SECTION

EDITOR

its and prosthodontics: enneth

A. Malament,

DDS,

Goals,

o

M&Da

Boston,Mass. I’rostbodontics and periodontics are collaborative disciplines. A successful prosthesis depends on a healthy periodontal environment, and periodontal health depends on the continued integrity of the prosthodontic restoration. To facilitate this collaboration, prosthodontists should not only appreciate the periodontic implications of gingival displacement procedures and tooth preparation, but should be knowledgeable about the types of gingival tissues, osseous topography, occlusal effects, and their implications for abutment choice. Working as a team, the periodontist can identify for the prosthodontist a patient’s periodontal strengths and limitations. In that way, the prosthodontist can then assume responsibility for a given treatment plan based on a mutual understanding of the critical factors involved. (J PROSTHET DENT 1992;67:259-63.)

reatment of patients with complex restorative problemsoften involves practitioners from more than one dental specialty. A mutual understanding among specialists regarding a planned therapeutic regimenis paramount to successful restoration of the teeth. Although each specialist may view the ultimate restorative goal from a different point of view, a common perspective on the patient’s therapy should be establishedbefore treatment is begun.It is especiallyimportant for the prosthodontist and periodontist to communicate and cooperate. A tooth restored on a weak periodontal foundation will not have a predictable prognosis;a failed prosthesiscan be a factor in future periodontal damage. In diagnosing and treating patients, the dentist faces difficult problemsoften unseenbelow the gingival margin. Such conditions include: (1) extensive decay, (2) endodontic failure, (3) clinical crown fracture, (4) root fracture, (5) root resorption-external or internal, (6) root perforation, (7) bone loss-horizontal, vertical, or oblique, (8) furcation involvement, (9) inadequateattached gingiva, (10) gingival recessionor clefts, and (11) root proximity. Although this list concerns periodontal pathoses and anatomic aberrations, the patient is usually unaware of their pathologic or functional implications and seeks prosthodontic care becausethese problems often affect appearance. Periodontal therapy aids patients in many ways. First, it can alter a patient’s oral hygiene habits. Periodontal care can minimize the causative factors of periodontal dis-

at the Academyof DentureProstheticsmeeting,Palm Springs,Califemia. “Private practice. Presented

10/l/33589 THE

JOURNAL

OF PROSTHETIC

DENTISTRY

ease.l-sPeriodontal therapy can also establish a healthy gingival state and topography to support teeth, and create a better, more esthetic dentogingival interface.gW1lThese changesenhancea patient’s resistanceto oral mechanical forces that may ultimately break down the gingival complex and affect teeth. In addition, by regenerating attachment and enhancing gingival tissues,periodontal therapy has the potential to improve topographic defects and cosmetic problemssuchasgingival discolorationsand gingival asymmetry of teeth and edentulous regions. The periodontist canalsohelp the prosthodontist restore teeth. Using surgical apical positioning procedures, periodontal therapy increases the available coronal tooth structure while creating commensurate,adequateinterroot space.12-14 For example, when gingiva is in a state of incomplete passiveeruption, minimal coronal tooth structure is present. Periodontal therapy can lengthen the exposedcrown and allow interocclusal tooth reduction to be madewithout compromisingthe retention of the future prosthodontic restoration or the health of the gingival complex.15-l7

GINGIVA A basicunderstanding of gingival tissuesis necessaryin establishinga rationale and treatment goal for restorative dentistry. Six types of tissuenormally surround the tooth. They are attached gingiva, unattached gingiva, alveolar mucosa,co1 epithelium, sulcular epithelium, and junctional epitheliurn.’ The epithelium is supported by a dense fibrous connective tissue corium through a basement membrane.l*, 18-2o The basallayer of the epithelium is attached to the basementmembraneand is the main germinal layer for epithelial growth. Through this layer, with extensive epithelial mitosis, cells migrate out into the prickle cell 259

