Journal of Interdisciplinary Dentistry

: 2012  |  Volume : 2  |  Issue : 2  |  Page : 84--91

Significance and clinical relevance of biologic width to implant dentistry

Sangeeta Dhir 
 Department of Periodontology and Implantology, Sudha Rustagi College of Dental Sciences and Research, Faridabad, Haryana, India

Correspondence Address:
Sangeeta Dhir
Department of Periodontology and Implantology, Sudha Rustagi College of Dental Sciences and Research, Faridabad, Haryana


The concept of biologic width forms the basis for a successful peri-implant soft tissue integration around titanium implants. The purpose of this review is to evaluate the present knowledge about this important zone that forms the basis for a successful implant. Methodology: Electronic search of the Medline/PubMed was done using the search words and MeSH Headings including, biologic width, peri-implant soft tissue, crestal bone loss, platform switch, biologic width and dental implant, implant abutment junction. Hand search of the prosthetic,implantology, and the periodontology journals was also undertaken for the collection of the data. Clinical Relevance to Interdisciplinary Dentistry
  1. Implant dentistry involves an interdisciplinary treatment approach of prosthodontics, periodontics, and surgical aspects.
  2. A profound knowledge of the biologic response and the underlying anatomical/histologic aspects of the bone and the overlying soft tissues is critical for the success of the implant.
  3. Biologic width is a healthy self-limiting zone around implant. It acts as a mirror for the underlying health of the supporting tissues.
  4. Violation of the biologic width generates a revoking response from the tissues, which then tries to accommodate at the stake of the crestal bone.
  5. This review article tries to demystify the conveniently overlooked biologic zone and the affecting factors/variables responsible for the viability of this zone.

How to cite this article:
Dhir S. Significance and clinical relevance of biologic width to implant dentistry.J Interdiscip Dentistry 2012;2:84-91

How to cite this URL:
Dhir S. Significance and clinical relevance of biologic width to implant dentistry. J Interdiscip Dentistry [serial online] 2012 [cited 2021 Nov 26 ];2:84-91
Available from:

Full Text


The use of dental implants to replace the missing teeth is becoming a preferred alternative. With the gained awareness and the improved quality of life, analyses indicate that patients perceive their oral health status as improved by their experience with dental implants. [1] Root form dental implants comprises the most widely used form of treatment and it consists of two basic types. The first category was introduced and developed by Branemark and was referred to as two-piece implant. [2] The second category was developed by Schroeder and was referred to as one-piece implant. [3]

Natural teeth are surrounded by gingival soft tissues that provide a biologic seal between the oral cavity and the inside of the body. This unique structure is composed of epithelium and soft connective tissue that are continually bathed in a transudate called gingival fluid. The term biologic width was based on the work of Gargiulo et al. who described the dimensions of dentogingival junction in human cadavers. [4] Average dimension counted was 2.04 mm comprising supraalveolar connective tissue and junctional epithelial attachment. It has been hypothesized that a similar relationship of bone to overlying soft tissues exists around implants, and changes in this relationship may be one of the reasons for the early crestal bone loss. [5] The presence of biologic width around implants has also been investigated. Multiple research groups have also verified that biologic width also exists around implants. [6],[7],[8] This is true for implants of all shapes after the implant uncovery stage (stage 2).

In the most simplified form, biologic width refers to the height of the dentogingival attachment apparatus around a normal tooth and is defined as the distance necessary for a healthy existence of bone and soft tissue from the apical extent of the dental restoration. In a more clinical sense, there must not be any encroachment within 2 mm of the bone that surrounds the tooth.

Vacek et al. [9] reported in their study the revised range of this zone as 0.75-4.33 mm. It was observed that of all the tissue dimensions measured, the length of connective tissue attachment varied the least.

