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Review Article 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

Address for correspondence: Dr. Sangeeta Dhir, E‑mail:

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.


(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
(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.

Key words: Biologic width, biologic width and dental implant, crestal bone loss, implant abutment junction,
peri‑implant soft tissue

INTRODUCTION was referred to as two‑piece implant.[2] The second

category was developed by Schroeder and was

T he use of dental implants to replace the missing

teeth is becoming a preferred alternative. With
the gained awareness and the improved quality of
referred to as one‑piece implant.[3]

Natural teeth are surrounded by gingival soft tissues

life, analyses indicate that patients perceive their that provide a biologic seal between the oral cavity
oral health status as improved by their experience and the inside of the body. This unique structure is
with dental implants.[1] Root form dental implants composed of epithelium and soft connective tissue that
comprises the most widely used form of treatment are continually bathed in a transudate called gingival
and it consists of two basic types. The first category fluid. The term biologic width was based on the work
was introduced and developed by Branemark and of Gargiulo et al. who described the dimensions of
dentogingival junction in human cadavers.[4] Average
Access this article online dimension counted was 2.04 mm comprising
Quick Response Code: supraalveolar connective tissue and junctional
Website: 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

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around implants has also been investigated. Multiple

Table 1: Differences between the peri-implant mucosa
research groups have also verified that biologic width also
and gingiva
exists around implants.[6‑8] This is true for implants of all
Features Tooth Implant
shapes after the implant uncovery stage (stage 2).
Clinical characteristics
Biologic width Supracrestal Subcrestal
In the most simplified form, biologic width refers to the Probing depth Normal = 2–3 mm Increased ≥4 mm
height of the dentogingival attachment apparatus around Bleeding on Reliable inflammatory sign Less reliable as bleeding
a normal tooth and is defined as the distance necessary probing is unrelated to the amount
of inflammation in the
for a healthy existence of bone and soft tissue from the peri-implant tissue[13]
apical extent of the dental restoration. In a more clinical Tissue quality
sense, there must not be any encroachment within 2 mm CT composition Low collagen and high High collagen and low
of the bone that surrounds the tooth. fibroblast fibroblast
Vascular supply Increased (supraperiosteal, Less (supraperiosteal only)
vascular plexus of PDL)
Vacek et al. reported in their study the revised range of
Hard tissue Resilient connection Rigid connection
this zone as 0.75–4.33 mm. It was observed that of all interface
the tissue dimensions measured, the length of connective Bone–periodontal Osseointegration,
ligament–cementum periodontal ligament and
tissue attachment varied the least. connection cementum absent
Others Periodontal ligament can No adaptive capacity and
The proceedings of the 3 rd European workshop on allow tooth movements no movements possible
with its adaptive capacity
periodontology and implant dentistry state that the
Soft tissue interface
function of peri‑implant seal is “to maintain homeostasis Connective tissue Perpendicular insertion Collagen fibers parallel to
of the internal environment in response to challenges from fibers into cementum the tooth surface
the external environment.”[10] Junctional Originates from the Originates from the
epithelium reduced enamel adjacent oral epithelium
PDL= Periodontal ligament
Electronic search of the Medline was done with the interface of natural teeth. These relationships depend
search words. The key words used for the search were: on the cervical design of the implant, location of the
biologic width, peri‑implant soft tissue, crestal bone loss, implant components relative to the crestal bone,
platform switch, biologic width and dental implant, implant implant abutment junction (IAJ), insertion depth, surface
abutment junction. Additionally, a manual search of the technology of the implant, and the soft and hard tissue
major dental implant, prosthetic, and periodontal journals dimensions. Bone remodeling around the implant
and books was performed. The following journals were continues until the biologic width is formed around the
searched: Clinical Oral Implant Research, Implant Dentistry, implant and is stabilized thereafter. The biologic rationale
International Journal of Oral and Maxillofacial Implants, behind the biologic width formation lies in the fact that
Clinical Implant Related Research, Journal of Prosthetic bone when exposed to the oral cavity is always covered
Dentistry, Journal of Periodontology, Journal of Biomedical with periosteum, connective tissue, and epithelium.
Research, Journal of Clinical Periodontology. The articles In the presence of the chronic irritation, e.g. bacteria
included in the review comprised in vitro studies, in vivo accessing the implant abutment interface, or when the
(animal and human) studies, abstracts, and review articles. abutment is removed during two‑stage implants after the
initial healing phase for prosthesis fabrication, the bone
Biology of peri‑implant mucosa starts resorbing to create a distance from this chronically
exposed/irritated area.[14] There exists a vertical and
There exists a significant difference between the tissues horizontal component of biologic width as it forms and
surrounding the natural tooth and the peri‑implant remodels itself around the implant. It is important to
mucosa. The mucosa that encircles the implant has maintain a minimum distance of 3 mm between the two
more of collagen and fewer fibroblasts as opposed to implants for a stable interimplant bone and soft tissue
gingival tissues. The collagen fiber bundles run parallel with a stable biologic width.[15]
to the titanium surface without attaching to it versus
the perpendicular direction around the tooth.[11] The The smooth polished collar of the conventional implant
supracrestal vascular topography surrounding the fixture and their relative insertion depth have revealed a varying
is reduced and diversely arranged[11,12] [Table 1]. biologic width.[16] Literature has reported the evidence of
biologic width of 3.6 mm and 4.1 mm in the mandible
Bone and implant junction
and maxillary implant, respectively, in the ITI (International
The healed bone and soft tissues around the implant and Team of Implantology )implants with a polished cervical
tooth are similar but do differ from the dentogingival collar placed at the crest of the bone.[17] In the event

