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245
Histologic Evidence of a Connective

Tissue Attachment to Laser
Microgrooved Abutments:
A Canine Study
Myron Nevins, DDS1/David M. Kim, DDS, DMSc2 The preservation of stable relation-
Sang-Ho Jun, DDS, MS3/Kevin Guze, DMD4 ships between overlying soft tissues
Peter Schupbach, PhD5/Marc L. Nevins, DMD, MMSc6 and the underlying supporting crestal
bone is critical for optimal form and
function in implant-supported resto-
Previous research has demonstrated the effectiveness of laser-ablated
rations. Such morphologic stability
microgrooves placed on implant collars to support direct connective tissue attach- is particularly important in the anterior
ments to altered implant surfaces. Such a direct connective tissue attachment esthetic zone of the maxilla, where
serves as a physiologic barrier to the apical migration of the junctional epithelium the anatomical integrity of esthetically
and prevents crestal bone resorption. The current prospective preclinical trial critical marginal and papillary tissues
sought to evaluate bone and soft tissue healing patterns when laser-ablated is intimately dependent on stable
microgrooves were placed on the abutment. A canine model was selected for crestal bone levels. Unfortunately, loss
comparison to previous investigations that examined the negative bone and soft of crestal bone, or “dieback,” to the
tissue sequelae of the implant-abutment microgap. The results demonstrate sig- first coronal implant thread is com-
nificant improvement in peri-implant hard and soft tissue healing compared to monly observed following abutment
traditional machined abutment surfaces. (Int J Periodontics Restorative Dent
attachment, resulting in an average
2010;30:245–255.)
of 1.5 to 2.0 mm of bone loss after the
first year in function, often followed by
an ongoing 0.1-mm loss each year
thereafter.1–7
1Associate Clinical Professor, Division of Periodontology, Department of Oral Medicine, The relationship between the
Infection and Immunity, Harvard School of Dental Medicine, Boston, Massachusetts.
2Assistant Professor, Division of Periodontology, Department of Oral Medicine, Infection and implant-abutment junction (IAJ) and
Immunity, Harvard School of Dental Medicine, Boston, Massachusetts. implant-related crestal bone loss has
3Research Fellow, Department of Plastic and Oral Surgery, Children’s Hospital Boston,
received increased attention and
Boston, Massachusetts. concern.1,4,8–11 Preclinical trials using a
4Research Fellow, Division of Periodontology, Department of Oral Medicine, Infection and
Immunity, Harvard School of Dental Medicine, Boston, Massachusetts.

canine model have confirmed a 3-mm
5PSchupbach Histology, Research Laboratory, Biomaterials, Horgen, Switzerland. dimension of the peri-implant soft
6Assistant Clinical Professor, Division of Periodontology, Department of Oral Medicine,
tissues.1–4 The microgap created at
Infection and Immunity, Harvard School of Dental Medicine, Boston, Massachusetts.
the IAJ consistently resulted in an
Correspondence to: Dr Myron Nevins, Harvard School of Dental Medicine, 188 Longwood inflammatory infiltrate that drove the
Avenue, Boston, Massachusetts 02115; email: [email protected]. healthy peri-implant connective
Volume 30, Number 3, 2010
246
tissue component apically, resulting attachments occurring at the micro-

