OAI ORAL & Implantology CIC Edizioni Internazionali 2016 January-March; 9(Suppl. 1/2016 to N. 4/2016): 10–20. ISSN: 2035-2468
Published online 2017 February 14. doi: 10.11138/orl/2016.9.1S.010.

Implant Dentistry: Monitoring of Bacteria Along the Transmucosal Passage of the Healing Screw in Absence of Functional Load


1Private practice, Mondovi, Italy
2Private practice, Milan, Italy
3Private practice, Varese, Italy
4Private practice, Venice, Italy
5Ministry of Public Health, Rome, Italy
6Department of Clinical Sciences and Translational Medicine, University of Tor Vergata, Rome, Italy

Correspondence to: Marco E. Pasqualini, MD, Galleria Strasburgo, 3, 20122 Milan, Italy, Phone/fax: +39.02.799.651, E-mail: dott.marcopasqualini@tiscali.it


To assess the changes in bacterial profile along the transmucosal path of healing screws placed immediately after insertion of two-piece endosseus implants during the 4-month osseointegration phase, in absence of functional load.

Materials and methods
Two site-specific samples were collected at the peri-implant mucosa of the healing screws of 80 two-piece implants, for a total of 640 samples. Implants placement was performed following a single protocol with flapless technique, in order to limit bacterial contamination of the surgical site. Identical healing screws (5 mm diameter/4 mm height) were used for each of the 80 implants. During the 4 months of the study, the patients followed a standard oral care regimen with no special hygiene maneuvers at the collection sites.

The present research documents that during the 4-month period prior to application of function load the bacterial profile of all sites exhibited a clear prevalence of cocci at the interface between implant neck and osteoalveolar crest margin.

A potentially pathogenic bacterial flora developed only along the peri-implant transmucosal path.

Keywords: bacterial morphological profile, transmucosal peri-implant path, healing screw, two-piece implant, absence of functional load


Dental plaque is the accumulation of organic and inorganic mixed material with a significant microbial content, especially bacteria, which – in addition of depositing on the teeth surface – can also adhere tenaciously to implant fixtures (13).

Previous studies underscored the similarities in composition between the plaque found on teeth and that found on implant abutments. The latter type is mostly made up of Gram-positive aerobic cocci and non-motile bacteria (4, 5).

In experiments on dogs, Berglundh and Ericsson (6, 7) found existing similarities between the amount and composition of the plaque formed on teeth and that observed at implant sites. Implants as well as teeth surrounded by healthy mucosa, are invariably associated with a plaque composed mainly by cocci and Gram-positive bacteria while the sites affected by diffused periodontal and peri-implant disease exhibit biopellicles rich in rod-shaped, fusiform and spiral bacteria, which – in addition of being motile bacteria – greatly outweighs the number of cocci (8, 9).

The above corroborates the results of Listgarten, according to whom the proportion of cocci found at the implant site corresponds to 71.3% of the total bacteria, while other types of bacteria are a minority, especially the non-motile strains (0.4%) (10). These data differ significantly in those sites with periodontal and peri-implant inflammation, where the percentage of cocci is markedly decreased. The aim of the study was to evaluate the bacterial profile from a morphological standpoint, and the ratio of the different types of bacteria found along the transmucosal path of healing screws placed after insertion of two-piece fixtures during the 4-month osseointegration phase in absence of load.

Specifically, the research aimed at assessing the differences in bacterial composition of the plaque accumulated on the mucosa surrounding titanium healing screws, before insertion of the definitive abutment and application of the functional load (Figure 1).

Figure 1Figure 1
Healing titanium screw of one of the 80 cases analyzed.

Materials and methods

All implant placements were performed following the same general protocol and flapless technique, in order to limit bacterial contamination of the surgical site. At the edentulous sites, complete perforation of the attached mucosa was achieved by means of a 4.1 mm O tissue punch. Identical healing screws (5 mm O, height 4 mm) were used for each of the 80 implants. Starting the month following implant placement, each site was followed-up for four months, a period corresponding to the so-called osseointegration phase, under non-functional loading conditions.