layer.21 The cells of the granular layer contain hydrolytic enzymes that begin the cellular protein synthesis forming keratinization. Although not proven, it has been postulated that these hydrolytic enzymes have the ability to alter the pathogenicity of bacterial endotoxin. The granular layer contains keratohyalin granules and cells that have been degraded by hydrolytic enzymes and remain in the intracellular spaces. lo The horny layer is a dense cell layer consisting of horny sheets of keratinization that eventually slough off. The horny layer contains lipid and calcium, which allow only lipid-soluble and nonionized materials to pass. It is mechanically protective and is often described as a stable barrier to toxic products and debris. Periodontal inflammation decreases the level of keratinization of gingiva.22 Keratinization is related to the underlying connective tissue, anatomy, and cellular activity.lg, 23-27From a physical “barrier theory” position, keratinization is the key to determining the type of tissue that would best surround an abutment tooth for prosthodonticsll Attached gingiva is a better tissue than unattached gingiva or alveolar mucosa in that its connective tissue support is dense and rich in collagen. Its small amount of matrix limits the lateral spread of inflammation. Furthermore, a strong continuity exists between this epithelium, its connective tissue, periosteum, and bone. Alveolar mucosa,2g unattached gingiva, and gingival co1 epithelium are anatomically similar to each other and are more easily injured. Lacking a keratinized layer, they are susceptible to bacterial products. The connective tissue supporting alveolar mucosa is loose with a haphazard fiber arrangement.28 Its tissue matrix, fluid, and vascular components give it a greater potential for cellular productivity and resorbability, and its continuity with periosteum and bone is weak. Hence, this type of epithelium (supported by the connective tissue just described), when injured or inflamed, tends to overgrowth or loss, which may result in gingival hyperplasia or create gingival dehiscenses or denuded roots. Certain gingival factors maintain periodontal health by decreasing the quantity and antigenic activity of harmful microorganisms. First, gingival epithelium continuously desquamates, thus shedding the microorganism attached to its surface.lOs 30,31 The outward flow of gingival fluid within the sulcus removes microorganisms and inhibits their ability to adhere to cementum.32, 33 Inflammatory cells such as neutrophils and macrophages from the gingival microcirculation kill microorganisms and remove debris while antibodies and complement neutralize endotoxin and debris.iO Finally, Socransky et al. 34and Tanner et al.35have shown that periodontal disease is site specific and is affected not only by destructive microorganisms, but by protective species that restrict growth of pathogenic microorganisms. When these protective factors fail, periodontal disease occurs and is spread from bacterial accrual in the form of plaque connected to root surfaces found next to sulcular epithelium.36-42 This periodontal disease may lead to 260

pocketing and apical migration of the junctional epithelium. In many instances, the apical penetration of disease may involve the alveolar mucosa. A knowledge of sulcular epithelial physiology is crucial to the understanding of how disease can most affect the prosthetic-gingival interface. Sulcular epithelium, junctional epithelium, and co1 epithelium are composed of cells similar to the prickle cell and basal layers and have no keratinized layer. This means that even without inflammation, breaks in the basement membrane and disruption of the hemidesmosomal connections of epithelial cells to each other render these tissues vulnerable to bacterial toxins.41,42 The path of periodontal inflammation is through these tissues. Theories that accept or advocate as ideal a long junctional epithelial attachment to abutment teeth fail to mention that, even in an ideal prosthetic-gingival interface, this tissue and environment is less stable than a short junctional epithelial attachment in the presence of inflammation.43, 44 If subjected to inflammation or mechanical trauma, a long junctional epithelium or deep, probeable sulcus may be prone to recession and more inflammation, often leading to gingival recession and further recurrence of periodontal pockets. The prosthodontic implications of a deep, probeable sulcus are that the dentist is unable to assess the junctional epithelial attachment level or, in multirooted teeth, its position relative to tooth furcations. This condition poses a greater risk of prosthodontic failure than one with shallow sulci. The ideal gingival form at the prosthetic-gingival interface is attached gingiva with a short, intact, sulcular and junctional epithelium.45-50 The gingival wall should be firm, densely fibrous, and highly collagenous. It should be noninflamed clinically and histologically. After periodontal treatment, gingival and osseous architecture should follow a parabolic form. If the underlying osseous architecture is flat or concave the gingiva will still grow parabolically, resulting in overgrowth of the connective tissue and epithelial migration creating psuedo pockets. ALVEOLARBONE The osseous structure in the human maxillae and mandible varies considerably in quantity and quality.l”, Is, l7 Generally where a thick periodontium is observed, the alveolar bone is thick with cortical plates of bone sandwiching cancellous bone. However, where there is root prominence or root proximity, the supporting boae is thin.i5, l7 In instances where the alveolar bone thickness is minimal and consists of cort.ical bone, dehiscenses or fenestrations may occur. Thin cortical bone containing few blood vessels has poor reparative qualities and, if injured, often resorbs, leaving exposed denuded roots and gingival dehiscences.s If this type of anatomy is present, the prostbodontist must be cautious during treatment. Alveolar bone can have different degrees of porosity; increased porosity may allow teeth to move in a variety of ways, including apically, especially after bone grafting or guided tissue regeneration FE&RUARY