in at least 1.5 to 2 mm of crestal grooved abutment surface during
bone loss.1,12 healing through histologic, micro–
Preclinical and clinical studies have computed tomographic (micro-CT),
been conducted to reduce or mini- and scanning electron microscopic
mize crestal dieback by examining the (SEM) analyses.
role that microchannels, with defined
three-dimensional shapes and depths,
might play in controlling fibroblastic Method and materials
and osteoblastic behavior by limiting
the apical migration of the junctional The current study, which was approved
epithelium.13,14 The significant results under the Institutional Animal Care
of a prospective proof-of-principle and Use Committee protocol, was
human histologic study demonstrated designed to examine the effects of
direct connective tissue attachment to two different implant and abutment
precisely generated Laser-Lok micro- surfaces on epithelial and connective
grooves on the implant collar.15 This tissue attachment, as well as peri-
raises the question of whether similar implant bone levels. The sites were
results would occur if configured laser- randomly assigned to receive tapered
ablated microgrooves were placed on internal implants (BioHorizons) with
the abutment surface. Such an altered either resorbable blast texturing (RBT)
surface, unlike traditional machined- or RBT with a 0.3-mm machined col-
surface abutments, might provide lar (Fig 1a). Each implant was 3.8 mm
improved opportunities for a direct in diameter and 9.0 mm in length. In
fibrocollagenous attachment and thus addition, either machined-surface or
potentially limit the apical epithelial Laser-Lok 8-µm microchannel healing
migration that is common in more tra- abutments were assigned randomly
ditional abutment-implant complexes. to each implant, with the Laser-Lok
In addition, direct connective tissue microchannels applied to a 0.7-mm-
attachment to the abutment surface tall band located immediately coro-
may potentially mitigate or altogether nal to the IAJ or microgap (Fig 1b). The
eliminate the negative sequelae sec- width of the band evaluated was the
ondary to microbial leakage from the same dimension as the portion of the
IAJ microgap, thereby reducing the band on the Laser-Lok implant that
potential for peri-implant crestal bone comes into contact with the soft tissue.
loss. The abutments were placed at the
The purpose of the current pre- time of surgery.
clinical proof-of-principle study was to Six foxhounds, each weighing at
determine whether precisely config- least 25 kg, were selected for this
ured Laser-Lok microgrooves placed study. Each dog received 6 implants in
within a defined healing abutment the bilateral mandibular premolar and
region prevent or reduce crestal bone first molar extraction sites, for a total of
loss when compared to a machined 36 implants for six dogs. Figure 2
abutment, and to determine the tissue describes the four cohorts (groups A,
247
Fig 1a (left) Resorbable blast texturing

(RBT) implant with a 0.3-mm machined 0.3-mm
collar (left) and an RBT implant without the machined
machined collar (right). collar
Fully
0.7-mm machined
Fig 1b (right) Healing abutment with a RBT Laser-Lok
0.7-mm Laser-Lok microgrooved zone (left) zone
and fully machined abutment without the
laser-ablated microgrooves (right).
Fig 2 (right) The four cohorts. LL = Laser-Lok;

RBT = resorbable blast texturing;
M = machined surface.
M M
Soft tissue LL LL
Bone M M
RBT RBT RBT RBT
Group A: Group B: Group C: Group D:

Laser-Lok Laser-Lok Machined Machined
healing healing healing healing
abutment on an abutment on an abutment on an abutment on an
RBT implant RBT implant with RBT implant RBT implant with
a machined area a machined area
B, C, and D) included in this study. Each foxhound received 1 g of each animal according to a random-
Each group received 9 implants. cefazolin (Apotex), intravascularly or ized distribution pattern generated
intramuscularly, every 3 days for the prior to surgery. No two adjacent
first week postoperative. Postoperative implants were of the same type.
Surgical extraction phase pain was managed with 0.3 mg of Implant osteotomies were performed
buprenorphine HCl (Reckitt Benckiser with torque-reducing rotary instru-
Full-thickness flaps were reflected Healthcare) intramuscularly once every ments at 500 rpm using a sterile saline
under 10 to 12 mL of thiopental 12 hours for the first 48 hours. solution. All implants were placed
sodium (Pentothal, Hospira) and local according to manufacturer guidelines.
anesthesia via 2% lidocaine with Every effort was made to place the
1:100,000 epinephrine for the bilat- Surgical implant placement implant platforms level with the
eral removal of the four mandibular osseous crest to allow for an accurate
premolars and first molars. The flaps Crestal incisions were made and full- histologic and micro-CT assessment of
were coapted and sutured without ten- thickness mucoperiosteal flaps were crestal bone levels (Fig 3). Laser-Lok
sion with multiple 4.0 chromic gut reflected 45 days postextraction. Three microchanneled healing abutments
interrupted sutures (Ethicon). implants per side were inserted into and standard machined surface healing
248
Fig 3 (left) Implant platforms were placed

as level as possible with the osseous crest
M to allow for accurate histologic and micro-
L CT assessment of crestal bone levels.
M
Fig 4 (right) A Laser-Lok microgrooved