The bacterial plaque accumulated on the 80 implants was collected on a monthly basis, for a total of 640 samples at the two considered sites:

  • along the transmucosal path of the healing screw;
  • at the interface between implant neck and osteoalveolar crestal margin.

Each collected sample was submitted to morphological assessment of the non-fixated vital bacteria by means of a technique employed by our study group for over 20 years, and following Listgarten’s principles, according to whom a bacterial profile composed mainly of cocci (70%) should be regarded as normal and saprophytic compared to a high percentage of pathogenic bacteria such as rod-shaped, fusiform and spiral types (11).

The samples were labeled as follows:

  • TMP: sample collected along the transmucosal path;
  • CMI: sample collected at the crestal margin interface.

The first collection phase was performed with a sterile point along the transmucosal path (TMP), leaving the healing screw and its bacterial film (plaque) in place to avoid alteration of the microbiota conditions at the different levels of the collection site (Figure 2).

Figure 2Figure 2
The first phase of withdrawal was performed using a sterile tip in scope of the transmucosal route (TMP), indicated by the arrows, while maintaining the healing screw in situ with the presence of its bacterial film (plaque) does not vary the conditions (more ...)

The second collection phase (CMI) was performed after removal of the healing screw, taking care to avoid contamination of the sterile tool used for sampling along the transmucosal path, characterized by abundant plaque (Figures 35). The healing screw was then repositioned to preserve the environmental conditions for the three following monthly collections.

Figure 3Figure 3
Second phase of withdrawal (CMI): blue arrows show the margin-alveolar crestal bone after the healing screw removal. Observe the amount of plaque.
Figure 4Figure 4
The arrows indicate the sampling sites. The transmucosal route TMP (yellow arrows) and the margin alveolar crestal bone-CMI (blue arrows).
Figure 5Figure 5
Position provides amply TMP (yellow arrows) and marginalveolar crestal bone IMC (blue arrows) seen in the image Xray.

The removed healing screws have constantly exhibited a significant amount of bacterial plaque on their entire surface (Figure 6). A massive presence of plaque was also found on the inner surface of the fixture, despite the presence of the healing screw (Figure 3).

Figure 6Figure 6
The plaque adherent to the surface of the titanium healing screw.

The bacterial morphology assessment of the vital intact bacteria was carried out by means of contrast-phase microscopy (Figure 7).

Figure 7Figure 7
40x microscope view of the levy of TMP provides amply when you notice the presence of all bacterial morphology (cocci, rods, filaments and convoluted).

The material collected with a sterile point from the sample sites (TMP – CMI) was diluted with 1% lyophilized gelatin in saline solution.

With a variable volume micropipette (Socorex – Isba S.A.-Switzerland), 1000 μL of solution were withdrawn and dissolved in the master vial (MV).

The MV underwent dynamization by agitator heatable magnetic (I.S.Co.,Mod. AMR 2T-Italy) so as to obtain an uniform distribution of the sample in the test vial. The sample was then allowed to rest for 3 minutes.

With a new sterile tip on the micropipette, 100 μL of diluted sample were transferred in a derived vial (DV) containing 900 μL of saline, thus obtaining a 1:10 dilution ratio. This vial also underwent dynamization similarly to the MV so as to achieve a homogeneous dispersion of the bacterial content, and the sample was allowed to rest for 3 minutes.

Subsequently, 100 μL of diluted sample were withdrawn from the vial, deposited on the surface of a Burker chamber, and covered with a coverslip.

The slide was then examined at 40x with a contrast-phase microscope.

Reading was performed for every surface unit (1/25 mm2) proceeding from top to bottom and left to right and the results were noted on an ad hoc table.


Results are summarized in Table 1. The data show a significant evolutionary differentiation in terms of percentage of cocci in the samples collected at the TMP compared to the CMI sites, during the 4 months of the study. The progressive reduction of the number of cocci at the TMP sites in favor of other forms of bacteria indicates that the microbiota niche can be easily colonized by bacterial plaque. At the IMC sites, the presence of cocci remains practically constant and they are clearly more prevalent than other bacterial types, meaning that the overall the echo-microbiota conditions are unfavorable to the growth of rod-shaped, fusiform and spiral-type bacteria.

