Periodontal Surgery: Resection to Regeneration

The focus of periodontal surgery has shifted over time from a philosophy based on resection to one based on regeneration. This shift has particular significance in cases of advanced periodontitis in the anterior maxilla, which may be associated with an unaesthetic smile. When severe attachment loss is present, comprehensive cosmetic reconstruction cannot take place until the periodontitis has been treated and the ongoing loss of attachment has been arrested. In the past, resective surgical techniques did not adequately address aesthetic concerns, whereas surgical periodontal techniques directed toward regeneration have as their ideal outcome the restoration of lost periodontal tissues.

This article will review the history of periodontal surgery and the shift from resection to regeneration.



Historically, periodontitis has been treated by resective techniques to reduce probing depths. The aim of resective procedures is the re-establishment of a healthy periodontium at a reduced level, accepting as irreversible the destruction that has already occurred. In essence, these procedures are all designed to achieve pocket elimination or reduction by the apical shift of the gingival margin.

The earliest form of resection was the gingivectomy. The gingivectomy procedure dates back to the Romans, who burned the diseased tissue. Pierre Fauchard1 described a resective procedure in 1742 and designed specific instrumentation to remove the excessive tissue. The technique of gingival excision or elimination of granulomatous tissue and bone removal was modified and improved over time. In 1884, Robicsek2 described a procedure very similar to what was later termed the “gingivectomy” by Pickerill in 1912.3 A partial list of those who contributed to the continued development of this technique includes G. V. Black,4 Ward,5 and Crane and Kaplan.6 All these practitioners advocated the need to remove infected bone as part of the gingivectomy procedure. It is important to recognize that the prevailing thought at that time was that the bone loss associated with periodontitis occurred because the bone in the area was infected or necrotic. Ward5 designed his own armamentarium, and his procedure – called “the obliteration method”– was a good example of the type of gingivectomy performed in the first half of the 20th century.

Another category of resective technique is the flap procedure. This procedure was introduced in periodontics during the beginning of the 20th century. Widman7, Neumann,8 Cieszynski,9 and others are associated with the initial descriptions of periodontal flap surgery. Neumann claimed to use the mucoperiosteal flap in periodontal surgery as early as 1911.8 His technique involved up to 6 teeth, used vertical releasing incisions at the interdental papillae that extended to the mucobuccal fold. A third incision was made apically through the gingival crevice to the alveolar crest and raised both buccal and lingual flaps. Neumann described his technique as “the radical treatment of alveolar pyorrhea.”8

A modification of Neumann’s flap was presented by Widman to the Scandinavian Dental Association in 1916 and was later published by Widman in 1918.7 He also claimed to have been performing this procedure as early as 1911. His technique involved 2 to 3 teeth, using 2 vertical releasing incisions at the midline of the teeth that extended to the apical level of the teeth to create a trapezoidal flap. A third reverse bevel incision was made parallel to the surfaces of the teeth 1 mm from the free gingival margin to the alveolar crest, and raised both buccal and lingual flaps. The third incision extended through the interdental papillae at their highest points, giving the flap a scalloped appearance.

Cieszynski is credited with the introduction of the reverse bevel incision in the periodontal flap operation.9 It is important to note that these flap techniques all advocated thorough scaling of the teeth, removal of granulomatous tissue, and also the removal of bone. This brief synopsis of the development of periodontal surgical techniques lends support to the point of view, although extremely dated, that surgical treatment for periodontitis was radical.

In 1935, Kronfeld10 published a classic paper demonstrating that the bone adjacent to periodontal pockets was neither necrotic nor infected but was destroyed by an inflammatory process. He supported his findings with autopsy material. This “state of osteitis” could be replaced by bone reformation if the etiologic factors were controlled. This concept was also substantiated by Orban11 in 1939. Consequently, the need for removal of marginal bone as a part of therapeutic treatment was not justified. This classic publication eliminated one of the main reasons for flap surgery. As a consequence of this, the gingivectomy techniques became increasingly popular. The gingivectomy allowed for the consistent elimination of the pocket after surgery, a goal that was not always met with flap surgery.

During the early 1950s, concerns were expressed regarding the unsatisfactory outcome when pocket depths extended beyond the mucogingival line.12,13 Incising horizontally through the depths of these pockets removed all the attached gingiva, and the wound healed with alveolar mucosa at the gingival margin. Alveolar mucosa was considered structurally and functionally unfit to replace the excised gingiva. As a result of this and other shortcomings, new flap procedures were designed. Bone denudation procedures (pushback and pouch operations13), periosteal retention,14 and periosteal fenestration15 were among these newly developed techniques.