healing abutment (L) and standard
machined-surface healing abutments (M)
were placed on the implants at the time of
implant placement.
abutments were connected to the using special software (Scanco

implants (Fig 4) following a randomized Medical), creating high-resolution
distribution pattern. Mucoperiosteal images of bone-to-implant contact.
flaps were closed tension-free and
sutured with multiple expanded poly- Light microscopy
tetrafluoroethylene interrupted and Fixed samples were dehydrated in a
horizontal mattress sutures (Gore-Tex, graded series of ethanols using a dehy-
W. L. Gore). All sutures were removed dration system with agitation and a
within 2 weeks. vacuum. The blocks were infiltrated
All six foxhounds received a soft with Kulzer Technovit 7200 VLC resin.
diet for the duration of the 3-month Infiltrated specimens were placed into
healing period. At 3 months following embedding molds, and polymeriza-
implant surgery, all six foxhounds were tion was performed under ultraviolet
sacrificed. Each mandible was resected light. Polymerized blocks were sec-
en bloc and placed immediately in fix- tioned in a mesiodistal direction and
ative for histologic preparation and parallel to the long axis of each
evaluation. implant. The slices were reduced by
microgrinding and polishing using an
Exakt grinding unit to an even thick-
Specimen preparation and ness of 30 to 40 µm. Sections were
analysis stained with toluidine blue–Azure II
and examined using both a Leica
Micro–computed tomography MZ16 stereomicroscope and a Leica
The specimens were scanned using a 6000DRB light microscope.
high-resolution micro-CT system (µCT
40, Scanco Medical) in multislice Scanning electron microscopy
mode. Each image data set consisted Specimens intended for SEM were
of approximately 600 micro-CT slice dehydrated through a graded series
images. The specimens were scanned of acetones and dried by the critical
in high resolution with an x-, y-, and z- point method16 using carbon dioxide
resolution of 16 µm. The image data as a transitory fluid. Specimens were
sets were used to produce three- examined in a scanning electron
dimensional views of the specimens microscope.
249
Fig 5 At the end of 3 months, the peri-

implant mucosa appeared normal with
little evidence of inflammation around the M
Laser-Lok microgrooved (L) and standard L
machined-surface (M) healing abutments. M
Results dicular to the microgrooved band.

There was coronal bone attachment to
All test and control implants were suc- the microchannel abutment surface
cessfully osseointegrated at the time of apical to the perpendicularly oriented
the 3-month sacrifice. Peri-implant CT fibers in two group A specimens
mucosal soft tissue healing proceeded (Figs 6b and 6c). The IAJ-mediated
uneventfully with little evidence of microgap was thus eliminated by
inflammation (Fig 5). No evidence of bone-implant contact coronal to the
localized infection was present IAJ (Figs 6b to 6e). Importantly, a long
throughout the entire 3-month healing JE was not observed in group A histo-
period at any of the implant sites. The logic sections.
unintentional loss of 11 abutments, a
result of the animals chewing on their Micro-CT and SEM observations
cages, reduced the number of avail- Micro-CT examination corroborated
able abutments to study. The resulting the histologic findings. Intimate bone-
lower number precluded a meaningful to-implant contact was seen extending
quantitative analysis. onto the RBT implant collar (Fig 6f).
SEM analysis demonstrated
intense connective tissue networks
Group A attached to the entire laser-ablated
abutment surfaces (Fig 6g). This
Histologic observations appeared to serve as an impenetrable
The peri-implant soft tissues consisted barrier to apical migration of the JE.
of an epithelial barrier composed of The normal circumferentially oriented
sulcular epithelium merging with junc- collagen fibers were noted to inter-
tional epithelium (JE). A discrete, digitate with the previously mentioned
supracrestal connective tissue barrier perpendicularly oriented connective
was seen in all group A sites apical to tissue fibers.
the JE (Fig 6a).
The JE ended at the coronal-most
position of the abutment’s Laser-Lok
microchannels, where a zone of con-
nective tissue fibers was seen perpen-
250
Fig 6a At group A sites, the JE ended at Fig 6b In this group A specimen, regener- Fig 6c A polarized light image demon-
the coronal-most Laser-Lok grooved area. ated bone was attached to the Laser-Lok strates perpendicularly inserting connective
Apical to the JE, healthy connective tissue abutment surface and the IAJ microgap was tissue fibers into the microgrooved abut-
fibers attached perpendicularly to the laser- eliminated. ment surface.
ablated channels.
Fig 6d (left) Light microscopic view of a