Table 1Table 1
Percentage of cocci in the samples collected at the TMP compared to the CMI sites, during the 4 months of the study.

Due to the fact that the results were expressed in percentages, the analysis was performed with non-parametric methods (12, 13).

The Mann-Whitney test was used to assess the statistical significance of the differences between the two simultaneous sample collections (TMP - CMI) (14).

Therefore, for the four timepoints, the TMP samples show a highly significant reduction of cocci compared to the IMC samples.

The Kruskal-Wallis test was used to assess the statistical significance of the variation at the different time-points, for each site (15) (Graphics 14).

Graphic 1Graphic 1
One-month follow-up. The differences in bacterial loading in CMI and TMP are statistical significant by using Mann-Whitney U test.
Graphic 2Graphic 2
Two-month follow-up. The differences in bacterial loading in CMI and TMP are statistical significant by using Mann-Whitney U test.
Graphic 3Graphic 3
Three-month follow-up. The differences in bacterial loading in CMI and TMP are statistical significant by using Mann-Whitney U test.
Graphic 4Graphic 4
Fou-month follow-up. The differences in bacterial loading in CMI and TMP are statistical significant by using Mann-Whitney U test.

The above shows that the progressive reduction of cocci along the transmucosal path is highly significant, while the interface with the crestal margin remains pretty much unchanged and has no pathogenic significance (10).


The research aims to highlight that in the absence of occlusal loading and in particular of environmental stressors (dysfunctional occlusal loading) the peri-implant tissue at the crestal margin undergoes spontaneous stabilization of the bacterial profile (1619).

The orderly and relatively repetitive presence of Gram+ cocci prevents the development of peri-implant pathogenic microbial conditions conducive to bacterial invasion of the deeper tissues which can cause infection followed by peri-implantitis (20, 21).

The ecosystem relationships between host organism and bacteria are therefore well maintained in terms of integrated ecological component (microbioma) (22, 23).

The above mentioned evaluation are of paramount importance especially in patients with oral disease (2433).

The absence of biomechanical stress (occlusal-static-dynamic load), permits maintenance of a balance between the system consisting of implant screw-bone-mucosa on one side and bacterial front on the other side.

Bacterial component maintains a non-invasive/aggressive saprophytic-commensal profile, regardless of the types of bacteria that progressively develop along the transmucosal path (TMP) and at the interface implant-crestal bone margin (CMI).

This study shows that in a multifactorial biological context in non-loading conditions, a massive presence of bacteria is not sufficient per sé to have a destabilizing effect on the balance between host and bacterial front (3441).

The dysfunctional load – i.e. occlusal trauma – could be a predisposing factor able to trigger the change in bacterial profile from saprophyte to pathogen (1619). Peri-implant disease could represents a biomechanic dysfunctional based syndrome whom damage it’s mainly atrophyc-distrophyc. Talking about implant-protesis, this pathological manifestation (peri-implantitis) it becomes stronger due to the lack of those organs of functional manifestation with a modulated distribution of loads, in fact the periodontal ligament, avoiding the contact between the root surface and the bone, represents the optimum biomechanical condition, even if is impossible in case of implant-bone ankylosis. However, unfortunately implant failure is often attributed to microbial causes, systemic diseases, inadequate hygiene and / or smoking (4279).


We thank Dr. Giorgio Comola for his precious collaborations and also special thanks to Doctor OS for letting us reproduce part of his original manuscript in Italian.