The proceedings of the 3 rd European workshop on periodontology and implant dentistry state that the function of peri-implant seal is "to maintain homeostasis of the internal environment in response to challenges from the external environment." [10]

 Materials and Methods

Electronic search of the Medline was done with the search words. The key words used for the search were: biologic width, peri-implant soft tissue, crestal bone loss, platform switch, biologic width and dental implant, implant abutment junction. Additionally, a manual search of the major dental implant, prosthetic, and periodontal journals and books was performed. The following journals were searched: Clinical Oral Implant Research, Implant Dentistry, International Journal of Oral and Maxillofacial Implants, Clinical Implant Related Research, Journal of Prosthetic Dentistry, Journal of Periodontology, Journal of Biomedical Research, Journal of Clinical Periodontology. The articles included in the review comprised in vitro studies, in vivo (animal and human) studies, abstracts, and review articles.

Biology of peri-implant mucosa

There exists a significant difference between the tissues surrounding the natural tooth and the peri-implant mucosa. The mucosa that encircles the implant has more of collagen and fewer fibroblasts as opposed to gingival tissues. The collagen fiber bundles run parallel to the titanium surface without attaching to it versus the perpendicular direction around the tooth. [11] The supracrestal vascular topography surrounding the fixture is reduced and diversely arranged [11],[12] [Table 1].{Table 1}

Bone and implant junction

The healed bone and soft tissues around the implant and tooth are similar but do differ from the dentogingival interface of natural teeth. These relationships depend on the cervical design of the implant, location of the implant components relative to the crestal bone, implant abutment junction (IAJ), insertion depth, surface technology of the implant, and the soft and hard tissue dimensions. Bone remodeling around the implant continues until the biologic width is formed around the implant and is stabilized thereafter. The biologic rationale behind the biologic width formation lies in the fact that bone when exposed to the oral cavity is always covered with periosteum, connective tissue, and epithelium. In the presence of the chronic irritation, e.g. bacteria accessing the implant abutment interface, or when the abutment is removed during two-stage implants after the initial healing phase for prosthesis fabrication, the bone starts resorbing to create a distance from this chronically exposed/irritated area. [14] There exists a vertical and horizontal component of biologic width as it forms and remodels itself around the implant. It is important to maintain a minimum distance of 3 mm between the two implants for a stable interimplant bone and soft tissue with a stable biologic width. [15]

The smooth polished collar of the conventional implant and their relative insertion depth have revealed a varying biologic width. [16] Literature has reported the evidence of biologic width of 3.6 mm and 4.1 mm in the mandible and maxillary implant, respectively, in the ITI (International Team of Implantology )implants with a polished cervical collar placed at the crest of the bone. [17] In the event of the smooth collar being placed subcrestally, it leads to the bone being resorbed to the transition level of the smooth and rough surface. With the introduction of the microrough/nanorough implant, neck surface osseointegration has been seen along the entire implant surface. [16]

Biologic width and crestal bone

Stability of the biologic width is chiefly dependent on the type of the implant (one piece versus two piece) and the crestal bone, which further influences the healthy peri-implant tissues and ultimately the long-term success of the implant therapy. Multiple theories have been put forward for the observed changes in the crestal bone height following the implant restoration: authors suggest that dental implants, when placed into function, lead to crestal bone remodeling as a result of the stress concentration at the coronal region of the implant. [18] Some authors are of the opinion that the post-restorative crestal bone remodeling is a result of the localized inflammation within the tissues located at the implant abutment interface in the process of forming the biologic width. [19] Based on these theories, it was suggested that as long as the soft tissue covering the implant remains closed (sealed) during healing, crestal bone remodeling does not occur and the crestal height is maintained at the pre-surgical levels. On second surgical exposure or the implant getting prematurely exposed, the crestal bone begins the remodeling to approximately lie at the first thread 1.5-2 mm apical to the IAJ. The one-stage surgical technique exposes the IAJ to the oral environment following the implant placement and abutment connection, and hence the bone remodeling begins immediately. Biologic width formation takes place since the time of placement of the implants. [20]

Biologic width and surgical technique of implant placement (Submerged/non-submerged implant)

