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» Articles -> Smile Journal Issue 9 September 2008-> Mind the Gap, The Platform Switching Concept
Dated : 2008-09-30
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Mind the Gap
The Platform Switching Concept

 

» By: Dr. Stewart Harding
Master of Science in Implant Dentistry, Fellow of the International Congress of Oral Implantologists
Associate Director - Postgraduate Dental Education Unit, Institute of Clinical Education
Honorary Associate Clinical Professor at the University of Warwick
Honorary Senior Lecturer in Implant Dentistry at Warwick and Ajman Universities
ste@osteo-ti.com

 

After exposing a submerged implant to the oral environment, bone loss occurs downwards along the implant body and stops at some predefined position.1 The implant abutment interface (IAI) is the joint between the implant and the abutment that is a feature common to two-piece implants (Fig. 1). A current area of hot debate is the significance of the IAI and its influence on crestal bone level in relation to the first thread. Several theories have been proposed based on a number of studies which attempt to explain this phenomenon. These range from trauma during surgery to load shielding resulting in crestal bone loss to the first thread or the inherent need for a minimum Biologic Width as seen in the natural dentition.2-4

(Figure 1): Passage of fluids through the microgap. ML = microleakage, S = soft tissue interface, B = bone interface

(Figure 2): IAI = Implant Abutment Interface, aICT = Abutment Inflammatory Cell Infiltrate (1.5mm = 0.75mm above IAI + 0.75mm below the IAI), CT = Zone of healthy connective tissue between the base of the aICT and crestal bone (1mm thick)

Criteria for Implant Success
Part of the early generally accepted criteria for implant success, is that less than 0.2 mm of alveolar bone loss occurs per year after the first year in function.5 However what is overlooked is that the success of implant therapy is determined after the first year of service because most of the bone loss occurs during the first 12 months following abutment connection.6 Therefore the loss of 2.0 mm of crestal bone over the first year has been considered a normal characteristic of a healthy functioning implant and this change in bone height is merely due to remodeling in responses to loading. In another words the bone is adapting to changes in load following prosthetic restoration.
The question that needs to be redressed is, does this small amount of bone loss have any clinical significance and can it be considered acceptable. Dental implants unlike implants employed in other areas of medicine have two roles to fulfill, aesthetic and functional. The loss of seemingly small amounts of bone and soft tissue can have important implications on aesthetics of implant-borne restorations, which are reliant on healthy and vertically constant bony supported soft tissue dimensions over time.

Part of the early generally accepted criteria for implant success, is that less than 0.2 mm of alveolar bone loss occurs per year after the first year in function.5 However what is overlooked is that the success of implant therapy is determined after the first year of service because most of the bone loss occurs during the first 12 months following abutment connection.6 Therefore the loss of 2.0 mm of crestal bone over the first year has been considered a normal characteristic of a healthy functioning implant and this change in bone height is merely due to remodeling in responses to loading. In another words the bone is adapting to changes in load following prosthetic restoration.The question that needs to be redressed is, does this small amount of bone loss have any clinical significance and can it be considered acceptable. Dental implants unlike implants employed in other areas of medicine have two roles to fulfill, aesthetic and functional. The loss of seemingly small amounts of bone and soft tissue can have important implications on , which are reliant on healthy and vertically constant bony supported soft tissue dimensions over time.

The Microgap
In recent years the microgap which exists at the connection between the implant body and the restorative abutment-That is the IAI, has been implicated. This gap permits micro-leakage of fluids containing small molecules in the range of disaccharides and short peptides that contain bacterial by products or nutrients required for bacterial growth or abutment inflammatory cell infiltrate (a- lCT).7-9

The sustained activation of inflammatory cells has been shown to promote osteoclast formation and activation, which can result in alveolar bone loss. It has been proposed that this in turn may initiate the one to two millimeters apical bone loss that occurs around submerged implants. This however remains to be clarified and distinguished from the phenomenon of bone resorption adjacent to the smooth implant neck.10,11 These infiltrates are invariably separated from the alveolar bone by a zone of non-inflammatory connective tissue (CT) showing clinically stable conditions (Fig. 2).12