1992

VOLUIME

67

NUMBER

2

BERIQDONTICS

AND

PROSTMODONTICS

procedures to establish new attachment.51S56 In situations where new attachment procedures have been performed, the new attachment (connective tissue to cementum with or without bone growth) presents uncertainty to prosthodontists. How such new bone, if it regrows, will respond to stress applied through teeth is not predictable, although it appears to function as normal bone. TOOTH

~~~PA~AT~ON

Tooth preparation procedures always have the potential to improve or to harm gingiva. Individual conditions and some of the anatomic considerations already mentioned require teeth to be prepared in many different ways. The ability of a complete or partial coverage restoration to remain luted to a tooth is a function of the retention, which is related to preparation length, width, taper, margin design, and bevel, and resistance form, which minimizes internal forces on the luting agent-tooth interface, thus reducing the likelihood of lingual displacement of the restoration.jl Ideally, the coronal aspect of a prepared tooth should be continuous with subgingival root contour, because tooth undercuts below the gingival margin potentially act as cul-de-sacs for plaque formation. Teeth should, if possible, be prepared to the free gingival margin. With anterior teeth, such preparation maintains the coronal width in the gingival third and will not result in undercontoured restorations. Anteriorly, symmetry should be respected so that the restored tooth maintains the same shape and contour as neighboring unrestored teeth. This symmetry applies to the surrounding gingival form and color as well. If one is able to eliminate subgingival undercuts and open or make wider interroot spaces, the co1 shaped gingival interproximal form or co1 epithelium will transform into keratinized non-col-formed tissue, which is potentially a healthier and more resistant tissue.r3, l6 If many anterior teeth are involved, gingival symmetry can be maintained, even with changed or eliminated interproximal papilla. If a few anterior teeth are involved, however, with reduced gingival neck contour and the gingival papillae lost, cosmetic results are poor. The consequences of poor appearance of posterior teeth are less important than those of anterior teeth. Here, interroot spaces can be widened and, with time, interproximal changes might allow a healthier gingiva to develop. Teeth requiring periodontal therapy can be prepared to the gingival crest and restored with a provisional acrylic resin prosthesis. After periodontal therapy and healing, teeth can be reprepared to the apically positioned gingival margin. These procedures can establish a new prostheticgingival interface that is stable and can be examined and cleaned easily.@, 5g GINGIVAL MP~ESS~~N

DISPLACEMENT

FOR

TOOTH

Gingival displacement and impression procedures are ideally done when gingival tissue is healthy and healed. THE

JOURNAL

OF PROSTHETIC

DENTISTRY

Maturation of the connective tissue corium and epitbelium after periodontal procedures will ensure ease of displacement and impression making. Usually a minimum of 6 weeks’ healing time is required after the surgical operation, but a previously diseased, incompetent periodontium may require months to achieve health. During the healing time a poor periodontal condition may persist, making an abutment tooth incompetent for prosthodontics and weakening the treatment prognosis. The final shape of the healed gingiva can also determine where the gingival margin will be in the final prosthesis. All displacement techniques have the potential to damage gingiva, attachment apparatus, and bone, especially if anatomic forms are weak or if disease is present. In healthy patients, properly used cord displacement or copper band methods have proved to be atraumatic. Rue1 et alS60demonstrated in humans that copper band displacement that pierced the connective tissue healed histologically within 8 days and caused 0.1 mm recession after 