Listgarten MA. The structure of dental plaque. Periodontol. 2000;1994(5):52–65.
Lindhe, J.; Nyman, S. Textbook of clinical periodontology. Place: Munksgaard; 1989.
Meynardi F, Pasqualini ME, Rossi F, Biancotti P. Confronto del profilo batterico presente in siti implantari con mesostruttura solidarizzata mediante barra saldata e con perno moncone singolo. Doctor Os. 2013;5:411–15.
Listgarten MA. The role of dental plaque in gingivitis and periodontitis. J Clin Periodontol. 1988;15:485–7.
Gandolfo S, Meynardi F, Corrente G, Nelken A. Analisi microbiologica a fresco della placca dento-gengivale. RIS. 1994:275–86.
Berglundh T, Lindhe J, Marinello C, Ericsson I, Liljenberg B. Soft tissue reaction to de novo plaque formation on implants and teeth. An experimental study in the dog. Clin Oral Implants Res. 1992;3:1–8.
Ericsson I, Berglundh T, Marinello C, Liljenberg B, Lindhe J. Long-standing plaque and gingivitis at implants and teeth in the dog. Clin Oral Implants Res. 1992;3:99–103.
Mombelli, A. Prevention and therapy of peri-implant infections. In: Lang NP, Karring T, Lindhe J. , editors. Proceedings of the 3rd European Workshop on Periodontology. Berlin: Quintessence; 1999. pp. 281–303.
Meynardi F, Pasqualini M, Biancotti PP. Analisi batteriologica nel follow up in Parodontologia. Doctor Os. 2011;22:120–27.
Listgarten MA. Structure of the microbial flora associated with periodontal health and disease in man. A light and electron microscopic study. J Periodontol. 1976;47:1–18.
Listgarten MA, Loomer PM. Microbial identification in the management of periodontal diseases. A systematic review. Ann Periodontol. 2003;8:182–92.
Peat, J.; Barton, B. Medical Statistics: A guide to data analysis and critical apptaisal. Place: Blackwell Publishing; 2005.
Hollander, M.; Wolfe, DA.; Chikchen, E. Nonparametrical Statistical Methods: John Wiley & Sons; New York: 2013.
Mann AB, Whitney DR. On a test whether one of two random variables is stochastically larger than the other. Annals of Mathematical Statistics. 1947;18:50–60.
Kruskal W, Wallis WA. Use of ranks in one criterion variance analysis. Journal of the American Statistical Association. 1952;47:583–621.
Pasqualini, U. Le Patologie Occlusali Eziopatogenesi e terapia. Place: Masson; 1993.
Meynardi F, Rossi F, Grivet Brancot L, Pasqualini ME. Non solo batteri ma un trauma occlusale all’origine della malattia parodontale. Dental Tribune. 2013;9:19–20.
Meynardi F, Pasqualini ME, Rossi F, Dal Carlo L, Biancotti P, Carinci F. Correlation between dysfunctional occlusion and periodontal bacterial profile. J Biol Regul Homeost Agents. 2016;30:115–21.
Meynardi F, Rossi F, Battaglio C, Biancotti PP, Pasqualini ME. Correlation beetwen periodontal-peri-implant bacterial profile and abnormal occlusal loads. Doctor Os. 2011;22:341–45.
Vettore MV, Leao AT, Monteiro Da Silva AM, Quintanilha RS, Lamarca GA. The relationship of stress and anxiety with chronic periodontitis. J Clin Periodontol. 2003;30:394–402.
Genco RJ, Ho AW, Grossi SG, Dunford RG, Tedesco LA. Relationship of stress, distress and inadequate coping behaviors to periodontal disease. J Periodontol. 1999;70:711–23.
Blaser MJ. Who are we? Indigenous microbes and the ecology of human diseases. EMBO Rep. 2006;7:956–60.
Lee YK, Mazmanian SK. Has the microbiota played a critical role in the evolution of the adaptive immune system? Science. 2010;330:1768–73.
Corsalini M, Di Venere D, Pettini F, Lauritano D, Petruzzi M. Temporomandibular disorders in burning mouth syndrome patients: an observational study. Int J Med Sci. 2013;10:1784–9.
Petruzzi M, Lucchese A, Lajolo C, Campus G, Lauritano D, Serpico R. Topical retinoids in oral lichen planus treatment: an overview. Dermatology. 2013;226:61–7.
