vitality are indications that treatment will result in a favorable outcome.

Surgical treatment consists of elevation of full-thickness mucoperiosteal flaps and thorough defect and root surface debridement. This is performed with a combination of rotary and ultrasonic instruments. The defect is probed using the lowest wall as reference. If the defect is greater than 5 mm, it is a good candidate for repair by flap debridement. Ochsenbein⁹ described the relationship of the defect to the surrounding bony walls. He reported that bony walls of the same height never surround three-walled intrabony defects. He recommended that the highest wall be reduced to the level of the adjacent walls. Adjusting the bony walls should allow for complete repair of the defect. The clot is then allowed to stabilize after which the flap margins are sutured with interrupted sutures. Postoperatively, patients can be placed on antimicrobial rinses, and the sutures are removed in a week. Oral hygiene is reinstituted and the area is evaluated by probing and radiographic examination after nine months of healing. These defects likely repair with a long junctional epithelium.

Allografts and Alloplasts

During the 1970s, the use of alloplastic filler and allogenic bone were introduced for treatment of periodontal defects.^10-17 Freeze-dried bone became a popular filling material, since early reports indicated this material was osteoinductive. The principle of osteoinduction means that bone morphogenetic proteins or other growth factors or proteins can affect undifferentiated mesenchymal cells to differentiate into cartilage and subsequently bone.

Figure 1a Deep three wall intrabony defect distal to the mandibular second molar. The defect is contained, and furcation is not involved.

Urist, in a series of rodent studies, first described bone formation in ectopic sites (muscle tissue) by induction.^18-20 Urist isolated a complex series of inductive proteins known as bone morphogenetic proteins.^{20, 21} The indications, expectations, and contraindications of when and where to use allogenic bone became confusing. Numerous clinical studies have demonstrated that placement of allografts into periodontal defects will result in decreased probing depths, bone fill, and gains in clinical attachment levels.^13,14,22

Figure 1b An ePTFE barrier has been fitted to cover the defect.

Other investigators have presented histologic evidence of periodontal regeneration following implantation of demineralized bone matrix.^15,23 When interproximal defects were treated with either barrier membranes alone or with allogenic bone, the results were similar.²⁴ Unfortunately, clinical studies do not demonstrate evidence of bone induction by the implanted material. Recently bone induction with commercially available allogenic bone has been questioned.^25-27 There is sufficient scientific evidence that commercially available bone matrix has varying amounts of bone-inductive activity. The capacity of the bone implants to initiate bone induction diminishes with age and varies from batch to batch. The quantity of bone matrix proteins or other growth factors or proteins necessary to induce clinically relevant amounts of bone is unknown. Commercially available bone allografts can be considered osteocondutive. When the allogenic bone particles are in contact with host bone over time, new bone will surround the bone matrix particles. Allogenic bone away from native bone will remain unresorbed for long periods. There is insufficient evidence to indicate that graft particles will ever be totally replaced by host bone. There is also insufficient evidence to indicate that allografts will be resorbed by osteoclasts, hence replacement by substitution is highly variable. Healing of defects treated with allogenic bone implants likely occurs by repair. This may be sufficient to prolong the life span of the tooth.

Investigators created furcation defects in baboons.²⁸ They implanted bone morphogenetic proteins extracted from bovine demineralized bone utilizing the demineralized matrix as the carrier for test sites. Collagen matrix alone was used for control defects.

Figure 1c The defect was re-entered 11 months after treatment to reduce a residual defect. Note defect bone fill.

Figure 1d The initial defect appears wide and extends close to the root apex

Histologic evaluation of treated defects indicated significant periodontal regeneration within the test furcations; however, large quantities of unresorbed demineralized matrix carrier was present within the surrounding connective tissue.

Alloplastic materials are synthetic bone substitutes. These materials are biocompatible, osteoconductive, and either resorbable or nonresorbable. They are of questionable value as regenerative materials. They can effectively be used for ridge augmentation, providing that dental implants do not significantly contact these fillers. Treatment of periodontal defects with filler materials results in decreased probing depths, gains in clinical attachment levels, and radiographic evidence of "bone like" material within the defects. The defects heal by repair. Long-term follow-up studies of teeth treated with these materials are not available, and the patient benefits are questionable.

Figure 2a Radiograph demonstrates deep, intrabony defect distal to the maillary right first bicuspid. Figure 2b Buccal view, showing inconsistent bony margin. Figure 2c Palatal view demonstrates contained, three-walled intrabony defect. Figure 2d An ePTFE barrier membrane has been used to isolate the defect. Figure 2e Three-year follow-up radiograph demonstrating bone fill of original defect. Compare with Figure 2a.