As this trend continued, in 1954 Nabers described a procedure he called “repositioning of the attached gingiva.”16 For the first time, a mucoperiosteal flap was apically positioned after treatment. He described only one vertical releasing incision, which was placed mesially to the area of the deepest pocket. A mucoperiosteal flap was raised and the teeth thoroughly scaled. The width of the flap was curetted, all granulomatous tissue removed, and the gingiva trimmed along the margin to a depth of at least 2 mm. The flap was then moved apically to the crest of the bone and sutured loosely into position. Thus, the procedure allowed for the retention of existing mature attached gingiva while eliminating the pocket.

In 1957, Nabers proposed replacing the marginal trimming of the gingiva with an internal incision from the gingival margin to the alveolar crest.17 This resulted in a thinner gingival margin that was positioned apically and sutured loosely without leaving alveolar bone uncovered. Also in 1957, Ariaudo and Tyrrell18 modified Nabers’ technique by using 2 vertical releasing incisions, which provided greater flexibility in flap management. The only difference between this technique and that proposed by Widman in 1918 was the apical positioning. The same authors later recommended small vertical incisions through the flap in the center of the interproximal spaces. This allowed the flaps to collapse. The resulting depressions would favor good gingival contour. Although effective in arresting periodontitis, pocket reduction, and preserving the attached gingiva, surgical pocket elimination often left the patient with long clinical crowns, root exposure, interproximal spacing, and an unnatural and unaesthetic smile. This history has frequently resulted in the misconception among practitioners that, due to the limitations of resective periodontal techniques, the treatment of periodontitis in the maxillary anterior area of the mouth should be limited to nonsurgical debridement therapy or tooth extraction followed by prosthetic replacement.



Currently, the focus of treatment of severe periodontitis is regenerative in nature. The surgical treatment of periodontal disease has evolved from a discipline characterized by resection as the primary means for pocket elimination to one where regeneration is the primary theme. The concept of periodontal regeneration has also evolved as considerable histologic and other basic scientific knowledge and clinical evidence has been amassed over the last 2 decades, indicating that the regeneration of periodontal tissues lost as a result of periodontitis can be achieved in humans.19,20

As regenerative therapy for periodontal disease has evolved, various treatment modalities have been developed. Bone grafts, root surface demineralization, and guided tissue regeneration have all been used with varying degrees of success to regenerate lost attachment in deep intrabony defects.19,20 Histologic observations and controlled clinical trials have demonstrated that some of the available regenerative procedures may result in healing that can be termed “periodontal regeneration.”21-24 Clinically, several factors may affect the extent of clinical attachment gain and bone regrowth as a case outcome.25-28

Of the different clinical obstacles in regenerative therapy, primary soft-tissue closure over the treated area seems to be of paramount importance. A list of other obstacles to be overcome includes behavioral risk factors such as plaque control and smoking; intrinsic risk factors such as general health, diabetes, and genetic predisposition; local risk factors such as pulpal health, root anatomy, osseous defect morphology, and root preparation; selection of the appropriate surgical technique to achieve the intended goals of treatment; and lastly, clinical skill.28



Bone grafting is one of the therapeutic modalities employed to fulfill the ideal goal of periodontal therapy– the reconstruction of bone and connective tissue that had been previously destroyed by the disease process. The interest in the use of bone grafts and hard- tissue grafting techniques dates from Schallhorn’s reports of the use of hematopoietic marrow to eradicate furcation and interproximal crater defects in humans.29,30 Subsequent case reports attested to the efficacy of this approach.31-34 All of these reports presented evidence of reduced probing depths and increased radiodensity in the osseous defects after treatment.

Bone-grafting techniques have used many different materials with varying degrees of success. Although new attachment and subsequent periodontal regeneration have not been universal findings following bone grafting procedures, many contributors have noted that new attachment is more likely to occur with the use of a graft35 and should therefore be included in the therapeutic armamentarium to treat periodontitis.36



In 1976, after an extensive series of laboratory studies, Melcher37 presented the basic concepts that led to the development of the clinical techniques known as Guided Tissue Regeneration (GTR). He suggested that the cells that repopulate the root surface after periodontal surgery will determine the type of attachment that forms on the root surface. Subsequently, animal studies were published indicating different healing responses when various periodontal tissues came in contact with the root surface.38-42 From these and other studies, the concept of GTR evolved, in that barrier membranes could be used to promote selective cell repopulation of the root surface, thus facilitating periodontal regeneration.43

In humans, histologic evidence of new connective tissue attachment using GTR was first demonstrated in 1982.44 Since the initial publication using a millipore filter as a barrier, the most commonly used membrane material has been made of expanded polytetraflourethylene (ePTFE).