Petruzzi M, Campus G, Paparusso F, Lucchese A, Lauritano D, De Benedittis M, Serpico R. Analysis of plasma fibronectin levels in patients affected by oral lichen planus. European Journal of Inflammation. 2012;10:45–50.
Lauritano D, Bussolati A, Baldoni M, Leonida A. Scleroderma and CREST syndrome: a case report in dentistry. Minerva Stomatol. 2011;60:443–65.
Petruzzi M, Lucchese A, Campus G, Crincoli V, Lauritano D, Baldoni E. Oral stigmatic lesions of gastroesophageal reflux disease (GERD). Rev Med Chil. 2012;140:915–8.
Petruzzi M, Lucchese A, Nardi GM, Lauritano D, Favia G, Serpico R, Grassi FR. Evaluation of autofluorescence and toluidine blue in the differentiation of oral dysplastic and neoplastic lesions from non dysplastic and neoplastic lesions: a cross-sectional study. J Biomed Opt. 2014;19:76003.
Lauritano D, Silvestre FJ, Borgia R, Carini F, Baldoni M. Oral manifestation of neutropenic patients. Dental Cadmos. 2007:43–51.
Lauritano D, Petruzzi M, Di Stasio D, Lucchese A. Clinical effectiveness of palifermin in prevention and treatment of oral mucositis in children with acute lymphoblastic leukaemia: a case-control study. Int J Oral Sci. 2014;6:27–30.
Lauritano D, Petruzzi M. Decayed, missing and filled teeth index and dental anomalies in long-term survivors leukaemic children: a prospective controlled study. Med Oral Patol Oral Cir Bucal. 2012;17:e977–80.
Lucchese A, Guida A, Capone G, Petruzzi M, Lauritano D, Serpico R. Designing a peptide-based vaccine against Porphyromonas gingivalis. Front Biosci (Schol Ed). 2013;5:631–7.
Margulis L, Dorion S. Microcosmos. Place: Press. Berkeley. 1997
Meynardi F, Biancotti PP. Correlazioni eziopatogenetiche tra parodontopatia e trauma occlusale. IAPNOR - International Academy of Posture and Neuromuscolar Occlusion Research. 2009;13:3.
Greenteing G, Lamter I. Cambiamenti dei modelli parodontali: implicazioni terapeutiche. International Journal of Periodontics & Restorative Dentistry. 2003;4:18–24.
Kawai T, Ito HO, Sakato N, Okada H. A novel approach for detecting an immunodominant antigen of Porphyromonas gingivalis in diagnosis of adult periodontitis. Clin Diagn Lab Immunol. 1998;5:11–7.
Wimmer G, Janda M, Wieselmann-Penkner K, Jakse N, Polansky R, Pertl C. Coping with stress: its influence on periodontal disease. J Periodontol. 2002;73:1343–51.
Van Dyke TE, Serhan CN. Resolution of inflammation: a new paradigm for the pathogenesis of periodontal diseases. J Dent Res. 2003;82:82–90.
Page RC, Schroeder HE. Current status of the host response in chronic marginal periodontitis. J Periodontol. 1981;52:477–91.
Fanali S, Perrotti V, Riccardi L, Piattelli A, Piccirilli M, Ricci L, Artese L. Inflammatory infiltrate, microvessel density, vascular endothelial growth factor, nitric oxide synthase, and proliferative activity in soft tissues below intraorally welded titanium bars. J Periodontol. 2010;81:748–57.
Lombardo L, Carinci F, Martini M, Gemmati D, Nardone M, Siciliani G. Quantitive evaluation of dentin sialoprotein (DSP) using microbeads - A potential early marker of root resorption. ORAL and Implantology. 2016;9:132–42.
Lauritano D, Cura F, Candotto V, Gaudio RM, Mucchi D, Carinci F. Evaluation of the Efficacy of Titanium Dioxide with Monovalent Silver Ions Covalently Linked (Tiab) as an Adjunct to Scaling and Root Planing in the Management of Chronic Periodontitis Using Pcr Analysis: A Microbiological Study. J Biol Regul Homeost Agents. 2015;29:127–30.
Scapoli L, Girardi A, Palmieri A, Martinelli M, Cura F, Lauritano D, Carinci F. Quantitative Analysis of Periodontal Pathogens in Periodontitis and Gingivitis. J Biol Regul Homeost Agents. 2015;29:101–10.