group A specimen demonstrating bone-to-
implant contact.
Fig 6e (right) A high-power view of Fig 6d

demonstrates bone regeneration at the IAJ
interface, effectively eliminating the IAJ
microgap.
251
Fig 6f (left) Micro-CT of a group A speci-

men corroborates the light microscopic
findings, including excellent bone-to-
implant contact up to the IAJ. No crestal
bone resorption occurred.
Fig 6g (right) Intense fibroblastic cellular

activity occurred at the Laser-Lok
microgrooved areas in all group A speci-
mens. Dense networks of connective tissue
fibers can be seen attached to the laser-
ablated microchannels.
Group B Group C
Histologic observations Histologic observations

The epithelial peri-implant soft tissues Apical migration of the JE was demon-
were identical to those seen in group A. strated in some group C sites (Fig 8a).
The JE terminated at the coronal-most The imposition of a long JE along the
position of the Laser-Lok abutment abutment and implant collar surfaces
microgrooves (Fig 7a). Functionally (Fig 8b) prevented connective tissue
oriented, perpendicularly directed fibers from forming the protective bar-
connective tissue fibers were juxta- rier and may be responsible for a more
posed intimately against the entire apical bone level.
band of the Laser-Lok microchannels
(Fig 7b). Apical to this band of connec- SEM observations
tive tissue fibers, newly regenerated Group C ultrastructural views demon-
bone was seen osseointegrating with strated an almost complete lack of
the machined collar of the RBT connective tissue fiber attachment to
implants. No group B site exhibited either the abutment or implant sur-
apical migration of the JE. faces (Fig 8c). No regenerated bone
was seen apposed to either the abut-
SEM observations ment or implant collar surfaces.
Ultrastructural examination of group B Significantly, the IAJ microgap
specimens proved identical to group A remained exposed to the surrounding
SEM findings. Dense masses of inter- environment.
lacing connective tissue fibers occu-
pied all surfaces of the Laser-Lok
microchannels (Fig 7c).
252
Fig 7a Group B specimens demonstrated Fig 7c SEM image of group B specimen

native and new bone (darker stain) on the demonstrated intense fibroblastic activity at
implant surface. This probably is the result the laser grooved surfaces, resulting in a
of the correction of drilling disparity, but it is dense network of interlacing connective tis-
evidenced that the supracrestal connective sue fibers that served as a natural barrier to
tissue fiber has prohibited apical migration apical epithelial migration.
of epithelium, allowing the bone to respond
in an aseptic environment.
Fig 7b Group B specimen demonstrating

perpendicularly oriented connective tissue
fibers against the entire surface of the
Laser-Lok grooved area.
Fig 8a A long JE is seen along the abut- Fig 8b A polarized light image of a group Fig 8c An SEM of a group C specimen
ment and implant collar surfaces, preventing C site demonstrates connective tissue fibers showing no connective tissue fiber attach-
connective tissue fibers from forming the parallel to the machined healing abutment ment to either the abutment or implant sur-
protective barrier seen in groups A and B. with no evidence of perpendicularly insert- faces. The IAJ microgap remains exposed
ing connective tissue fibers. to the surrounding tissue bed.
253
Fig 9c As in group C, SEM imagery

demonstrated the almost total absence of
connective tissue fibers covering either the
healing abutment or implant collar surfaces.
The IAJ microgap remained exposed to the
surrounding tissue bed.
Fig 9a A group D high-power specimen Fig 9b In a polarized light view, this group
demonstrated apical JE migration, resulting D site clearly demonstrates parallel running
in significant crestal bone resorption. connective tissue fibers against both the
abutment and implant collar surfaces. In
addition, significant crestal bone loss is seen.
Group D Discussion mate 1.5- to 2-mm apical position of