The stability of the biologic width depends on the technique of implant placement, i.e. submerged (two piece) or non-submerged (one piece). Amongst the one piece or two piece implant a one-piece non-submerged implant or two-stage implant with single-stage non-submerged protocol is more predictable than the submerged technique owing to its added advantages i.e - lack of the interface/microgap, lack of a second surgical procedure to connect a transgingival component to the top of the implant, a more mature soft tissue healing due to lack of the second stage surgery, and a small crown to root ratio for one-piece designed non-submerged implants. [21] The fact that one-stage implants have no implant abutment interface leads to less bone remodeling, hence a stable biologic width. This phenomenon is not related to loading and will occur whether the implant is loaded or unloaded. [22]

Factors affecting the crestal bone loss [5]

Biologic width/seal

Biologic width forms within the first 6 weeks after the implant/abutment junction has been exposed to the oral cavity. It is a barrier against bacterial invasion and food ingress at the implant-tissue interface. The ultimate location of epithelial attachment following stage 2 surgery in part determines early post-surgical bone loss. Thus, implant bone loss is in part a process of establishing the biologic seal.

Surgical trauma

Surgical trauma due to heat generated during drilling elevation of the periosteal flap and excessive pressure at the crestal region during implant placement may contribute to implant bone loss during the healing period. Wildermann et al. [23] reported that bone loss due to periosteal elevation was restricted to the area just adjacent to the implant, even though a larger surface area of the bone was exposed during surgery. Early implant bone loss is in the form of horizontal saucerization. However, bone loss after osseous surgery in natural teeth is more vertical. Signs of bone loss from surgical trauma and periosteal reflection are not commonly observed at the implant stage 2 surgery in successfully osseointegrated implants. Thus, surgical trauma is unlikely to cause early crestal bone loss.


In most of the two-stage implant systems, after abutment is connected, a microgap exists between the implant and the abutment at or below the alveolar crest. For all two-stage implants, the crestal bone levels are dependent upon the location of the microgap ~2 mm below it. The countersinking below the crest is done to minimize the risk of implant interface movement during bone remodeling, to prevent implant exposure during healing, and also to enhance the emergence profile. Countersinking places the implant microgap below the crestal bone. The microgap-crestal bone level relationship was studied radiographically by Hermann et al., [17],[24] who for the first time, demonstrated that the microgap between the implant/abutment has a direct effect on crestal bone loss, independent of surgical approaches. Epithelial proliferation to establish biologic width could be responsible for crestal bone loss found about 2 mm below the microgap.

Occlusal overload

Excessive stress on the immature implant-bone interface in the early stage of prosthesis in function is likely to cause crestal bone loss. Cortical bone is least resistant to shear force, which is significantly increased in bending overload. However, bone loss from occlusal overload is considered to be progressive rather than limited to the first year of loading.

Crest module

The transosteal region of the implant receives crestal stresses after loading. The crest module design can transmit different types of forces onto the bone, which depends upon its surface texture and shape. A polished collar and a straight crest module design transmit shear force, whereas a rough surface with an angled collar transmits beneficial compressive force to the bone.

Evidence-based review of the biologic width around implants

Important gray areas of concern

What is the structure of the biologic width around implants?What is the function of the biologic width?What is the influence of the mucosal thickness on the biologic width?Does abutment connection/disconnection have influence on biologic width?What is the effect of macrostructure of the neck of the implant?

