Journal of Dental Implants
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REVIEW ARTICLE
Year : 2013  |  Volume : 3  |  Issue : 2  |  Page : 148-152

Bioseal: The physiological and biological barrier for osseointegrated supported prosthesis


Department of Prosthodontics and Crown and Bridge, A.B.Shetty Memorial Institute of Dental Sciences, Nitte University, Deralakatte, Mangalore, India

Date of Web Publication25-Sep-2013

Correspondence Address:
Krishna D Prasad
Department of Prosthodontics and Crown and Bridge, A.B.Shetty Memorial Institute of Dental Sciences, Nitte University, Deralakatte, Mangalore 575 018
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-6781.118855

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   Abstract 

The success of osseointegrated supported prosthesis is dependent on the establishment of a soft-tissue barrier that is able to shelter the underlying osseous structures and the osseointegration surrounding the implant body. The esthetics of dental implant prosthesis depends on the health and stability of the peri-implant mucosa. The biological seal refers to the soft tissue seal around the dental implants that prevents the ingress of toxins. A thorough understanding of soft-tissue healing and maintenance of dental implants is of paramount importance for the success of an implant. This review article describes the components of the surrounding tissue and the healing process.

Keywords: Biological width, dental implants, seal


How to cite this article:
Alva H, Prasad KD, Prasad AD. Bioseal: The physiological and biological barrier for osseointegrated supported prosthesis. J Dent Implant 2013;3:148-52

How to cite this URL:
Alva H, Prasad KD, Prasad AD. Bioseal: The physiological and biological barrier for osseointegrated supported prosthesis. J Dent Implant [serial online] 2013 [cited 2019 Sep 16];3:148-52. Available from: http://www.jdionline.org/text.asp?2013/3/2/148/118855


   Introduction Top


Replacement of missing teeth by means of endosseous implants has proven to be the most predictable and successful treatment modality over the decades. The dental implants are unique as they consist of abutments that emerge and support one or more prosthetic component that extrudes through the lamina propria and stratified squamous epithelium in the oral cavity. This transmucosal tunnel is a weak junction between the prosthetic structure and the underlying bone that surrounds the dental implant. It is in this region that the peri-implant lesions might originate with consequent osteoclastic activity and resorption of the supporting bone.

Weinmann in 1956, first theorized the concept of a 'seal' around the dental implants, which was later researched by other authors like Lavelle et al., James et al., and McKinney et al. The term 'biological seal' refers to the soft tissue around a dental implant, which provides an essential physiological and biological barrier from the external environment. It is an entity whose integrity prevents the toxins that originate in the oral cavity from passing through the implant-tissue interface. Healthy soft tissue surrounding a dental implant is essential for its health, function, and esthetics. [1]


   Epithelial Components Forming the Bioseal Top


The components of a bioseal include the epithelial cell with the cell membrane, the basal lamina outside the cell membrane, which consists of lamina lucida, lamina densa, sub lamina lucida and the hemidesmosomes on the cell membrane, which consist of peripheral densities, pyramidal particles, fine filaments, and the linear body of the implant. [1] The collagenous components of the linear body cannot physiologically adhere to or become embedded in the implant body as they do in case of the living cementum of a natural tooth. The high content of glycosaminoglycans on the linear body provides the sufficient stickiness to form a biologically active and trauma-resistant attachment at the base of the regenerated sulcus.

Peri-implant mucosa

The soft tissue that surrounds the dental implants is termed as 'peri-implant mucosa'. The mucosal tissues around the implants form a tightly adherent band consisting of a dense collagenous lamina propria covered by a stratified squamous keratinizing epithelium. The implant-epithelium junction is analogous to the junctional epithelium around the natural teeth, in that, the epithelial cells attach to the titanium implant by means of hemidesmosomes and a basal lamina.

Similarities between periodontal and peri-implant soft tissues are limited to the form and function of the epithelial structures. The outer surface is covered by a well-keratinized oral epithelium and this outer epithelium connects with a barrier epithelium that faces the implant surface.

Mucosal barrier is composed of:

  • Zone of junctional epithelium (2 mm)
  • Zone of connective tissue (1-1.5 mm)


Hemidesmosomal attachment

The presence of the basal lamina and hemidesmosomal adherence of the junctional epithelium to the dental implant surface was first described in monkeys by James and Schultz (1974). This 'junctional epithelium', with a thickness of only a few cells, attaches to the titanium via the hemidesmosomes. The hemidesmosomal seal only has a circumferential band of tissue to provide mechanical protection against tearing, with no fibers extending into the implant.