Lauritano D, Cura F, Candotto V, Gaudio RM, Mucchi D, Carinci F. Periodontal Pockets as a Reservoir of Helicobacter Pylori Causing Relapse of Gastric Ulcer: A Review of the Literature. J Biol Regul Homeost Agents. 2015;29:123–6.
Scapoli L, Girardi A, Palmieri A, et al. Interleukin-6 Gene Polymorphism Modulates the Risk of Periodontal Diseases. J Biol Regul Homeost Agents. 2015;29:111–6.
Carinci F, Girardi A, Palmieri A, et al. LAB®-Test 1: Peri-Implantitis and bacteriological analysis. European Journal of Inflammation. 2012;10:91–93.
Carinci F, Girardi A, Palmieri A, et al. LAB®-test 2: Microflora and periodontal disease. European Journal of Inflammation. 2012;10:95–98.
Carinci F, Girardi A, Palmieri A, et al. Lab®-test 3: Genetic susceptibility in periodontal disease. European Journal of Inflammation. 2012;10:99–101.
Scapoli L, Girardi A, Palmieri A, et al. IL6 and IL10 are genetic susceptibility factors of periodontal disease. Dent Res J (Isfahan). 2012;9:S197–201.
Gargari M, Ottria L, Morelli V, Benli M, Ceruso FM. Conservative zirconia-ceramic bridge in front teeth. Case report. Oral Implantol (Rome). 2015;7:93–98.
Andreasi Bassi M, Andrisani C, Lopez MA, Gaudio RM, Lombardo L, Carinci F. Guided bone regeneration by means of a preformed titanium foil: A case of severe atrophy of edentulous posterior mandible. J Biol Regul Homeost Agents. 2016;30( S2):35–41.
Milillo L, Fiandaca C, Giannoulis F, Ottria L, Lucchese A, Silvestre F, Petruzzi M. Immediate vs non-immediate loading post-extractive implants: A comparative study of Implant Stability Quotient (ISQ). Oral Implantol (Rome). 2016;9:123–31.
Bartuli FN, Luciani F, Caddeo F, et al. Piezosurgery vs High Speed Rotary Handpiece: a comparison between the two techniques in the impacted third molar surgery. Oral Implantol (Rome). 2013;6:5–10.
Clementini M, Ottria L, Pandolfi C, Agrestini C, Barlattani A. Four impacted fourth molars in a young patient: a case report. Oral Implantol (Rome). 2012;5:100–3.
Gargari M, Comuzzi L, Bazzato MF, Sivolella S, Di Fiore A, Ceruso F. Treatment of peri-implantitis: Description of a technique of surgical 2 detoxification of the implant. A prospective clinical case series with 3-year follow-up. Oral Implantol (Rome). 2015;8:1–11.
Inchingolo F, Marrelli M, Annibali S, et al. Influence of endodontic treatment on systemic oxidative stress. Int J Med Sci. 2014;11:1–6.
Cura F, Palmieri A, Girardi A, Martinelli M, Scapoli L, Carinci F. Lab-Test((R)) 4: Dental caries and bacteriological analysis. Dent Res J (Isfahan). 2012;9:S139–41.
Roncati M, Lauritano D, Cura F, Carinci F. Evaluation of light-emitting diode (led-835 nm) application over human gingival fibroblast: An in vitro study. Journal of Biological Regulators and Homeostatic Agents. 2016;30:161–67.
Lauritano D, Bignozzi CA, Pazzi D, Palmieri A, Gaudio RM, Di Muzio M, Carinci F. Evaluation of the efficacy of a new oral gel as an adjunct to home oral hygiene in the management of chronic periodontitis. A microbiological study using PCR analysis. J Biol Regul Homeost Agents. 2016;30:123–8.
Carinci F, Palmieri A, Girardi A, Cura F, Lauritano D. Aquolab ® ozone-therapy is an efficient adjuvant in the treatment of chronic periodontitis: A case-control study. Journal of Orofacial Sciences. 2015;7:27–32.
Lauritano D, Cura F, Gaudio RM, Pezzetti F, Andreasi Bassi M, Carinci F. Polymerase Chain Reaction to Evaluate the Efficacy of Silica Dioxide Colloidal Solutions in the Treatment of Chronic Periodontitis: A Case Control Study. J Biol Regul Homeost Agents. 2015;29:131–5.