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of the smooth collar being placed subcrestally, it leads Factors affecting the crestal bone loss[5]
to the bone being resorbed to the transition level of
the smooth and rough surface. With the introduction Biologic width/seal
of the microrough/nanorough implant, neck surface Biologic width forms within the first 6 weeks after the
osseointegration has been seen along the entire implant implant/abutment junction has been exposed to the oral
surface.[16] cavity. It is a barrier against bacterial invasion and food
ingress at the implant–tissue interface. The ultimate location
Biologic width and crestal bone of epithelial attachment following stage 2 surgery in part
Stability of the biologic width is chiefly dependent on determines early post‑surgical bone loss. Thus, implant
the type of the implant (one piece versus two piece) and bone loss is in part a process of establishing the biologic seal.
the crestal bone, which further influences the healthy
peri‑implant tissues and ultimately the long‑term success Surgical trauma
of the implant therapy. Multiple theories have been put Surgical trauma due to heat generated during drilling
forward for the observed changes in the crestal bone height elevation of the periosteal flap and excessive pressure at
following the implant restoration: authors suggest that the crestal region during implant placement may contribute
dental implants, when placed into function, lead to crestal to implant bone loss during the healing period. Wildermann
bone remodeling as a result of the stress concentration at et al.[23] reported that bone loss due to periosteal elevation
the coronal region of the implant.[18] Some authors are of the was restricted to the area just adjacent to the implant, even
opinion that the post‑restorative crestal bone remodeling though a larger surface area of the bone was exposed
is a result of the localized inflammation within the tissues during surgery. Early implant bone loss is in the form of
located at the implant abutment interface in the process horizontal saucerization. However, bone loss after osseous
of forming the biologic width.[19] Based on these theories, surgery in natural teeth is more vertical. Signs of bone
it was suggested that as long as the soft tissue covering loss from surgical trauma and periosteal reflection are
the implant remains closed (sealed) during healing, crestal not commonly observed at the implant stage 2 surgery
bone remodeling does not occur and the crestal height is in successfully osseointegrated implants. Thus, surgical
maintained at the pre‑surgical levels. On second surgical trauma is unlikely to cause early crestal bone loss.
exposure or the implant getting prematurely exposed, the
crestal bone begins the remodeling to approximately lie at Microgap
the first thread 1.5–2 mm apical to the IAJ. The one‑stage
surgical technique exposes the IAJ to the oral environment In most of the two‑stage implant systems, after abutment
following the implant placement and abutment connection, is connected, a microgap exists between the implant
and hence the bone remodeling begins immediately. and the abutment at or below the alveolar crest. For all
Biologic width formation takes place since the time of two‑stage implants, the crestal bone levels are dependent
placement of the implants.[20] upon the location of the microgap ~2 mm below it. The
countersinking below the crest is done to minimize the risk
Biologic width and surgical technique of implant interface movement during bone remodeling,
of implant placement (Submerged/non- to prevent implant exposure during healing, and also to
submerged implant) enhance the emergence profile. Countersinking places the
implant microgap below the crestal bone. The microgap–
The stability of the biologic width depends on the technique crestal bone level relationship was studied radiographically
of implant placement, i.e. submerged (two piece) or by Hermann et al.,[17,24] who for the first time, demonstrated
non‑submerged (one piece). Amongst the one piece or that the microgap between the implant/abutment has a
two piece implant a one‑piece non‑submerged implant direct effect on crestal bone loss, independent of surgical
or two‑stage implant with single‑stage non‑submerged approaches. Epithelial proliferation to establish biologic
protocol is more predictable than the submerged width could be responsible for crestal bone loss found
technique owing to its added advantages i.e – lack of the
about 2 mm below the microgap.
interface/microgap, lack of a second surgical procedure
to connect a transgingival component to the top of the
Occlusal overload
implant, a more mature soft tissue healing due to lack of
the second stage surgery, and a small crown to root ratio Excessive stress on the immature implant–bone interface
for one‑piece designed non‑submerged implants.[21] The in the early stage of prosthesis in function is likely to
fact that one‑stage implants have no implant abutment cause crestal bone loss. Cortical bone is least resistant to
interface leads to less bone remodeling, hence a stable shear force, which is significantly increased in bending
biologic width. This phenomenon is not related to overload. However, bone loss from occlusal overload is
loading and will occur whether the implant is loaded or considered to be progressive rather than limited to the
unloaded.[22] first year of loading.