As the understanding of the development of the periodontal attachment apparatus progressed, the hypothesis of cellular mediators expressed by Hertwig’s epithelial root sheath playing a role in the development of the periodontal ligament was suggested.45 Subsequent animal studies by Hammarstrom46 and Schonfeld and Slavkin47 led to the identification of enamel matrix proteins in the development of the root and the adjacent periodontal ligament. In light of earlier observations, it was suggested in the late 1980s that growth factors could be used to achieve periodontal regeneration.48

The rationale for this therapy is based on mimicking the physiologic processes that take place during the formation of the developing root and periodontal tissues. It has been shown that the cells of Hertwig’s epithelial root sheath have a secretory phase during which enamel- related matrix proteins are secreted and deposited onto the root surface. This deposition appears to provide an initial, essential step in the formation of acellular cementum.46 It has also been reported that the cells close to the root surface appear to carry the message not only to form acellular cementum, but also to form an associated periodontal ligament and alveolar bone.47,48 Prior to the formation of acellular cementum, enamel matrix proteins are secreted and temporally deposited onto the root surface, providing an essential surface for the expression of cementum-forming cells. Subsequently, when cementum has been deposited onto the enamel matrix-covered dentin surface, the proper attachment apparatus will develop. The discovery of the enamel layer between the peripheral dentin and the developing cementum provided the fundamental concept for development of EMD (Emdogain, Biora) and supported the viability of tissue engineering for regenerative periodontal therapy.49,50

Studies were designed to determine if enamel matrix proteins are involved in the formation of acellular cementum and also to determine if they have the potential to induce regeneration of the same type of cementum. In vitro tests were used to determine if amelogenin, the major constituent of the developing enamel matrix and a component of the Tomes’ granular layer of human teeth, had the potential to regenerate cementum.51 The results of these in vitro studies showed that when mesenchymal cells of the dental follicle were exposed to the enamel matrix, a noncellular hard-tissue matrix was formed at the enamel surface. Application of porcine enamel matrix in experimental cavities in the roots of monkey incisors induced formation of acellular cementum that was well attached to the dentin. In control cavities without enamel matrix, a cellular, poorly attached, hard tissue was formed.

Furthermore, investigations were designed to determine the ability of EMD to influence specific properties of periodontal ligament cells in vitro.52 Properties of cells examined included migration, attachment, proliferation, biosynthetic activity, and mineral nodule formation. Results demonstrated that under in vitro conditions, EMD formed protein aggregates, thereby providing a unique environment for cell/matrix interaction. Under these conditions, EMD (a) enhanced proliferation of periodontal ligament cells (PDL), but not of epithelial cells; (b) increased total protein production by PDL cells; (c) promoted mineral nodule formation of PDL cells as assayed by von Kossa staining; and (d) had no significant effect on migration or attachment and spreading of cells within the limits of the assay systems used. Lastly, human clinical studies have demonstrated that the local application of EMD during surgical periodontal treatment for intraosseous defects can result in improved probing depths, gain of clinical attachment, and defect bone fill.53-57 These clinical results following treatment with EMD are not different from those obtained with guided tissue regeneration, 56,58,60 and based on previously reported human histologic data, it can be assumed that these improved clinical measurements reflect regenerative healing to a greater extent than reparative healing. 61-65



This article has reviewed the history of periodontal surgical technique, demonstrating the shift in philosophy from an emphasis on resection to a focus on regeneration. Accompanying this shift in philosophy has been a change in scientific emphasis from clinical observation to histologic understanding of tissue formation and the unraveling of the role of specific molecular signaling.


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2. Stern T, Everett F, Robicsek K. S. Robicsek—a pioneer in the surgical treatment of periodontal disease. J Periodontol. 1965;36:265-268.

3. Pickerill H. Stomatology in General Practice: A Textbook of the Teeth and Mouth. London, England: Frowde, Hodder and Stoughton; 1912.

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10. Kronfeld RJ. Condition of the bone tissue of the alveolar process below the periodontal pockets. J Periodontol. 1935;6:22-29.