Soft Tissue Interface
Although the gingiva at teeth and the keratinized mucosa (peri-implant mucosa, PM) at titanium implants have features in common such as the relative proportions of epithelium and connective tissue as well as the length of the junctional epithelium, there are, however, also important differences between the two tissues. From the cementum, collagen fibers project laterally and run a course in the gingiva perpendicular to the root. Implants lack cementum and the orientation of the attachment fibers in the supracrestal soft tissue compartment is parallel to the implant surface and perpendicular to the periosteum of the marginal bone crest (Figs. 3, 4).

(Figure 3): Histomorphometric Landmarks: GM= gingival margin, aS= apical extension of sulcus, aJE= apical extension of junctional epithelium, IAI=implant abutment interface, BC= bone contact. SD= sulcus depth, JE= junctional epithelium, CTC=connective tissue contact. BW=biologic width = SD+JE+CTC. From the cementum collagen fibers project laterally into the gingiva

(Figure 4): Histomorphometric Landmarks: PM= margin of peri-implant mucosa, aS= apical extension of sulcus, aJE= apical extension of junctional epithelium, IAI=implant abutment interface, BIC= Bone implant contact. BW=biologic width = SD+JE+CTC. There is no cementum or attached lateral collagen fibers

In the natural dentition, the junctional epithelium provides a seal at the base of the sulcus against bacterial penetration. The other line of defense present in the natural dentition and absent in implants is the periodontal ligament. Since no cementum or fibers are present on the surface of an implant, infection has the potential to spread directly into the osseous structures resulting in bone loss and ultimately implant failure. Thus, the maintenance of osseointegration and long term success of implants depends on the presence of a leak-proof peri-implant soft tissue cuff. This requires the formation of a biological seal dependent on the tight contact between the epithelium and adjacent connective tissue with the implant surface.

Biologic Width
The majority of research has been directed towards hard tissue integration with less emphasis on soft tissue integration involving epithelium and connective tissue. It is important to understand the mechanisms which permit the implant or abutment to transverse the soft tissues while maintaining a seal against bacterial ingress. The biologic width, is a soft tissue barrier composed of an epithelial component continuous with a zone of connective tissue.13,14 For natural teeth and implants alike, the biologic width is a physiologically formed and stable dimension. It is suggested that a certain width of peri-implant mucosa is essential in order to enable proper epithelial-connective tissue attachment and, if this absolute soft tissue dimension is not satisfied, bone resorption will occur to ensure the reestablishment of an attachment of the appropriate biologic width.15 Therefore, the “Biologic Seal” is composed of junctional epithelium (JE) attachment to either the abutment of a 2-stage implant or neck section of a 1-stage implant and a tight band of connective tissue contact (CTC).

Platform Switching
Recently it has been suggested that the presence and position of the microgap may not be the principal cause of bone resorption phenomenon, but instead that it is due to the relative diameters of the abutment and the implant platform (Fig. 5). Radiographically the anticipated change in crestal bone level does not occur if the implant is restored with an abutment having a smaller diameter than the corresponding implant (Figs. 6, 7).This observation has given birth to the concept of “Platform Switching”.16-18
It is proposed that horizontal positioning of the implant abutment interface (IAI) has two effects.

1- The increased surface area created by the exposed implant seating surface, reduces the amount of crestal bone resorption necessary to expose a minimum vertical amount of implant surface for soft tissue attachment. In effect, the biologic width has been repositioned horizontally (Fig. 8).

2- Repositioning the IAI away from the outer edge of the implant and adjacent bone, confines the abutment inflammatory cell infiltrate (aICT) and reduces the overall effect on the surrounding tissues thus decreasing the resorptive effect on the crestal bone
(Fig. 9).