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Crest module changes as evident around the tooth, independent of

tissue biotype (thick/thin).
The transosteal region of the implant receives crestal
stresses after loading. The crest module design can Function of biologic width
transmit different types of forces onto the bone, which
depends upon its surface texture and shape. A polished Biologic width serves as protective mechanism for
collar and a straight crest module design transmit shear underlying bone. The function of junctional epithelium
force, whereas a rough surface with an angled collar was investigated by Sanz[29] in a comparative histologic
transmits beneficial compressive force to the bone. study of healthy and infected implant sites, revealing
high transmigration of inflammatory cells in sulcular
Evidence‑based review of the biologic width epithelium of infected sites. A case control study showed
around implants significant increase of T‑lymphocytes in sulcular epithelium
in peri‑implantitis human biopsies when compared with
Important gray areas of concern healthy peri‑implant tissue.[30] Chavrier in his histologic
• What is the structure of the biologic width around biopsy study on the connective tissue around implants
implants? revealed predominance of type 1 collagen fiber.[31]
• What is the function of the biologic width?
• What is the influence of the mucosal thickness on the Some animal studies revealed migration of leukocytes
biologic width? through junctional epithelium toward bacterial plaque.
• Does abutment connection/disconnection have Accumulation of these cells in the presence of infection
influence on biologic width? may demonstrate the possible defense mechanism of
• What is the effect of macrostructure of the neck of the biologic width.[32] The evidence of protective peri‑implant
implant? seal abilities may be found in the peri‑implantitis models in
animal studies which confirm that combination of plaque
Structure of biologic width around implant accumulation and biologic width injury can result in crestal
bone loss around implants.[33]
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] Effect of mucosal thickness on biologic width
in a study on anterior implants after bone sounding on the around implants
specific sites calculated a mean dimension of 6.17 mm on
mesial, 3.63 mm at midfacial, and 5.93 mm at distal sites It has been hypothesized that a certain width of peri‑implant
of implants. Epithelium around two‑piece implants was mucosa is required to enable a proper epithelial–connective
always located apical to the microgap.[27] tissue seal, and if this tissue dimension is not satisfied,
bone resorption might occur. Albrektsson[34] noticed that
A biologic width dimension around two‑piece implants implant sites with thin tissues were more prone to form
is larger than that of one‑piece implants and natural angular defects. Clinically, thin tissues can be expected if
teeth. Presence of microgap and its location influences thin gingival biotype is present. Tissue thickness is vital for
the marginal bone levels and the biologic width of the the marginal bone integrity.[35] Thin biotype leads to poor
surrounding soft tissue. Hermann et al.[28]evaluated the papilla fill and buccal recession.[35]
changes over time and determined that the connective
tissue around implants are more stable than the epithelial Abutment disconnection and connection and its
dimension, as evident around natural teeth. The biologic effect on the stability of biologic width
width did not vary significantly regardless of whether Abrahamson in his histologic study in animals suggested
the implant was loaded (with restoration) for a short or that healing abutment disconnection as a part of the
long time. This suggests the formation of biologic width prosthetic treatment results in disruption of epithelial
is a physiologic response in the oral cavity and is not seal, causing bleeding and ulceration of the site.
dependent on the presence or absence of loading or the This mechanical disruption of the site may result in
length of loading time. Connective tissue dimensions inflammatory responses. The re‑establishment of the
being more stable around one‑piece implants and biologic width in more apical position may be the
natural teeth relates to the fact that once formed, they explanation of crestal bone loss.[14]
are predominated by protein collagen, and as collagen
matures, more cross‑linkages occur which stabilize this However, a retrospective 3‑year clinical study suggested
tissue and make it more resistant to dimensional change no evidence of any adverse outcomes on the implant
over time. Junctional epithelium, however, is constantly stability results in terms of the crestal bone loss following
being challenged by microbial growth and pathologic shift from the healing abutment to prosthetic analog. Small
microbial products. Biologic width once invaded around and Tarnow[36] revealed a vestibular recession at the end
the implant undergoes similar structural and histologic of 3 months in 80% cases, the average being 1mm after