Structure of biologic width around implant

Glauser et al. [25] in their study on one-piece mini implants calculated the mean dimensions as 4-4.5 mm. Kan et al. [26] in a study on anterior implants after bone sounding on the specific sites calculated a mean dimension of 6.17 mm on mesial, 3.63 mm at midfacial, and 5.93 mm at distal sites of implants. Epithelium around two-piece implants was always located apical to the microgap. [27]

A biologic width dimension around two-piece implants is larger than that of one-piece implants and natural teeth. Presence of microgap and its location influences the marginal bone levels and the biologic width of the surrounding soft tissue. Hermann et al. [28] evaluated the changes over time and determined that the connective tissue around implants are more stable than the epithelial dimension, as evident around natural teeth. The biologic width did not vary significantly regardless of whether the implant was loaded (with restoration) for a short or long time. This suggests the formation of biologic width is a physiologic response in the oral cavity and is not dependent on the presence or absence of loading or the length of loading time. Connective tissue dimensions being more stable around one-piece implants and natural teeth relates to the fact that once formed, they are predominated by protein collagen, and as collagen matures, more cross-linkages occur which stabilize this tissue and make it more resistant to dimensional change over time. Junctional epithelium, however, is constantly being challenged by microbial growth and pathologic microbial products. Biologic width once invaded around the implant undergoes similar structural and histologic changes as evident around the tooth, independent of tissue biotype (thick/thin).

Function of biologic width

Biologic width serves as protective mechanism for underlying bone. The function of junctional epithelium was investigated by Sanz [29] in a comparative histologic study of healthy and infected implant sites, revealing high transmigration of inflammatory cells in sulcular epithelium of infected sites. A case control study showed significant increase of T-lymphocytes in sulcular epithelium in peri-implantitis human biopsies when compared with healthy peri-implant tissue. [30] Chavrier in his histologic biopsy study on the connective tissue around implants revealed predominance of type 1 collagen fiber. [31]

Some animal studies revealed migration of leukocytes through junctional epithelium toward bacterial plaque. Accumulation of these cells in the presence of infection may demonstrate the possible defense mechanism of biologic width. [32] The evidence of protective peri-implant seal abilities may be found in the peri-implantitis models in animal studies which confirm that combination of plaque accumulation and biologic width injury can result in crestal bone loss around implants. [33]

Effect of mucosal thickness on biologic width around implants

It has been hypothesized that a certain width of peri-implant mucosa is required to enable a proper epithelial-connective tissue seal, and if this tissue dimension is not satisfied, bone resorption might occur. Albrektsson [34] noticed that implant sites with thin tissues were more prone to form angular defects. Clinically, thin tissues can be expected if thin gingival biotype is present. Tissue thickness is vital for the marginal bone integrity. [35] Thin biotype leads to poor papilla fill and buccal recession. [35]

Abutment disconnection and connection and its effect on the stability of biologic width

Abrahamson in his histologic study in animals suggested that healing abutment disconnection as a part of the prosthetic treatment results in disruption of epithelial seal, causing bleeding and ulceration of the site. This mechanical disruption of the site may result in inflammatory responses. The re-establishment of the biologic width in more apical position may be the explanation of crestal bone loss. [14]

However, a retrospective 3-year clinical study suggested no evidence of any adverse outcomes on the implant stability results in terms of the crestal bone loss following shift from the healing abutment to prosthetic analog. Small and Tarnow [36] revealed a vestibular recession at the end of 3 months in 80% cases, the average being 1mm after a year. Bengazi [37] observed a greater recession in cases where there was keratinized tissue.

Macrostructure of the neck of the implant

Use of retention elements like microthreads favors the biomechanical adaptation to the functional loads due to which the forces of shear are transmitted into forces of compression, stimulating in this manner the surrounding bone, and reducing the bone resorption by the formation of biologic width. [38]

The IAJ (implant abutment junction)

The microgap

This is the joint/gap between the implant and abutment in two-piece implant. Here, the junctional epithelium extends to the implant abutment interface (or even slightly below that level) and connective tissue borders the implant collar. This gap permits microleakage of fluids containing small molecules in the range of disaccharides and short peptides that contain bacterial by products or nutrients required for bacterial growth - better known as abutment inflammatory cell infiltrate. [39] This results in horizontal and vertical bone resorption within 1.5-2 mm. [40] This phenomenon could explain the typical saucerization, which is possibly the cause of bone loss due to mechanical stress exerted by the implant body at the alveolar crestal level. Currently, the causes of the crestal bone loss, apart from the mechanical stress, are also attributed to lack of space for biologic width and existence of microgap at the alveolar crest level.