Lauritano D, Petruzzi M, Nardi GM, Carinci F, Minervini G, Di Stasio D, Lucchese A. Single Application of a Dessicating Agent in the Treatment of Recurrent Aphthous Stomatitis. J Biol Regul Homeost Agents. 2015;29:59–66.
Carinci F, Lauritano D, Cura F, Lopez MA, Bassi MA, Confalone L, Pezzetti F. Prevention of bacterial leakage at implant-Abutment connection level: An in vitro study of the efficacy of three different implant systems. Journal of Biological Regulators and Homeostatic Agents. 2016;30:69–73.
El Haddad E, Giannì AB, Mancini GE, Cura F, Carinci F. Implant-abutment leaking of replace conical connection nobel biocare® implant system. An in vitro study of the microbiological penetration from external environment to implant-abutment space. ORAL and Implantology. 2016;9:76–82.
Mancini GE, Gianni AB, Cura F, Ormanier Z, Carinci F. Efficacy of a new implant-abutment connection to minimize microbial contamination: An in vitro study. ORAL and Implantology. 2016;9:99–105.
Roncati M, Lucchese A, Carinci F. Non-Surgical treatment of peri-Implantitis with the adjunctive use of an 810-nm diode laser. Journal of Indian Society of Periodontology. 2013;17:812–15.
Scarano A, Tripodi D, Carinci F, Piccolomini R, D’Ercole S. Biofilm formation on titanium alloy and anatase-Bactercline® coated titanium healing screws: An in vivo human study. Journal of Osseointegration. 2013;5:8–12.
Brunelli G, Carinci F, Zollino I, Candotto V, Scarano A, Lauritano D. Sem evaluation of 10 infected implants retrieved from man. European Journal of Inflammation. 2012;10:7–12.
Scarano A, Sinjari B, Di Orio D, Murmura G, Carinci F, Lauritano D. Surface analysis of failed oral titanium implants after irradiated with ErCr:ysgg 2780 laser. European Journal of Inflammation. 2012;10:49–54.
Brunelli G, Carinci F, Girardi A, Palmieri A, Caccianiga G, Sollazzo V. Osteobiol effect on dental pulp derived stem cells. European Journal of Inflammation. 2012;10:27–30.
Scarano A, Piattelli A, Polimeni A, Di Iorio D, Carinci F. Bacterial adhesion on commercially pure titanium and anatase-coated titanium healing screws: An in vivo human study. Journal of Periodontology. 2010;81:1466–71.
Grecchi F, Zollino I, Candotto V, et al. A case of mandible osteonecrosis after a severe periimplant infection. Dent Res J (Isfahan). 2012;9:S233–6.
Pezzetti F, Carinci F, Palmieri A, et al. Diphenylhydantoin plays a role in gene expression related to cytoskeleton and protein adhesion in human normal palate fibroblasts. Pathology. 2009;41:261–68.
Stabellini G, Carinci F, Gagliano N, et al. Downregulated Gene Expression in Human Palate Fibroblasts after Cyclosporin A Treatment. Archives of Medical Research. 2007;38:717–22.
Stabellini G, Carinci F, Bedani PL, et al. Cyclosporin A and transforming growth factor β modify the pattern of extracellular glycosaminoglycans without causing cytoskeletal changes in human gingival fibroblasts. Transplantation. 2002;73:1676–79.
Mariani G, Calastrini C, Carinci F, Bergamini L, Calastrini F, Stabellini G. Ultrastructural and histochemical features of the ground substance in cyclosporin A-induced gingival overgrowth. Journal of Periodontology. 1996;67:21–27.
Pagliarini A, Stabellini G, Carinci F, Calura G, Tognon M, Evangelisti R. Heterogeneity of fibroblasts derived from human free and attached gingiva. Glycosaminoglycan synthesis and effects of phenytoin (PHT) treatment. Journal of oral pathology & medicine: official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology. 1995;24:72–77.
Mariani G, Calastrini C, Carinci F, Marzola R, Calura G. Ultrastructural features of cyclosporine A-induced gingival hyperplasia. Journal of Periodontology. 1993;64:1092–97.