Connective tissue attachment

Berglundh [2] stated that collagen fibers connecting at the marginal bone run parallel to the abutment surfaces, and do not attach to the titanium surface. He also stated that the main difference between the mesenchymal tissue present at the tooth and implant site is the occurrence of cementum. Fibers invest into the periosteum at the bone crest and project parallel to the implant surface. In areas distant to the implant the fibers run more or less perpendicular to the implant.

The connective tissue layer protects the underlying osseous area by restraining the apical migration of the epithelium. A high content of glycosaminoglycans associated with the linear body of the implant have sufficient 'stickiness' to form a biologically active and trauma-resistant attachment at the base of the regenerated gingival sulcus. The junctional and barrier epithelia are 2 mm long and the zone of supra-alveolar connective tissue is between 1 and 1.5 mm high. Both epithelia are attached to the surface by hemidesmosomes.

Vasculature

Berglundh [3] observed the vasculature of the peri-implant mucosa and concluded that it originates from large supra-periosteal blood vessels and branches into the supra-alveolar mucosa to supply the capillaries beneath the oral mucosa. The connective tissue surrounding the dental implant is free of vascular units.

Wound healing

Wound healing is a complex sequence of physiological events, which is accomplished in two ways:

  1. Healing by primary intention
  2. Healing by secondary intention


Healing by primary intention

Healing by primary intention occurs in wounds that are clean and uninfected and surgically incised wounds without much loss of cells and tissue. The edges of such wounds are approximated by sutures. The stages of healing by primary intention involve initial hemorrhage and the acute inflammatory response that occurs within 24 hours and is characterized by the presence of Poly Morpho Neuclear neutrophils (PMNs). Epithelial changes are characterized by basal cells, which start proliferating and migrate toward the incision space. By the fifth day a multiple-layered epithelium is formed. The next stage is 'Organization' where new collagen fibrils start forming by day, and by four weeks a scar tissue with scanty cellular and vascular elements is formed.

Healing by secondary intention

Healing by secondary intention occurs in wounds that are open and at times infected, having extensive loss of cells and tissue, with edges not approximated by sutures. The stages involve initial hemorrhage, the inflammatory phase, and epithelial changes that are characterized by proliferating epithelial cells that do not completely cover the surface. This is followed by granulation tissue formation, which forms the main bulk and is formed by the proliferation of fibroblasts and neovascularization. After granulation tissue formation, wound contraction takes place due to the action of myofibroblasts. The wound contracts to one-third to one-fourth its original size.

Healing of peri-implant mucosa

Healing of the peri-implant mucosa is a delicate process that requires several weeks of tissue remodeling. A large number of neutrophils infiltrate the compartment between the mucosa and the implant during the initial phase of healing. The first signs of epithelial proliferation begin after one to two weeks of healing. The collagen fibers of the mucosa get organized after four to six weeks. Subsequently, the mature barrier epithelium formation occurs by six to eight weeks.

Following implant surgery, healing occurs by regeneration of the attached gingiva around the implant, forming an epithelial cuff.



Moon (1999), [4] conducted a histological and morphometric examination of a 200 μm-wide zone of connective tissue interposed between the apical border of junctional epithelium and bone tissue.

This zone was divided into two units:

  • Zone A
  • Zone B.


Zone A

Zone A was the central zone, which was a 40 μm-wide unit, located immediately next to the implant surface. It was characterized by the absence of blood vessels and an abundance of fibroblasts (28%) interposed between the collagen fibers, which were oriented with their long axes parallel to the adjacent collagen fibers and implant surface.

Zone B

Zone B is a 160 μm-wide zone, which is continuous with zone A laterally. Compared to zone A, zone B consists of fewer fibroblasts (10%), more collagen Fibers, and more vascular structures.

Biological width

The biological width is a term used to describe the junctional epithelium and connective tissue that attaches to the root surface. The average length of the biological width is 2 mm (±30%). The connective tissue occupies 1.07 mm of the space above the crest of the alveolar bone and the junctional epithelium occupies 0.97 mm of the space below the gingival sulcus. These two spaces combine to form the biological width.