11. Orban B. Gingivectomy or flap operation? J Am Dent Assoc. 1939;26:1276.

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15. Robinson RE. Periosteal fenestration in mucogingival surgery. J West Soc Periodont. 1961;9:107.

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20. Karring T, Nyman S, Gottlow J, et al. Development of the biological concept of guided tissue regeneration—animal and human studies. Periodontol 2000. 1993;1:26-35.

21. Bowers G, Chadroff B, Carnevale R, et al. Histologic evaluation of new attachment apparatus formation in humans. Part I. J Periodontol. 1989;60:664-674.

22. Nyman S, Lindhe J, Karring T, et al. New attachment following surgical treatment of human periodontal disease. J Clin Periodontol. 1982;9:290-296.

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25. Tonetti MS, Pini-Prato G, Cortellini P. Effect of cigarette smoking on periodontal healing following GTR in infrabony defects. A preliminary retrospective study. J Clin Periodontol. 1995;22:229-234.

26. Rosen PS, Marks MH, Reynolds MA. Influence of smoking on long-term clinical results of intrabony defects treated with regenerative therapy. J Periodontol. 1996;67:1159-1163.

27. Trombelli L, Kim CK, Zimmerman GJ, et al. Retrospective analysis of factors related to clinical outcome of guided tissue regeneration procedures in intrabony defects. J Clin Periodontol. 1997;24:366-371.

28. Kornman KS, Robertson PB. Fundamental principles affecting the outcomes of therapy for osseous lesions. Periodontol 2000. 2000;22:22-43.

29. Schallhorn RG. Eradication of bifurcation defects utilizing frozen autogenous hip marrow implants. Periodontal Abstr. 1967;15:101-105.

30. Schallhorn RG. The use of autogenous hip marrow biopsy implants for bony crater defects. J Periodontol. 1968;39:145-147.

31. Baumhammers A. Use of autogenous bone grafts in periodontal therapy. II. Intra-oral grafts. Pa Dent J (Harrisb). 1970;37:226-232.

32. Haggerty PC, Maeda I. Autogenous bone grafts: a revolution in the treatment of vertical bone defects. J Periodontol. 1971;42:626-641.

33. Dragoo MR, Sullivan HC. A clinical and histological evaluation of autogenous iliac bone grafts in humans. I. Wound healing 2 to 8 months. J Periodontol. 1973;44:599-613.

34. Mattout P, Roche M. Juvenile periodontitis: healing following autogenous iliac marrow graft, long-term evaluation. J Clin Periodontol. 1984;11:274-279.

35. Bowers GM, Schallhorn RG, Mellonig JT. Histologic evaluation of new attachment in human intrabony defects. A literature review. J Periodontol. 1982;53:509-514.

36. Mellonig JT. Bone grafts in periodontal therapy. N Y State Dent J. 1986;52:27-29.

37. Melcher AH. On the repair potential of periodontal tissues. J Periodontol. 1976;47:256-260.

38. Karring T, Nyman S, Lindhe J. Healing following implantation of periodontitis affected roots into bone tissue. J Clin Periodontol. 1980;7:96-105.

39. Nyman S, Karring T, Lindhe J, et al. Healing following implantation of periodontitis-affected roots into gingival connective tissue. J Clin Periodontol. 1980;7:394-401.

40. Isidor F, Karring T, Nyman S, et al. The significance of coronal growth of periodontal ligament tissue for new attachment formation. J Clin Periodontol. 1986;13:145-150.

41. Aukhil I, Pettersson E, Suggs C. Periodontal wound healing in the absence of periodontal ligament cells. J Periodontol. 1987;58:71-77.

42. Karring T, Isidor F, Nyman S, et al. New attachment formation on teeth with a reduced but healthy periodontal ligament. J Clin Periodontol. 1985;12:51-60.

43. Gottlow J. Periodontal regeneration. In: Lang NP, Karring T, eds. Proceedings of the 1st European Workshop on Periodontology. London, England: Quintessence Pub Co; 1994; 172-192.

44. Nyman S, Lindhe J, Karring T, et al. New attachment following surgical treatment of human periodontal disease. J Clin Periodontol. 1982;9:290-296.

45. Slavkin HC. Towards a cellular and molecular understanding of periodontics. Cementogenesis revisited. J Periodontol. 1976;47:249-255.