24 hours. Tissues displaced with cord impregnated with 1:lOOO epinephrine healed histologically after 16 days, causing 0.2 mm recession. The same study also showed that although electrosurgery did not pass into the connective tissue, as did both other techniques, it caused damage. The gingiva did not begin to heal for 4 days because of vasoconstriction and the lack of immediate polymorphonuclear leukocyte infiltration. Complete healing was seen after 24 days, but with gingival recession of 0.6 mm. A study done by Wilhelson et a1.61on baboons supports the need for extreme caution in the use of electrosurgery. The procedure produced burn marks in the dentin of the root surfaces where contact was made by the electrode, produced cemental destruction with subsequent impaired cementogenesis, and ultimately inhibited epithelial and connective tissue reattachment at the burn sites. OCCLUSAL

EFFECTS

Teeth requiring prosthodontic treatment are often affected by the combined lesion of marginal periodontitis and occlusal trauma. Meitner,62 P01son”~ and Lindbe et a1.64-68have observed that occlusal trauma alters the periodontal tissue below the connective tissue attachment to the tooth. It is well known that thin plates of facial bone can be resorbed after occlusal trauma, resulting in dehiscences and fenestrations. As these plates are resorbed and the periodontal ligament becomes confluent with the periodontium, the union between tooth and gingiva (or mucosa) becomes more membranous and tenuous. The involved tissues are highly vulnerable to physical or inflammatory trauma, which results in recession. COMMUNICATION If excellent periodontal care and patient cooperation have been achieved, the prosthodontist can routinely make restorations that are harmonious with and contribute to periodontal health. The prosthodontist must make decisions regarding tooth strength, prosthetic design, and the 261

choice of prosthetic materials to be used in treatment. The choice of a prosthetic material is dictated by material strength, durability, potential wear, esthetics, and prosthetic design. If problems appear after prosthodontic treatment and are not discovered quickly, they can become causative factors in periodontal breakdown, decay, and further material fail.ure. Periodontists and prosthodontists often speak of an ideal periodontal environment. Perfection cannot exist in an altered biologic environment. There is no single ideal gingival form for the interface of all teeth. Distinctions are made, for example, between the preferred gingival form surrounding anterior teeth and that surrounding posterior teeth. Levels of excellence, if not ideals, can be attained in treating individual patients. Periodontal practice today is moving toward presenting a holistic, nonsurgical philosophy, and periodontal education is placing heavy emphasis on bacteriology, immunology, bone growth factors, and genetics. While this approach has appealing aspects, the fact remains that prosthodontists require specific periodontal anatomy, which can be provided only by a periodontist who is well disciplined in practical surgical technique. As part of a treatment team, periodontists have the responsibility to guide prosthodontists in their decisions regarding the prognosis of abutment teeth and implants. Because potential problems always exist before, during, and after treatment, a team approach to monitoring patients is advantageous. Prosthodontists need to be knowledgeable about periodontics and those who teach should incorporate sound periodontal principles into their educational programs. This understanding will facilitate communication and allow prosthodontists to develop an appreciation of the periodontist’s goals and limitations imposed in a given situation. Periodontists and prosthodontists need to establish a common understanding for factors on which their views may differ.6g These include (1) predictability of treatment, (2) total patient responsibility, (3) undertreatment and overtreatment, (4) divergent