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a year. Bengazi[37] observed a greater recession in cases a marginal bone loss of 0.06 mm after the first year
where there was keratinized tissue. of load. The consequences of horizontal repositioning
lead to creation of increased surface area and reduce
Macrostructure of the neck of the implant the amount of the crestal bone resorption. This in turn
Use of retention elements like microthreads favors the maximizes the surface area desired for the soft tissue to
biomechanical adaptation to the functional loads due to attach. Repositioning of the IAJ inward and away from
which the forces of shear are transmitted into forces of the outer edge of the implant and adjacent bone leads to
compression, stimulating in this manner the surrounding reduction in the resorptive effect of the abutment ICT on
bone, and reducing the bone resorption by the formation crestal bone.[43]
of biologic width.[38]
Platform switching repositions the abutment ICT further
The IAJ (implant abutment junction) away from the crestal bone and locates inflammatory
infiltrate within an approximate <90° confined area
The microgap of exposure instead of 180° of direct exposure to the
surrounding hard and soft tissues.
This is the joint/gap between the implant and abutment
in two‑piece implant. Here, the junctional epithelium
Other clinical benefits
extends to the implant abutment interface (or even slightly
below that level) and connective tissue borders the implant Optimal management of prosthetic space: A good
collar. This gap permits microleakage of fluids containing amount of restorative volume is available for an optimally
small molecules in the range of disaccharides and short contoured restoration. With the crestal bone preserved
peptides that contain bacterial by products or nutrients both horizontally and vertically, support is thus retained
required for bacterial growth – better known as abutment for the papilla.
inflammatory cell infiltrate.[39] This results in horizontal
and vertical bone resorption within 1.5–2 mm.[40] This Improved bone support for short implants: Bone
phenomenon could explain the typical saucerization, remodeling around a platform‑switched implant is
which is possibly the cause of bone loss due to mechanical minimized, therefore there is potentially greater bone–
stress exerted by the implant body at the alveolar crestal implant contact for short implants. In order to benefit
level. Currently, the causes of the crestal bone loss, apart from the platform switching technique, reduced diameter
from the mechanical stress, are also attributed to lack of components, beginning with healing abutments, must
space for biologic width and existence of microgap at the be used from the moment the implant is exposed to the
alveolar crest level. oral environment because the process of biologic width
formation begins immediately following exposure to the
The histology of peri‑implant tissues was studied by oral environment.
Ericsson et al.[19] who identified two important entities
in the implant crestal region, viz., plaque associated Criteria for implant success
inflammatory cell infiltrate (PaICT) and implant associated Part of the early generally accepted criteria for implant
inflammatory cell infiltrate (IaICT). They observed that success is that less than 0.2 mm of alveolar bone loss
the peri‑implant bone crest was consistently located occurs per year after the first year in function.[44] However,
1.0–1.5 mm apical to IAJ. The apical border of an ICT what is overlooked is that the success of implant therapy is
was always separated from the bone crest at ~1.0 mm of determined after the first year of service because most of
healthy connective tissue. Thus, they concluded that IaICT the bone loss occurs during the first 12 months following
is the etiological factor for crestal bone loss. abutment connection.[45] Therefore, the loss of 2.0 mm
of crestal bone over the first year has been considered a
“Platform switching – The concept”
normal characteristic of a healthy functioning implant and
The discovery of this concept lies in the simple fact of this change in bone height is merely due to remodeling
horizontally repositioning the biologic width by using in response to loading.
undersized diameter of prosthetic component in relation
to the implant diameter in order to limit peri‑implant In other words, the bone is adapting to changes in load
bone resorption. Studies have shown that a minimum following prosthetic restoration. The question that needs
thickness of 3 mm of soft tissue is required to allow the to be addressed is: Does this small amount of bone loss
formation of biologic seal. Berglundh et al.[41] observed in have any clinical significance and can it be considered
the histologic section of the crestal bone and soft tissue acceptable? Dental implants unlike implants employed in
that crestal bone is always separated from the base of the other areas of medicine have two roles to fulfill, esthetics
abutment ICT by 1‑mm‑wide zone of healthy connective and function. The loss of seemingly small amounts of
tissue. Wennstrom[42] in a 5‑year clinical study reported bone and soft tissue can have important implications on