The histology of peri-implant tissues was studied by Ericsson et al. [19] who identified two important entities in the implant crestal region, viz., plaque associated inflammatory cell infiltrate (PaICT) and implant associated inflammatory cell infiltrate (IaICT). They observed that the peri-implant bone crest was consistently located 1.0-1.5 mm apical to IAJ. The apical border of an ICT was always separated from the bone crest at ~1.0 mm of healthy connective tissue. Thus, they concluded that IaICT is the etiological factor for crestal bone loss.

"Platform switching - The concept"

The discovery of this concept lies in the simple fact of horizontally repositioning the biologic width by using undersized diameter of prosthetic component in relation to the implant diameter in order to limit peri-implant bone resorption. Studies have shown that a minimum thickness of 3 mm of soft tissue is required to allow the formation of biologic seal. Berglundh et al. [41] observed in the histologic section of the crestal bone and soft tissue that crestal bone is always separated from the base of the abutment ICT by 1-mm-wide zone of healthy connective tissue. Wennstrom [42] in a 5-year clinical study reported a marginal bone loss of 0.06 mm after the first year of load. The consequences of horizontal repositioning lead to creation of increased surface area and reduce the amount of the crestal bone resorption. This in turn maximizes the surface area desired for the soft tissue to attach. Repositioning of the IAJ inward and away from the outer edge of the implant and adjacent bone leads to reduction in the resorptive effect of the abutment ICT on crestal bone. [43]

Platform switching repositions the abutment ICT further away from the crestal bone and locates inflammatory infiltrate within an approximate <90° confined area of exposure instead of 180° of direct exposure to the surrounding hard and soft tissues.

Other clinical benefits

Optimal management of prosthetic space: A good amount of restorative volume is available for an optimally contoured restoration. With the crestal bone preserved both horizontally and vertically, support is thus retained for the papilla.

Improved bone support for short implants: Bone remodeling around a platform-switched implant is minimized, therefore there is potentially greater bone-implant contact for short implants. In order to benefit from the platform switching technique, reduced diameter components, beginning with healing abutments, must be used from the moment the implant is exposed to the oral environment because the process of biologic width formation begins immediately following exposure to the oral environment.

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. [44] 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. [45] 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 response to loading.

In other words, the bone is adapting to changes in load following prosthetic restoration. The question that needs to be addressed 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, esthetics and function. The loss of seemingly small amounts of bone and soft tissue can have important implications on esthetics of implant-borne restorations, which are reliant on healthy and vertically constant bony supported soft tissue dimensions over time.

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 biologic seal dependent on the tight contact between the epithelium and adjacent connective tissue with the implant surface.


Historically, several clinical studies have documented on the high success rate of the end osseous implant therapy with the chief criteria of evaluating the bony integrity of the implant, with less reference to the dynamics of the soft tissue integration around. Schroeder reported on the non-submerged approach of the implant placement and described the soft tissue attachment/contact with the transgingival portion of the implant with its added benefits. [46] The design of the implant (one piece/two piece) and its clinical implications on the stability of the biologic width is the area of concern. Hermann et al. stated that the radiographic bone levels around the non-submerged one-piece implants do not significantly change over 6 months. [47] However a two piece submerged implant (with interface ) placed either in a nonsubmerged or submerged approach results in similar amount of bone loss. These studies do reveal that bone loss decreased as the interface was moved coronally and the bone loss increased with the more apical placement of the interface, suggesting that there appears to be the presence of the physiologic interaction to the presence of the interface, which leads to the dimensional changes of the biologic width. The possible reason for the reaction is the microbial contamination or micromovement of the interface between the implant and the abutment or the secondary implant components. [22]