Guided Tissue Regeneration

Scandinavian investigators introduced the principle of guided tissue regeneration.^29-35 The concept was based on isolating periodontal defects with barrier membranes.

Figure 1e Eleven-month follow-up X-ray. Note slight residual defect and extensive amount of bone fill.

The purpose of the barriers was to exclude epithelial down-growth and to allow periodontal ligament cells to repopulate the previously diseased root. The first commercial barrier membranes were made of expanded polytetrafluoroethylene (ePTFE) (WL Gore and Associates, Flagstaff, Ariz.) and were cell-occlusive. There was an open microstructure collar that was fitted around the tooth at or near the cementoenamel junction. The biologic rationale for using these barriers was based on scientific and clinical studies. These barriers have been used to treat intrabony and furcation defects.^32,33,35-44 Results after treatment of multiwalled defects with debridement and barrier membranes demonstrated improved probing depths and gains in clinical attachment levels with varying amounts of reported bone fill (Figures 1 and 2). Several studies provided evidence of sustained gains in clinical measures when compared with the short-term reports.

Barrier membrane treatment of furcation defects is technique-sensitive. There is minimal evidence of complete furcation closure with or without allogenic bone alone or with barrier membranes.^40,42 There are several reports in which barrier membranes have been used with allogenic bone.^45-47 The primary reason for adding the bone implants was to support the barrier membranes. Barrier membranes with allografts have primarily been used to treat furcation defects. Studies that compared debridement alone with barriers plus grafts generally demonstrated similar results.^48,49

Figure 3a A Class II furcation with a narrow buccal furcation defect after debridement Figure 3b Defect filled with demineralized freeze-dried bone. Figure 3c A barrier membrane was fitted over bone-filled defect. Figure 3d Flaps sutured in an attempt to completely cover the barrier membrane. Figure 3e Patient was maintained at four-month intervals for six years. Defect probed during a maintenance visit. Note proble penetration into furcation. Probing depth reduction originally recorded postoperatively has been lost. The defect probes to the original depth. Figure 3f Preoperative radiograph taken in 1990 Figure 3g Radiograph taken at follow-up visit in 1996. Compare with tradiographi taken in 1990. There was no apparent change in the furcation status.

Figure 3 demonstrate a furcation defect that was treated with a demineralized freeze-dried bone and an ePTFE barrier. Probing depth had decreased by the nine-month evaluation. The patient was maintained for six years with progressive loss of the initial soft tissue gains in clinical probing attachment and a return to preoperative probing depth. Failure to predictably close Class II furcations and the tendency for initial probing depth decreases to regress to pretreatment depths has brought into question the long-term patient benefits of treating furcation defects with barrier membranes alone or in combination with allografts. Moderately involved Class II defects can be effectively treated with open flap debridement, however long-term patient outcomes are unknown. There are no predictable methods for treating Class III furcations with regenerative procedures.

Bioabsorbable Barriers

Nonresorbable barriers required a second minor surgery for removal. These membranes frequently became exposed and plaque-infected. When this occurred, there was less improvement in clinical measures when compared with sites where the membranes remained unexposed.^50-52 As a consequence of these problems, a new generation of barrier membranes was developed. These barriers resorb and are manufactured from either polyglycolic and polylactic acids, collagen, or various combinations of these. Resorbable barriers have been used to treat intrabony as well as furcation defects. Results from studies comparing nonresorbable to resorbable membranes demonstrate comparable results.⁵³ Intrabony defects were treated with resorbable barriers and compared with flap debridement controls.⁵⁴ Findings indicated improved clinical measures for probing depth reduction and clinical attachment level gains. These improvements were not significantly enhanced with guided tissue regeneration therapy.

Conclusion

Technological and surgical techniques have been implemented to enhance periodontal regeneration. Results from these advances were met with enthusiasm because they provided the possibility for improving results from periodontal regenerative procedures. When these procedures are critically evaluated, they appear to have slightly better clinical outcomes than flap debridement procedures. These slight improvements may not provide cost or patient benefits in terms of improved periodontal health and may not increase the health or longevity of the treated teeth.

Author

William Becker, DDS, MSD, is a clinical associate professor in periodontics at the University of Southern California School of Dentistry and a clinical professor in periodontics at the University of Texas at Houston. He also maintains a private practice, limited to periodontics, in Tucson, Ariz.

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To request printed copies of this article, please contact: William Becker, DDS, MSD, 801 N. Wilmot, B-2, Tucson, AZ 85711