the bony crest relative to the implant-
Histologic observations Commonly observed crestal bone abutment interface.3,17,18
The absence of Laser-Lok microchan- resorption, or “dieback,” to the first Laser-ablated microgrooved
nels resulted in apical migration of the coronally positioned implant thread implant surface depths and widths in
JE and some crestal bone loss (Fig 9a). following abutment attachment threat- the range of 8 to 12 µm appear to reg-
The imposition of a long JE extending ens the needed balance between the ulate epithelial, fibroblastic, and
to the alveolar crest consistently stable underlying bone and overlying osteoblastic cellular migration and ori-
resulted in connective tissue fibers par- soft tissues. Multiple causes of such entation across these topographically
allel to the abutment and implant sur- undesirable crestal bone resorption altered surfaces.13,15,16,19–22 A recent
faces (Fig 9b). have been suggested, including the prospective proof-of-principle human
inherent need for a minimum biologic study demonstrated that these con-
SEM observations width dimension, as seen in the natural figured 8- and 12-µm microgrooves
Similar ultrastructural findings seen at dentition, and the bacterial and inflam- placed on the collar of dental implants
group C sites were also seen in group matory cell infiltrate present at the IAJ allowed direct supracrestal connective
D specimens. Minimal connective tis- microgap. 1,6,7 This inflammatory tissue attachment to the implant col-
sue attachment was demonstrated at cell–laden connective tissue adjacent lar.15 Abutment surface modifications
the abutment or implant surfaces. The to the IAJ microgap forces the reposi- may also be effective in preventing
SEM imagery revealed an IAJ covered tioning of noninflamed peri-implant commonly observed crestal bone loss,
with neither connective tissue fibers connective tissue and the crestal bone much like what has been shown with
nor bone, exposing the critically apically. The relatively constant spatial implant surface modifications. 22
important microgap to the surround- relationship between the IAJ and the Previous research examined multiple
ing environment (Fig 9c). alveolar crest confirms the approxi- abutment-related variables affecting
254
peri-implant and peri-abutment soft Conclusions