concepts of therapy, (5) research-clinical correlations, (6) end point of active therapy, (7) treatment time (projected/actual), (8) fees, (9) residual defects (compromise), and (10) maintenance. The past 30 years have seen the blossoming of the relationship between prosthodontics and periodontics. Faced with a given patient’s problem, each specialty can easily ignore its own idealistic goals and abdicate responsibility in treatment planning, design, and execution to a cotherapist. Each specialist may rely too much on the expertise of the other, or even too much on the theoretical, but impractical, ideas of treatment. However, using the periodontist’s philosophy in patient treatment as the only guideline cannot yield, by itself, a long-term successful prosthodontic result. Classic prosthodontic theory and practice is, at least, as relevant and should be respected. It is the prosthodontist who will be held responsible if the patient’s prosthesis fails.

262

Such failure may be very costly not only financially also, to the prosthodontist’s reputation and career.

but,

CONCLUSION Prosthodontics and periodontics are collaborative clinical sciences. Prosthodontists should work in three ways to facilitate this collaboration: 1. They should become knowledgeable in periodontics, and incorporate sound periodontic principles when teaching students and colleagues. 2. They should use a team approach with periodontists in monitoring patient care. 3. They should assume responsibility for a given treatment plan based on a mutual understanding of the critical factors involved. Periodontists should become knowledgeable about prosthodontics and better understand the limitations that face prosthodontists in their clinical and laboratory procedures. With this kind of knowledge and collaboration, better treatment decisions can be made and patients will be better served.

REFERENCES 1. Axelsson P, Lindhe. The significance of maintenance care in the treatment of periodontal disease. J Clin Periodontal 1981;8:281. 2. Lindhe J, Nyman S. Long term maintenance of patients treated for advanced periodontal disease. J Clin Periodontol 1984;11:504. 3. Axelsson P, Lindhe J. Effect of controlled oral hygiene procedures on caries and periodontal disease in adults, J Clin Periodontol 1978;5: 133. 4. Pihlstrom BL, McHugh B, Oliphant TH, Campos DO. Comparison of surgical and non-surgical treatment of periodontal disease: a review of current studies and additional results after 6.5 years. J Clin Periodonto1 1983;10:524. 5. Lindhe J, Haffajee AD, Socransky SS. Progression of periodontal disease in adult subjects in the absence of periodontal therapy, J Clin Periodontol 1983;10:433. 6. Lindhe J, Nyman S. The effect of plaque control and surgical pocket elimination on the establishment and maintenance of periodontal health: a longitudinal study of periodontal therapy in cases of advanced disease. J Clin Periodontol 1975;2:67. 7. Parma-Benfenati S, Fugazzotto PA, Ruben MP. The effect of restorative margins on the post surgical development and natxre of the periodontum. Part I. Int J Periodont Res Dent 1985;5:31. 8. Parma-Benfenati S, Fugazzotto PA, Ferreira PM, Ruben MP, Kramer GM. The effect of restorative margins on the post surgical development and nature of the periodontum. Part II. Int J Periodont Res Dent 1986;6:65. 9. Genco RJ, Goldman HM, Cohen DW. Contemporary periodontics. St. Louis: CV Mosby, 1990, 3-30. 10. Lindhe J. Textbook of clinical periodontology, 2nd ed. Copenhagen: Munksgaard, 1989, 27-35. 11. Kramer GM. Rationale of periodontal therapy. In NM Goldman et al, (eds). Periodontal therapy. 5th ed. St. Louis: CV Mosby, 1973,331. 12. Nyman S, Lindhe J. A longitudinal study of combined periodontal and prosthetic treatment of patients with advanced periodontal disease. J Periodontol 1979;50:163. 13. Carnevale GC, Sterrantino SF, DiFebo G. Soft and bard tissue wound healing following tooth preparation to the alveolar crest. Int J Periodont Res Dent 1983;6:37. 14. Ariaudo AA, Tyrell HA. Repositioning and increasing the zone of attached gingiva. J Periodontol 1987;28:106. 15. Kramer GM. A consideration of root proximity. Int J Periodont Res Dent 1987;7:9. 16. Boner C, Boner N. Restoration of the interdental space. Int J Periodont Res Dent 1983;3:31. FEBRUARY