Cochran [22] demonstrated the soft issue dimensions and the biologic width around the non-submerged one-piece implants. This study was in line with the previous reports on the soft tissues around the non-submerged, one-piece implants [48] and showed that an area of epithelial attachment with the implant surface occurs similar in morphology to that found around natural teeth. In addition, an area of the connective tissue contact was found between the apical extension of the junctional epithelium and alveolar bone comprising the first implant to bone contact. The dimensions of these tissues, the biologic width, for non-submerged one-piece implants were demonstrated to be similar to the dimensions of the same tissues described for natural teeth. [4],[9]

Hermann et al. evaluated the dimensional changes in the soft tissue around the non-submerged one-piece implants over a period of 15 months with a loaded and non-loaded period to reveal a significant finding that the biologic width did not change in the evaluation period despite the scheduled mechanical and chemical oral hygiene procedures, however, the soft tissue compartment did undergo significant changes within. Non-submerged one-piece implants do exhibit physiologically stable peri-implant tissues. [20]

Experimental studies have demonstrated that a minimum width of the peri-implant mucosa is required. If the thickness of the peri-implant mucosa is reduced, bone resorption occurs to re-establish the mucosal dimension that was required for protection of the underlying tissues. [49] This physiological dimension has been found to be similar in loaded and unloaded conditions. [20],[22] Peri-implant soft tissue mucosa is not influenced by the conventional or immediate functional loading. [50] In other studies, it was suggested that the one-piece implants had shorter soft tissue dimensions than the two-piece implants. [28] Healing after different surgical procedures has also been evaluated. It was reported that similar soft tissue dimensions were established using a submerged or a non-submerged technique, [21],[28],[48] but a long epithelial attachment was reported with the submerged implant. [51]

Several methods have been explored to preserve the crestal bone and stability of the biologic width, and hence maintaining the soft tissue integrity around the implants, e.g. use of non-submerged/one-piece implant and tapered abutment connection and platform switching. Hermann et al. [16] reviewed biologic width, platform switch, implant design in the cervical area, nanoroughness, fine threads, abutment design, and avoidance of microlesions in the peri-implant soft tissues as the factors that determine the preservation of the crestal bone levels. They stated that these factors along with the several other factors determine the esthetic outcomes of the implant restoration.

Vela Nobot et al. concluded that the platform switching improves the esthetic results and that when invasion of the biologic width is reduced, bone loss is reduced. [52] Lazzara in his pioneering study on the platform switch reported that wider implants with reduced diameter abutments improved crestal bone preservation. [43] Degidi et al. evaluated the histology and histomorphology of three platform-switched morse taper connection implants and reported a zero microgap and no micromovement. Results also revealed no resorption and enhanced esthetic results. [53] Bone remodeling is encountered during the first year of the final restoration with platform switching implants, yet enough data still need to be available to confirm the results. [54] Position of the implant abutment interface (microgap) with respect to the crestal bone affects the vertical dimension of biologic width, i.e. deeper the implant is placed, the longer is the biologic dimension formed. [28]


The concept of the biologic width forms the basis of the successful peri-implant soft tissue integration around the implant. The present analysis of the knowledge about the biologic width around implants is definitely evidence based; however, the revealing results are derived more from the animal studies. Controlled human clinical studies are deficient. Hence, future human clinical trials are recommended.