Violation of the biological width can have two different responses: It can either cause bone loss and gingival recession as the body tries to recreate room to allow space for tissue reattachment, or the bone level might remain unchanged and gingival inflammation develops and persists.

Berglundh and Lindhe [5] (1996) studied the dimensions of the peri-implant mucosa and concluded that the peri-implant mucosa is composed of a 2 mm-long junctional epithelium and a zone of connective tissue of around 1.3 mm. The author implied that a minimum width of peri-implant mucosa that may be required was around 3 mm, to allow a stable soft tissue attachment to form.


   Discussion Top


The peri-implant soft tissue acts as a transmucosal seal against bacterial irritants. It provides structural stability to withstand mechanical trauma, resist disruption of the junctional epithelial seal to the implant, and helps limit the apical spread of marginal inflammatory lesions that can lead to bone loss and eventually implant failure. The peri-implant soft tissues with appropriate contours create a self-cleansing environment for implant restoration, minimizing food accumulation, and thus, fulfilling the patient's expectation of a replacement that functions in the same fashion as the lost tooth, greatly increasing patient satisfaction.

One-stage (non-submerged) and Two-stage (initially submerged and subsequently exposed) peri-implant tissue was compared by Abrahamsson (1996). [6] Three implant fixtures (Astra Tech Implants Dental System, the Brånemark System, and the Bonefit - ITI system) were installed in beagle dogs. Histologically all tissue samples had a similar composition and dimensions. No quantitative or qualitative differences were observed. The junctional epithelium formed an attachment of about 2 mm to the abutment part of the fixture.

Weber et al., [7] in 1996 assessed healed tissues adjacent to 19 submerged and 19 non-submerged implants (rough surface Straumann titanium implants).He found no mean difference in the soft tissue height, and the marginal bone level was recorded from the implant tip to the coronal border of the mucosa. It was, therefore, concluded that a non-submerged one-stage installation technique may provide conditions for tissue integration that are similar to those obtained when using the submerged two-stage approach. The apical extension of the peri-implant epithelium was significantly greater for the submerged implants than for the intentionally non-submerged implants. Non-submerged implants displayed a greater mean height of connective tissue contact along the implant surface.

Abrahamsson et al., [8] conducted a study comparing four types of transmucosal abutments: Two commercially pure titanium (control), two ceramic abutments, one gold, and one short titanium abutment provided with dental porcelain fused to gold; placed onto Brånemark fixtures. Commercially pure titanium or ceramic abutment: Formation of mucosal attachment with an epithelial height of 2 mm and connective tissue height around 1-1.5 mm was observed.

Gold alloy or dental porcelain fused to gold abutment: No proper attachment formation at the abutment level was seen and the soft tissue margin receded, and bone resorption occurred, occasionally exposing the abutment fixture junction, and the mucosal seal became attached to the fixture portion of the implant. Furthermore, it is commonly accepted that ceramics and titanium dioxide are more resistant to corrosion than gold alloys or the surface layers of ceramics and titanium are chemically more stable, and therefore, readily allow cells to grow in contact with the surface. In all the specimens, infiltrates of inflammatory cells were consistently present in the mucosa lateral to the abutment/fixture junction - abutment ICT. The abutment ICT was greater in the ceramic abutment sites than in the controls, which was attributed to a larger microgap between the ceramic abutment and the fixture than titanium.

Abrahamsson et al., [9] conducted a study on five beagle dogs. Four implants made of commercially pure titanium were placed in the right edentulous mandibular premolar region. After three months, two different types of abutments were connected: Rough surface abutments (dual, thermal acid-etched surface 3I Osseotite® ) and regular smooth (turned) surface abutments were attached to the implant fixture. Both surfaces showed formation of barrier epithelium and a zone of connective tissue. Similar quantitative and qualitative soft tissue attachment occurred between the peri-implant mucosa and titanium abutments. The inner zone of the connective tissue attachment in both types of abutments was composed of about 30-33% fibroblasts and 63-66% collagen. The soft tissue attachment that formed on the implants made of C.P. titanium was not influenced by the roughness of the titanium surface.