tissue attachments important in deter-
mining subsequent peri-implant bone The current proof-of-principle preclin-
levels.12,23–29 Results suggest that ical study suggests that carefully
surface characteristics of abutment designed implant surface modifica-
components affect the epithelial, tions may effectively prevent what
fibroblastic, and osteoblastic cellular often is perceived as either physio-
behavior at the implant-abutment logic or inevitable crestal bony
interface. “dieback” following abutment con-
The current study dramatically nection. The results suggest that the
underscores the effects that three- 1.5 to 2.0 mm of crestal bone loss
dimensional surface geometry can following abutment connection to
have on cellular behavior at the accommodate the needed space for
abutment-tissue interface. The pres- the connective tissue component of
ence of the 0.7-mm laser-ablated the biologic width may in fact not be
microchanneled zone consistently a physiologically inevitable event. The
enabled intense fibroblastic activity to study also suggests that a change may
occur on the abutment-grooved sur- be required in how implant abutments
face, resulting in a dense interlacing are perceived and managed clinically.
complex of connective tissue fibers However, microgrooved surface abut-
oriented perpendicular to the abutments, while showing intriguing and
ment surface that served as a phys- thought-provoking results and insights,
iologic barrier to apical JE migration. should be evaluated in a human study
As a consequence of inhibiting JE to verify the current results. Addi-
apical migration, crestal bone resorp- tionally, the question of whether the
tion in groups A and B was prevented. beneficial soft and hard tissue effects
Significantly, in two cases, bone induced by this surface can be main-
regeneration coronal to the IAJ and tained with repetitive manipulation of
onto the abutment surface occurred, the implant-abutment interface should
completely eliminating the negative also be evaluated.
sequelae of the IAJ microgap.
In contrast, group C and D abut-
ments, devoid of laser-ablated Acknowledgments
microgrooved surfaces, exhibited little
evidence of robust fibroblastic activity The authors would like to thank Dr Stuart Kay
(Huntington, New York) for his help with the
at the abutment-tissue interface. A
organization and production of this manuscript.
long JE extended along the abutment This study was sponsored by a grant from
and implant collar surfaces, preventing BioHorizons.
formation of the physiologic connec-
tive tissue barrier and causing crestal
bone resorption. Parallel rather than
functionally oriented perpendicular
connective tissue fibers apposed the
abutment-implant surfaces.
255
References 11. Ericcson I, Persson LG, Berglundh T, 22. Pecora GE, Ceccarelli R, Bonelli M,
Marinello CP, Lindhe J, Klinge B. Different Alexander H, Ricci JL. Clinical evaluation of
1. Berglundh T, Lindhe J. Dimension of the types of inflammatory reactions in peri- laser microtexturing for soft tissue and
periimplant mucosa. Biological width revis- implant soft tissues. J Clin Periodontol bone attachment to dental implants.
ited. J Clin Periodontol 1996;23:971–973. 1995;22:255–261. Implant Dent 2009;18:57–66.
2. Hermann JS, Cochran DL, Nummikoski PV, 12. Abrahamsson I, Berglundh T, Lindhe J. The 23. Abrahamsson I, Berglundh T, Sekino S,
Buser D. Crestal bone changes around mucosal barrier following abutment Lindhe J. Tissue reactions to abutment
titanium implants. A radiographic evalua- dis/reconnection. An experimental study in shift: An experimental study in dogs. Clin
tion of unloaded nonsubmerged and sub- dogs. J Clin Periodontol 1997;24:568–572. Implant Dent Relat Res 2003;5:82–88.
merged implants in the canine mandible. 13. Weiner S, Simon J, Ehrenberg DS, Zweig 24. Welander M, Abrahamsson I, Berglundh T.
J Periodontol 1997;68:1117–1130. B, Ricci JL. The effects of laser microtex- The mucosal barrier at implant abutments
3. Hermann JS, Buser D, Schenk RK, tured collars upon crestal bone levels of of different materials. Clin Oral Implants
Higginbottom FL, Cochran DL. Biologic dental implants. Implant Dent 2008;17: Res 2008;19:635–641.
width around titanium implants. A physio- 217–228.
25. Welander M, Abrahamsson I, Berglundh T.
logically formed and stable dimension over 14. Alexander H, Ricci JL, Hrico GJ. Subcrestal placement of two-part implants.
time. Clin Oral Implants Res 2000;11:1–11. Mechanical basis for bone retention Clin Oral Implants Res 2009;20:226–231.
4. Hermann JS, Schoolfield JD, Nummikoski around dental implants. J Biomed Mater
26. Zitzmann NU, Abrahamsson I, Berglundh
PV, Buser D, Schenk RK, Cochran DL. Res B Appl Biomater 2009;88:306–311.
T, Lindhe J. Soft tissue reactions to plaque
Crestal bone changes around titanium 15. Nevins M, Nevins ML, Camelo M, Boyesen formation at implant abutments with dif-
implants: A methodologic study compar- JL, Kim DM. Human histologic evidence of ferent surface topography. An experimen-
ing linear radiographic with histometric a connective tissue attachment to a dental study in dogs. J Clin Periodontol
measurements. Int J Oral Maxillofac tal implant. Int J Periodontics Restorative 2002;29:456–461.
Implants 2001;16:475–485. Dent 2008;28:111–121.
27. Abrahamsson I, Berglundh T, Glantz PO,
5. Quirynen M, Naert I, van Steenberghe D, 16. Soboyejo WO, Nemetski B, Allameh S, Lindhe J. The mucosal attachment at dif-
Nys L. A study of 589 consecutive implants Marcantonio N, Mercer C, Ricci J. ferent abutments. An experimental study in
supporting complete fixed prostheses. Interactions between MC3T3-El cells and dogs. J Clin Periodontol 1998;25:721–727.
Part I: Periodontal aspects. J Prosthet Dent textured Ti6Al4V surfaces. J Biomed Mater
28. Moon IS, Berglundh T, Abrahamsson I,
1992;68:655–663. Res 2002;62:56–72.
Linder E, Lindhe J. The barrier between the
6. van Steenberghe D, Lekholm U, Bolender 17. Listgarten MA, Lang NP, Schroeder HE, keratinized mucosa and the dental implant.
C, et al. Applicability of osseointegrated Schroeder A. Periodontal tissues and their An experimental study in the dog. J Clin
oral implants in the rehabilitation of partial counterparts around endosseous implants. Periodontol 1999;26:658–663.
edentulism: A prospective multcenter Clin Oral Implants Res 1991;2:1–19.
29. Abrahamsson I, Zitzmann NU, Berglundh
study on 558 fixtures. Int J Oral Maxillofac
18. Buser D, Weber HP, Donath K, Fiorellini JP, T, Linder E, Wennerberg A, Lindhe J. The
Implants 1990;5:272–281.
Paquette DW, Williams RC. Soft tissue mucosal attachment to titanium implants
7. Richter EJ. Basic biomechanics of dental reactions to non-submerged unloaded with different surface characteristics: An
implants in prosthetic dentistry. J Prosthet titanium implants in beagle dogs. experimental study in dogs. J Clin
Dent 1989;61:602–609. J Periodontol 1992;63:225–235. Periodontol 2002;29:448–455.
8. Piattelli A, Vrespa G, Petrone G, Iezzi G, 19. Ellingsen JE. Surface configurations of
Annibali S, Scarano A. Role of the micro- dental implants. Periodontol 2000 1998;
gap between implant and abutment: A 17:36–46.
retrospective histologic evaluation in mon-
20. Boyan BD, Dean DD, Lohmann CH,
keys. J Periodontol 2003;74:346–352.
Cochran DL, Sylvia VL, Schwartz Z. The tita-
9. Quirynen M, van Steenberghe D. Bacterial nium bone cell interface in vitro: The role
colonization of the internal part of two- of the surface in promoting osseointegra-
stage implants. An in vivo study. Clin Oral tion. In: Brunette DM, Tengvall P, Textor
Implants Res 1993;4:158–161. M, Thomson P (eds). Titanium in Medicine.
10. Quirynen M, Bollen CM, Eyssen H, van Berlin: Springer-Verlag, 2001:561–585.
Steenberghe D. Microbial penetration 21. Frenkel SR, Simon J, Alexander H, Dennis
along the implant components of the M, Ricci JL. Osseointegration on metallic
Brånemark system. An in vitro study. Clin implant surfaces: Effects of microgeome-
Oral Implants Res 1994;5:239–244. try and growth factor treatment. J Biomed
Mater Res 2002;63:706–713.
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The International Journal of Periodontics & Restorative Dentistry