1Fienne JS, Carlsson JE. Mandibular two implant overdenture dentures as first choice standard of care for edentulous patients Int J Oral Maxillofac Implants 2002;17:601-2.
2Branemark PI, Adell R. Intraosseous anchorage of dental prosthesis Scand J Plast Reconstr Surg 1969;3:81-100.
3Schroeder A, van der Zypen E. Reactions of bone, connective tissue, and epithelium to endosteal implants with titanium sprayed surfaces J Maxillofac Surg 1981;9:15-25.
4Gargiulo AW, Wentz FM, Orban B. Dimensions and relations of the dentogingival junction in humans J Periodontol 1961;32:261-67.
5Oh TJ, Yoon J, Misch CE, Wang HL. The causes of early implant bone loss: Myth or science? J Periodontol 2002;73:322-33.
6Listgarten MA, Lang N. Periodontal tissues and their counterparts around endoosseous implants Clin Oral Implants Res 1991;2:1-19.
7Myshin HL, Weins JP. Factors affecting soft tissue around dental implants J Prosthet Dent 2005;94:440-44.
8Weber HP, Cochran LD. The soft tissue response to osseointegrated dental implants J Prosthet Dent 1998;79:79-89.
9Vacek JS, Gehr ME. Dimensions of the human dentogingival junction Int J Periodontics Restorative Dent 1994;14:154-65.
10Tonetti MS, Sanz M. Consesus Report, Proceedings of the 3 RD European Workshop on Periodontology and implant dentistryBerlin: Quintessesce ;1999; 85-8.
11Berglundh T, Lindhe J. Soft tissue barrier at implants and teeth Clin Oral Implants Res 1991;2:81-90.
12Berglundh T, Lindhe J. The topography of the vascular system in the periodontal and periimplant tissues J Clin Periodontol 1994;21:189-93.
13Lekhom U, Adell R. Marginal tissue reactions at osseointegrated titanium fixtures Int J Oral Maxillofac Surg 1986;15:39-52.
14Abrahamson I, Lindhe J. The mucosal barrier following abutment dis/reconnection. An experimental study in dogs J Clin Periodontol 1997;24:568-72.
15Tarnow DP, Cho SC, Wallace SS. The effect of interimplant distance on the height of inter implant bone crest J Periodontol 2000;71:546-9.
16Hermann F, Lerner H. Factors influencing the preservation of the periimplant marginal bone Implant Dent 2007;16:165-75.
17Weber HP, Buser D. Radiographic evaluation of crestal bone levels adjacent to nonsubmerged titanium implants Clin Oral Implants Res 1992;3:181-8.
18Pillar RM, Deporter DA. Dental implant design: Effect on bone remodeling J Biomed Mater Res 1991;25:467-83.
19Ericsson J, Persson LG. Different types of implant associated reactions in periodontal soft tissues J Clin Periodontol 1995;22:255-61.
20Hermann JS, Cochran DL, Schenk RK. Biologic width around titanium implants-A physiologically formed and stable dimension over time Clin Oral Implant Res 2000;11:1-11.
21Buser D, Mericske-Stern R, Dula K, Lang NP. Clinical experience with one stage, nonsubmerged dental implants. Adv Dent Res1999;13: 153-61,
22Cochran DL, Hermann JS, Schenk RK. Biologic width around titanium implants. A histometric analysis of the implantogingival junctionaround loaded & unloaded implants J Periodontol 1997;68:186-98.
23Wildermann MN, Wentz FN. Histogenesis of repair after osseous surgery J Periodontol 1970;41:551-65.
24Hermann J, Buser D, Schenk RK, Schoolfield JD. Influence of the size of the microgap on crestal bone changes around titanium implants. A histometric evaluation of unloaded non-submerged implants in canine mandible J Periodontol 2001;72:1372-83.
25Glauser R, Schunbach P. Perimplant soft tissue barrier at experimental one piece mini-implant-a light microscopic and histometric review Clin Implant Dent Relat Res 2005;7:S44-51.
26Kan JY. Dimensions of the periimplant mucosa J Periodontol 2003;74:557-62.
27Weber HP, Cochran DL. Soft tissue response to osseointegrated implants. J Prosthet Dent 1998;79:79-89.
28Hermann JS, Buser D. Biologic width around one and two piece titanium implants Clin Oral Implants Res 2001;12:559-71.