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esthetics of implant‑borne restorations, which are reliant found between the apical extension of the junctional
on healthy and vertically constant bony supported soft epithelium and alveolar bone comprising the first implant
tissue dimensions over time. to bone contact. The dimensions of these tissues, the
biologic width, for non‑submerged one‑piece implants
In the natural dentition, the junctional epithelium provides were demonstrated to be similar to the dimensions of the
a seal at the base of the sulcus against bacterial penetration. same tissues described for natural teeth.[4,9]
The other line of defense present in the natural dentition
and absent in implants is the periodontal ligament. Since Hermann et al. evaluated the dimensional changes in
no cementum or fibers are present on the surface of an the soft tissue around the non‑submerged one‑piece
implant, infection has the potential to spread directly implants over a period of 15 months with a loaded and
into the osseous structures, resulting in bone loss and non‑loaded period to reveal a significant finding that the
ultimately implant failure. Thus, the maintenance of biologic width did not change in the evaluation period
osseointegration and long‑term success of implants despite the scheduled mechanical and chemical oral
depends on the presence of a leak‑proof peri‑implant soft hygiene procedures, however, the soft tissue compartment
tissue cuff. This requires the formation of a biologic seal did undergo significant changes within. Non‑submerged
dependent on the tight contact between the epithelium one‑piece implants do exhibit physiologically stable
and adjacent connective tissue with the implant surface. peri‑implant tissues.[20]

Experimental studies have demonstrated that a minimum

DISCUSSION width of the peri‑implant mucosa is required. If the
thickness of the peri‑implant mucosa is reduced, bone
Historically, several clinical studies have documented on resorption occurs to re‑establish the mucosal dimension
the high success rate of the end osseous implant therapy that was required for protection of the underlying
with the chief criteria of evaluating the bony integrity of tissues.[49] This physiological dimension has been found
the implant, with less reference to the dynamics of the to be similar in loaded and unloaded conditions.[20,22]
soft tissue integration around. Schroeder reported on Peri‑implant soft tissue mucosa is not influenced by
the non‑submerged approach of the implant placement the conventional or immediate functional loading. [50]
and described the soft tissue attachment/contact with In other studies, it was suggested that the one‑piece
the transgingival portion of the implant with its added implants had shorter soft tissue dimensions than the
benefits.[46] The design of the implant (one piece/two two‑piece implants.[28] Healing after different surgical
piece) and its clinical implications on the stability of the procedures has also been evaluated. It was reported that
biologic width is the area of concern. Hermann et al. similar soft tissue dimensions were established using
stated that the radiographic bone levels around the a submerged or a non‑submerged technique, [21,28,48]
non‑submerged one‑piece implants do not significantly but a long epithelial attachment was reported with the
change over 6 months. [47] However a two piece submerged implant.[51]
submerged implant (with interface ) placed either in a
nonsubmerged or submerged approach results in similar Several methods have been explored to preserve the
amount of bone loss. These studies do reveal that bone crestal bone and stability of the biologic width, and
loss decreased as the interface was moved coronally and hence maintaining the soft tissue integrity around
the bone loss increased with the more apical placement the implants, e.g. use of non‑submerged/one‑piece
of the interface, suggesting that there appears to be the implant and tapered abutment connection and platform
presence of the physiologic interaction to the presence switching. Hermann et al.[16] reviewed biologic width,
of the interface, which leads to the dimensional changes platform switch, implant design in the cervical area,
of the biologic width. The possible reason for the reaction nanoroughness, fine threads, abutment design, and
is the microbial contamination or micromovement of the avoidance of microlesions in the peri‑implant soft tissues
interface between the implant and the abutment or the as the factors that determine the preservation of the
secondary implant components.[22] crestal bone levels. They stated that these factors along
with the several other factors determine the esthetic
Cochran[22] demonstrated the soft issue dimensions and outcomes of the implant restoration.
the biologic width around the non‑submerged one‑piece
implants. This study was in line with the previous Vela Nobot et al. concluded that the platform switching
reports on the soft tissues around the non‑submerged, improves the esthetic results and that when invasion of
one‑piece implants [48] and showed that an area of the biologic width is reduced, bone loss is reduced.[52]
epithelial attachment with the implant surface occurs Lazzara in his pioneering study on the platform switch
similar in morphology to that found around natural teeth. reported that wider implants with reduced diameter
In addition, an area of the connective tissue contact was abutments improved crestal bone preservation.[43] Degidi

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23. Wildermann MN, Wentz FN. Histogenesis of repair after osseous
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reactions to nonsubmerged unloaded titanium implants in beagle Source of Support: Nil, Conflict of Interest: None declared.

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