46. Hammarstrom L. Enamel matrix, cementum development and regeneration. J Clin Periodontol. 1997;24:658-668.

47. Schonfeld SE, Slavkin HC. Demonstration of enamel matrix proteins on root-analogue surfaces of rabbit permanent incisor teeth. Calcif Tissue Res. 1977;24:223-229.

48. Lynch SE, Colvin RB, Antoniades HN. Growth factors in wound healing. Single and synergistic effects on partial thickness porcine skin wounds. J Clin Invest. 1989;84:640-646.

49. Ten Cate AR, Mills C, Solomon G. The development of the periodontium. A transplantation and autoradiographic study. Anat Rec. 1971;170:365-379.

50. Andreasen JO. Interrelation between alveolar bone and periodontal ligament repair after replantation of mature permanent incisors in monkeys. J Periodontal Res. 1981;16:228-235.

51. Hammarstrom L. Enamel matrix, cementum development and regeneration. J Clin Periodontol. 1997;24:658-668.

52. Gestrelius S, Andersson C, Johansson AC, et al. Formulation of enamel matrix derivative for surface coating. Kinetics and cell colonization. J Clin Periodontol. 1997;24:678-684.

53. Heijl L, Heden G, Suardsrom G, et al. Enamel matrix derivative (Emdogain) in the treatment of infrabony periodontal defects. J Clin Periodontol. 1997;24:705-714.

54. Hammarstrom L, Heijl L, Gestrelius S, et al. Periodontal regeneration in a buccal dehiscence model in monkeys after application of enamel matrix proteins. J Clin Periodontol. 1997;24:669-677.

55. Zetterstrom O, Andersson C, Eriksson L, et al. Clinical safety of enamel matrix derivative (Emdogain) in the treatment of periodontal defects. J Clin Periodontol. 1997;24:697-704.

56. Sculean A, Donos N, Blaes A, et al. Comparison of enamel matrix proteins and bioresorbable membranes in the treatment of intrabony periodontal defects: a split mouth study. J Periodontol. 1999;70:255-262.

57. Sculean A, Chiantella G, Miliauskcite A, et al. Four year results following treatment of intrabony periodontal defects with an enamel matrix protein derivative: A report of 46 cases. Int J Perio Res Dent. 2003;32(4):345-351.

58. Silvestri M, Ricci G, Rasperini G, et al. Comparison of treatments of intrabony defects with enamel matrix derivative, guided tissue regeneration with a nonresorbable membrane and Widman modified flap. A pilot study. J Clin Periodontol. 2000;27:603-610.

59. Pontoriero R, Wennstrom J, Lindhe J. The use of barrier membranes and enamel matrix proteins in the treatment of angular bone defects. A prospective controlled clinical study. J Clin Periodontol. 1999;26:833-840.

60. Sculean A, Windisch P, Chiantella G, et al. Treatment of intrabony defects with enamel matrix proteins and guided tissue regeneration. A prospective controlled clinical study. J Clin Periodontol. 2001;28:397-403.

61. Hiejl L. Periodontal regeneration with enamel matrix derivative in one human experimental defect. A case report. J Clin Periodontol. 1997;24:693-696.

62. Mellonig J. Enamel matrix derivative for periodontal reconstruction surgery: Technique and clinical and histologic case report. Int J Perio Rest Dent. 1999;19:9-19.

63. Sculean A, Donos N, Windisch P, et al. Healing of human intrabony defects following treatment with enamel matrix proteins or guided tissue regeneration. J Perio Res. 1999;34:310-322.

64. Yukua R, Mellonig J. Histologic evaluation of periodontal healing in humans following regenerative therapy with enamel matrix derivative. A 10-case series. J Periodontol. 2000;71:752-759.

65. Sculean A, Chiantella G, Windisch P, et al. Clinical and histologic evaluation of treatment of intrabony defects with an enamel matrix protein derivative (Emdogain). Int J Perio Rest Dent. 2000;20:375-381.

Dr. Young graduated from the Indiana University School of Dentistry. After completing an advanced education in general dentistry at the Irwin Army Hospital in Fort Riley, Kan, Dr. Young practiced general dentistry for 5 years. He completed his residency in periodontology at The University of Michigan. Dr. Young maintains a private practice limited to periodontics in Des Moines, Iowa. His practice has an emphasis in aesthetic periodontal regeneration, cosmetic periodontal reconstruction, and dental implants. Dr. Young can be reached at (515) 224-1771 or This e-mail address is being protected from spambots. You need JavaScript enabled to view it .

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