Histologic Evidence of a Connective

Immunity, Harvard School of Dental Medicine, Boston, Massachusetts.

Volume 30, Number 3, 2010

tissue component apically, resulting attachments occurring at the micro-

The International Journal of Periodontics & Restorative Dentistry

Fig 1a (left) Resorbable blast texturing

Fig 2 (right) The four cohorts. LL = Laser-Lok;

Group A: Group B: Group C: Group D:

Volume 30, Number 3, 2010

Fig 3 (left) Implant platforms were placed

Fig 4 (right) A Laser-Lok microgrooved

abutments were connected to the using special software (Scanco

The International Journal of Periodontics & Restorative Dentistry

Fig 5 At the end of 3 months, the peri-

Results dicular to the microgrooved band.

Volume 30, Number 3, 2010

Fig 6d (left) Light microscopic view of a

Fig 6e (right) A high-power view of Fig 6d

The International Journal of Periodontics & Restorative Dentistry

Fig 6f (left) Micro-CT of a group A speci-

Fig 6g (right) Intense fibroblastic cellular

Histologic observations Histologic observations

Volume 30, Number 3, 2010

Fig 7a Group B specimens demonstrated Fig 7c SEM image of group B specimen

Fig 7b Group B specimen demonstrating

The International Journal of Periodontics & Restorative Dentistry

Fig 9c As in group C, SEM imagery

Group D Discussion mate 1.5- to 2-mm apical position of

Volume 30, Number 3, 2010

peri-implant and peri-abutment soft Conclusions

The International Journal of Periodontics & Restorative Dentistry

Volume 30, Number 3, 2010

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