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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: sangeeta_dhir@hotmail.com

ABSTRACT
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.

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
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
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DOI:
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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

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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
[9]
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
epithelium
PDL= Periodontal ligament
MATERIALS AND METHODS
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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Dhir: Biologic width and dental implants
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]
86
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.
Microgap
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.
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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
Journal of Interdisciplinary Dentistry / May-Aug 2012 / Vol-2 / Issue-2
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
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Dhir: Biologic width and dental implants
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
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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
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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.
DISCUSSION
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
Journal of Interdisciplinary Dentistry / May-Aug 2012 / Vol-2 / Issue-2
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
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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]
CONCLUSION
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.
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How to cite this article: Dhir S. Significance and clinical relevance of biologic
width to implant dentistry. J Interdiscip Dentistry 2012;2:84-91.
Source of Support: Nil, Conflict of Interest: None declared.

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