1992

VOLUME

87

NUMBER

2

PERIODONTICS

AND

PROSTHODONTICS

17. Nevins M. Interproximal periodontal disease: the embrasure as an etiologic factor. Int J Periodont Res Dent 1982;2:9. 18. Ainamo J, Loe H. Anatomical characteristics of gingiva. I. A clinical and microscopic study of the free and attached gingiva. J Periodontol 1966;37:5. 19. Schroeder HE, Listgarten MA. Fine structure of the developing epitheha1 attachment of human teeth. In Wolsky A, ed. Monographs in developmental biology, vol 2. Basel, Switzerland: S Karger, 1971, 9, 85. 20. Schroeder HE, Theilade J. Electron microscopy of normal human gingival epithelium. J Periodont Res 1966;1:95. 21. Karring T. Mitotic activity in the oral epithelium. J Periodont Res 1973;13(Suppl):l. 22. Freedman HL, Listgarten MA, Taichman NS. Electron microscopic features of chronically inflamed human gingiva. J Periodont Res 1968;3:313. 23. Karring T, Lang NP, Lee H. The role of gingival connective tissue in determining epithelial differentiation. J Periodont Res 1975;lO:l. 24. Listgarten MA. Electron microscopic study of the gingivo-dental junction of man. Am J Anat 1966;119:147. 25. Listgarten MA. Normal development, structure, physiology and repair of gingival epithelium. Oral Sci Rev 1972;1:3. 26. Karring T, Loe H. The three dimensional concept of the epitheliumconnective tissue boundary of gingiva. Acta Odontol Stand 1920;28:917. 27. Kuam E: Topography of principle fibers. Stand J Dent Res 1973;81:553. 28. Shultz-Naudt Sp AASE. Dynamics of the periodontal tissues II: the connective tissue. Odont Tidsskr 1962;70:397. 29. Cozdan 6, Squier CA. The histology of the mucogingival junction. J Periodont Res 1969;4:83. 30. Tinanoff N, Gross A. Epithelial cells associated with the development of dental plaque. J Dent Res 1976;55:580. 31. L&g&en MA, Ellegaard B. Electron microscopic evidence of a cellular attachment between junctional epithelium and dental calculus. J Periodont Res 1973;8:143. 32. Brill M, Bjorn H. Passage of tissue fluid into human gingival pockets. Acta Odontol Stand 1959;17:11. 33. Loe H, Helm-Pederson P. Absence and presence of fluid from normal and inflamed gingiva. Periodontics 1965;3:171. 34. Socransky SS, Manganiello AD, Propoas D, Oram V, van Haute. Bacteriological studies of developing supragingival dental plaque. J Periodont Res 1977;12:90. 35. Tanner ACR, Socransky SS, Goodson JM. Microbiota of periodontal pockets losing crestat alveolar bone. J Periodont Res 1984;9:279. 36. Arbuthnott JP. Membrane-damaging toxins in relation to interference with host defense mechanisms. In Grady FO, Smith H, eds. Microbial perturbation of host defenses. London: Academic Press, 1981;9’7-112. 37. Frank RM. Bacterial penetration in the apical pocket wall of advanced human periodontitis. J Periodont Res 1980;15:563. 38. Liakoni H, Barber P, Newman HN. Bacterial penetration of pocket soft tissues in chronic adult and juvenile periodontics case. J Clin Periodontol 1987;14:22. 39. Listgarten MA. Electron microscopic observations on the bacterial flora of acute necrotizing ulcerative gingivitis. J Periodontol 1965;36:328. 40. Nitzan D, Sperry JF, Wickins TD. Fibronolytic activity of oral anaerobic bacteria. Arch Oral Biol 1978;23:465. 41. Saglie R, Newman MG, Carranza Jr FA, Patison GL. Bacterial invasion of gingiva in advanced periodontitis in humans. J Periodontol 1982;53:217. 42. Steffen EK, Hen&es DG. Hydrolytic enzymes of anaerobic bacteria isolated from human infections. J Clin Microbial 1981;14:153. 43. Ramfjord SP, Knowles JW, Nissle RR, Schick RA, Burgett FG. Longitudinal study of periodontal therapy. J Periodontol 1973;46:66. 44. Ramfjord SP, Nissle RR, Schick RA, Cooper Jr H. Subgingival curettage versus surgical elimination of periodontal pockets. J Periodontol 1968;39:167. 45. Waerhaug J. Histologic considerations that govern where the margin of restorations should be located in relation to the gingiva. Dent Clin North Am 1960;167-i76.