29Sanz M, Alandez J. Histo-pathologic characteristics of periimplant soft tissues in clinical and radiologic patterns Clin Oral Implants Res 1991;2:128-34.
30Bullon P, Fioroni M. Immunohistochemical analysis of soft tissues in implants in healthy and periimplantitis conditions Clin Oral Implants Res 2004;15:553-9.
31Chavrier CA, Couble ML. Ultrastructural immunohistochemical study of interstitial collagenous components of healthy human keratinized mucosa surrounding implants. Int J Oral Maxillofac Implants 1999;14:108-12.
32Kawahara H, Hashimoto K. Morpholologic studies on the biologic seal of titanium dental implants Int J Oral Maxillofac Implants 1998;13:465-73.
33Lindhe J. Experimental breakdown of periimplant and periodontal tissues Clin Oral Implants Res 1992;3:9-16.
34Albrektsson T, Zarb G, Worthington P, Eriksson AR. The long-term efficacy of currently used dental implants: A review and proposed criteria of success Int J Oral Maxillofac Implants 1986;1:11-25.
35Linkevicius T, Apse P, Grybauskas S, Puisys A. The influence of soft tissue thickness on crestal bone changes around implants: A 1-year prospective controlled clinical trial Int J Oral Maxillofac Implants 2009;24:712-9.
36Small PN, Tarnow DP. Gingival recession around implants Int J Oral Maxillofac Implants 2000;15:527-32.
37Bengazi F. Recession of soft tissue margins at oral implants Clin Oral Implant Res 1996;7:303-10.
38Abrahmsson I Berglundh T. Tissue characteristics at microthreaded implants Clin Implant Dent Relat Res 2006;8:107-13.
39Quirynen M, Bollen MC, Eyssen H, van Steenberghe D. Microbial penetration along the implant components of the Brånemark System- An in vitro study Clin Oral Implants Res 1994;5:239-44.
40Piattelli A, Vrespa G. Role of microgap between implant and abutment J Periodontol 2003;74:346-52.
41Berglundh TLindhe J. Morphogenesis of the periimplant mucosa Clin Oral Implant Res 2007;18:1-8.
42Wennstorm JL. Implant supported single tooth restoration: 5 year prospective study J Clin Periodontol 2005;32:567-74.
43Lazzara RJ, Porter SS. Platform switching: A new concept in implant dentistry Intl J Periodontics Restorative Dent 2006;26:9-17.
44Smith DE, Zarb GA. Criteria for success of osseointegrated endosseous implants - A review J Prosthet Dent 1989;62:567-72.
45Adell R. Clinical results of osseointegrated implants supporting fixed prostheses in edentulous jaws J Prosthet Dent 1983;50:251-4.
46Schroeder A. Reactions of the bone, connective tissue and epithelium to endosteal implants with titanium sprayed surfaces J Maxillofac Surg 1981;9:15-25.
47Hermann JS, Cochran DS. Crestal bone changes around titanium implants. A radiographic evaluation of the unloaded nonsubmerged and submerged implants in canine mandible J Periodontol 1997;68:1117-30.
48Buser D, Weber HP, Donath K, Fiorellini JP, Paquette DW. Soft tissue reactions to nonsubmerged unloaded titanium implants in beagle dogs J Periodontol 1992;63:225-35.
49Berglundh T, Lindhe J. Dimensions of the periimplant mucosa. Biologic width revisited. J Clin Periodontol 1996;23:971-3.
50Siar HC, Swaminathan D. Periimplant soft tissue integration of immediately loaded implants- A histomorphometric study J Periodontol 2003;74:571-8.
51Weber HP, Buser D. Comparison of healed tissues adjacent to submerged/nonsubmerged implants Clin Oral Implants Res 1996;7:11-9.
52Vela-Nobot X, Rodríguez-Ciurana X, Rodado-Alonso C, Segalà-Torres M. Benefits of an implant modification technique to reduce the crestal bone resorption Implant Dent 2006;15:313-20.
53Degidi M, Lezzi G. Immediately loaded titanium implant with a tissue stabilizing/maintaining design retrieved from a man after 4 weeks: Histological and histomorphometric evaluation.A case report Clin Oral Implants Res 2008;19:276-82.
54Hurzeler M, Fickl S. Periimplant bone level around implants with platform switched abutments: preliminary data from prospective study J Oral Maxillofac Surg 2007;65:33-9.