The effect on the marginal peri-implant tissues following repeated abutment removal and the subsequent reconnection was studied. [10] Five beagle dogs were used. The mandibular premolars were extracted and two fixtures of the Brånemark system were installed, one in each mandibular quadrant. Three months later, the abutment connection was performed. A six-month period of plaque control was initiated. Once a month, during the plaque-control period, the abutment of the right side (test) in each dog was disconnected, cleaned, and reconnected to the fixture. Thus, every test abutment was removed and reconnected. The contralateral abutment remained undisturbed for six months and served as the control. One month after the last reconnection, examination of the tissues was performed. The findings indicate that the disconnections and subsequent reconnections of the abutment component of the implant compromised the mucosal barrier and resulted in a more 'apically' positioned zone of connective tissue. Bone resorption was also observed, which could be the result of tissue reactions initiated to establish a proper 'biological width' of the mucosal-implant barrier.

Cochran [11] examined the dimensions of the implantogingival junction in relation to clinically healthy, unloaded and loaded, non-submerged implants. In total, 69 titanium plasma-sprayed (TPS) and sandblasted acid-etched (SLA) implants were placed in an alternating fashion and allowed to heal for three months. Two dogs were sacrificed after the initial healing period. The remaining four dogs had crowns fabricated that were allowed to function for up to 12 months. These animals were sacrificed after three and twelve months of loading and histometric analysis was carried out. Biological width exists around unloaded and loaded, non-submerged, one-part, titanium implants and this is a physiologically formed and stable dimension as is found around teeth.

The seal, if violated, can lead to: [1] Inflammation of the adjacent soft tissue.




   Conclusion Top


An adequate zone of attached soft tissue with an intimate contact to the emerging implant structures thus becomes an important and pivotal factor for the long-term success of an implant restoration. This seal as a physiological barrier must be effective enough to prevent the ingress of bacterial plaque, toxins, oral debris or other deleterious substances from the oral environment.

 
   References Top

1.McKinney R, James RA: Tissues surrounding dental implants. In Misch CE, Contemporary implant dentistry, St Louis, Mosby 1993:369-86.  Back to cited text no. 1
    
2.Lindhe J, Lang NP, Karring T. Clinical periodontology and implant dentistry, 4 th edn, Blackwell Munksgaard, Oxford; 2003:830-7.  Back to cited text no. 2
    
3.Berglundh T, Lindhe J, Jonsson K, Ericsson I. The topography of the vascular systems in the periodontal and peri-implant tissues in the dog. J Clin Periodontol 1994;21:189-93.  Back to cited text no. 3
[PUBMED]    
4.Moon IS, Berglundh T, Abrahamsson I, Linder E, Lindhe J. The barrier between the keratinized mucosa and the dental implant. An experimental study in the dogs. J Clin Periodontol 1999;26:658-63.  Back to cited text no. 4
[PUBMED]    
5.Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's Clinical Periodontology: 10 th ed, Saunders, St.Louis Missouri; 2006:1072-87.  Back to cited text no. 5
    
6.Abrahamsson I, Berglundh T, Moon IS, Lindhe J. Peri-implant tissues at submerged and non-submerged titanium implants. J Clin Periodontol 1999;26:600-7.  Back to cited text no. 6
[PUBMED]    
7.Weber HP, Buser D, Donath K, Fiorellini JP, Doppalapudi V, Paquette DW, et al., Comparison of healed tissues adjacent to submerged and non-submerged unloaded titanium dental implants. A histomorphometric study in beagle dogs.Clin Oral Implants Res 1996;7:11-9.  Back to cited text no. 7
[PUBMED]    
8.Abrahamsson I, Berglundh T, Glantz PO, Lindhe J. The mucosal attachment at different abutments. An experimental study on dogs. J Clin Periodontol 1998;25:721-7.  Back to cited text no. 8
[PUBMED]    
9.Abrahamsson I, Zitzmann NU, Berglundh T, Linder E, Wennerberg A, Lindhe J. The mucosal attachment to titanium implants with different surface characteristics: An Experimental study in dogs. J Clin Periodontol 2002;29:448-55.  Back to cited text no. 9
[PUBMED]    
10.Abrahamsson I, Berglundh T, Lindhe J. The mucosal barrier following abutment dis/reconnection. An experimental study in dogs. J Clin Periodontol 1997;24:568-72.  Back to cited text no. 10
[PUBMED]    
11.Cochran DL, Hermann JS, Schenk RK, Higginbottom FL, Buser D. Biological width around titanium implants. A histometric analysis of the implanto-gingival junction around unloaded and loaded nonsubmerged implants in the canine mandible. J Periodontol 1997;68:186-98.  Back to cited text no. 11
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