TKE

JOURNAL

OF

PROSTHETIC

DENTISTRY

46. Dragoo MR, Williams GB. Periodontal tissue reactions to restorative procedures, part II. Int J Periodont Res Dent 1982;2:35. 47. Karlsen K. Gingival reactions to dental restorations. Acta Odontol Stand 1970;28:895. 48. Tarnow D, Stang SS, Magner A, Zamzok J. Human gingival attachment responses to subgingival crown placement: marginal remodeling. J Clin Periodontol 1986;13:563. 49. Newcomb GM. The relationship between location of subgingivai crown margins and gingival inflammation. J Periodontol 1974;45:151. 50. Richter WM, Ueno H. Relationship of crown margin placement to gingival inflammation. J Periodontol 1973;303156. 51. Bowers GM, Schallhorn RG, Mellonig JT. Histologic evaluation of new attachment in human intrabony defects, a literature review. J Periodontol 1982;53:509. 52. Schallhorn RG. Long term observation of the healing of an interbony lesion. Int Dent J 1989;30:101. 53. Nyman S, Lindhe J, Karring T, Rylander H. New attachment following surgical treatment of human periodontal disease. J Clin Periodontol 1982;9:290. 54. Gottlow J, Nyman S, Lindhe J, Karring T, Wennstron J. New attachment formation in the human periodontium by guided tissue regeneration. J Clin Periodontol 1986;13:604. 55. Becker W, Becker BE, Berg L, Prichard 3, Caffessee R, Rosenberg E. New attachment after treatment with root isolation procedures. Report for treated Class III and Class II furcations and vertical osseous defects, Int J Periodont Res Dent 1988;8:(3):9-23. 56. Schallhorn RG, McClain PR. Combined osseous composite grafting, root conditioning and guided tissue regeneration. Int J Periodont Res Dent 1988;8(4):9-31. 57. Shillingburg HT, Jacobi R, Brackett SE. Fundamentals of tooth preparationss for cast metal and porcelain restorations. Chicago: Quintessence, 1987. 58. Rosenberg MM, Kay HB, Keough BE, Holt RL. Periodontal and prosthetic management for advanced cases. Chicago: Quintessence, 1988. 59. Selvig KA. An ultrastructural study of cementurn formation. Acta Odonto1 &and 1964;22:105. 60. Rue1 J, Scbuessler PJ, Malament KA, Mori D. Effect of retraction procedures on the periodontium in humans. J PROSTHET DENT 1980;44:508. 61. Wilhelmson NR, Ramfjord SP, Blankenship JR. Effects of electrosurgery on the gingival attachment in rhesus monkeys. J Periodontol 1976;47:160. 62. Meitner SW. Co-destructive factors of marginal periodontitis and repetitive mechanical injury [Thesis]. Rochester: Eastmen Dental Center and the University of Rochester, 1975. 63. Polson A, Zander H. Effect of periodontal trauma upon infrabony pockets, J Periodontol 1983;54:586. 64. Ericsson I, Lindhe J. Lack of effect of trauma from occlusion on the recurrence of experiment periodontitis. J Clin Periodontol 1977;4:115. 65. Ericsson I, Lindhe J. The effect of long standing jiggling on experimental marginal periodontitis in the beagle dog. J Clin Periodontol 1982;9:497. 66. Lindhe J, Ericsson I. The effect of elimination of jiggling forces on periodontally exposed teeth in the dog. J Periodontol 1982;53:562. 67. Lindhe J, Svanberg G. Influences of trauma from occlusion on progression of experimental periodontitis in the beagle dog. J Clin Periodontol 1974;1:3. 68. Nyman S, Lindhe J, Ericsson I. The effect of progressive tooth mobility on destructive periodontitis in the dog. J Clin Periodontol1978;7:351. 69. Schallhorn RG. Third Int symposium on Perio and Rest Dent. Boston: April 1989. Reprint requests to: DR. KENNETH A. MALAMENT 50 STANFORD STREET BOSTON, MA 02114

263

Periodontics and prosthodontics: goals, objectives, and clinical reality.

Prosthodontics and periodontics are collaborative disciplines. A successful prosthesis depends on a healthy periodontal environment, and periodontal h...
876KB Sizes 0 Downloads 0 Views