      

(Figure 5):  Switching. Abutment diameter is within implant platform                                                                   

(Figure 6): Radiograph of implants at exposure

(Figure 7):  Radiograph of loaded platform switched implants after 2 years

(Figure 8): Histomorphometric Landmarks: PM= margin of peri-implant mucosa, aS= apical extension of sulcus, aJE= apical extension of junctional epithelium, IAI=implant abutment interface, BIC= Bone implant contact. The biologic width his changed horizontally within the implant        

(Figure 9):  Radiograph of loaded platform switched implants after 2 years

(Figure 10): Implant features designed to limit microleakage and reduce the effects of aICT                                           

Conclusion
It appears desirable to incorporate features into implant design which reduce microleakage or limit its effects. A tapered IAI creates a microseal and the hermetic seal produced eliminates the microgap preventing the passage of bacteria or aICT. Platform switching may limit or confine the effects of the aICT (Fig. 10).

References
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2. Williams WN, Levin AC, La Pointe LL, Cornell CE. Bite force discrimination by individuals with complete dentures. JProsthet Dent 1985 Jul;54(1):146-50.

3. Richter EJ. Basic biomechanics of dental implants in prosthetic dentistry. J Prosthet Dent 1989 May;61(5):602-9.

4. van Steenberghe D, Lekholm U, Bolender C, Folmer T, Henry P, Herrmann I et al. Applicability of osseointegrated oral implants in the rehabilitation of partial edentulism: a prospective multicenter study on 558 fixtures. Int J Oral Maxillofac Implants 1990 Fall;5(3):272-81.

5. Smith DE, Zarb GA. Criteria for success of osseointegrated endosseous implants. J Prosthet Dent 1989 Nov;62(5):567–72.Review.

6. Adell R. Clinical results of osseointegrated implants supporting fixed prostheses in edentulous jaws. J Prosthet Dent 1983 Aug;50(2):251–4.

7. Piatelli A, Vrespa G, Petrone G, lezzi G, Annibali S, Scarano A. Role of the microgap between implant and abutment: a retro¬spective histologic evaluation in monkeys. J Periodontol 2003 Mar;74(3):346-52.

8. Quirynen M, Van Steenberghe D. Bacterial colonization of the internal part of two stage implants. An in vivo study. Clin Oral Implants Res 1993 Sep;4(3):158-61.

9. Quirynen M, Bollen MC, Eyssen H, van Steenberghe D. Micro¬bial penetration along the implant components of the Brånemark System. An in vitro study. CIin Oral Implants Res 1994 Dec;5(4):239-44.

10. Buser D, Weber HP, Donath K, Fiorellini JP, Paquette DW, Williams RC. Soft tissue reactions to non-submerged unloaded titanium implants in beagle dogs. J Periodontol 1992 Mar;63(3):225-35.

11. Jung YC, Han CH, Lee KW. A 1-Year Radiographic Evaluation of Marginal Bone Around Dental Implants. Int J Oral Maxillofac Implants 1996 Nov-Dec;11(6):811-8.

12. Broggini N, McMmnus LM, Hermann JS, Medina RU, Oates TW, Schenk RK et al. Persistent acute inflammation at the implant-abutment interface. J Dent Res 2003 Mar;82(3):232-7.

13. Berglundh T, Lindhe J. Dimension of the periimplant mucosa. Biological width revisited. J Clin Periodontol 1996 Oct;23(10):971-3.

14. Gargiulo AW, Wentz FM, Orban B. Dimesions and relations of the dentogingival junction in humans. J Periodontol 1961;32:261-7.

15. Berglundh T, Lindhe J. Dimension of the periimplant mucosa. Biological width revisited. J Clin Periodontol 1996 Oct;23(10):971-3.

16. Lazzara RJ, Porter SS. Platform Switching: a new concept in implant dentistry for controlling postrestorative crestal bone levels. Int J Periodontics Restorative Dent 2006 Feb;26(1):9-17.

17. Hansson S. A conical implant-abutment interface at the level of the marginal bone improves the distribution of stresses in the supporting bone. An axisymmetric finite element analysis. Clin Oral Impl Res 2003 Jun;14(3):286-93.

18. Hansson S. Implant-abutment interface: bio-mechanical study of flat top versus conical. Clinical Implant Dent Relat Res 2000;2(1):33-41.

 
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