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The document discusses the biological seal formed by gingival tissues around dental implants. Key points:
1) The gingival epithelium forms a biological seal that is important for minimizing infection risk and preventing apical migration of tissues. This seal acts as a physiological barrier.
2) The peri-implant mucosa has an epithelial and connective tissue component. The epithelial attachment is characterized by hemidesmosomes and a basal lamina. The connective tissue attaches directly to the implant surface via parallel collagen fibers.
3) A minimum biological width of 3mm is needed around implants to accommodate soft tissue healing and prevent bone resorption. Factors like initial tissue thickness and biotype impact cre
The document discusses the biological seal formed by gingival tissues around dental implants. Key points:
1) The gingival epithelium forms a biological seal that is important for minimizing infection risk and preventing apical migration of tissues. This seal acts as a physiological barrier.
2) The peri-implant mucosa has an epithelial and connective tissue component. The epithelial attachment is characterized by hemidesmosomes and a basal lamina. The connective tissue attaches directly to the implant surface via parallel collagen fibers.
3) A minimum biological width of 3mm is needed around implants to accommodate soft tissue healing and prevent bone resorption. Factors like initial tissue thickness and biotype impact cre
The document discusses the biological seal formed by gingival tissues around dental implants. Key points:
1) The gingival epithelium forms a biological seal that is important for minimizing infection risk and preventing apical migration of tissues. This seal acts as a physiological barrier.
2) The peri-implant mucosa has an epithelial and connective tissue component. The epithelial attachment is characterized by hemidesmosomes and a basal lamina. The connective tissue attaches directly to the implant surface via parallel collagen fibers.
3) A minimum biological width of 3mm is needed around implants to accommodate soft tissue healing and prevent bone resorption. Factors like initial tissue thickness and biotype impact cre
THE PERI IMPLANT MUCOSA BIOLOGIC WIDTH AROUND DENTAL IMPLANTS PROBING THE PERIIMPLANT MUCOSA COMPARISON OF TISSUES SURROUNDING NATURAL DENTITION AND ORAL IMPLANTS FACTORS AFFECTING SOFT TISSUES AROUND IMPLANTS BONE LOSS AND SOFT TISSUE HEALTH PERI IMPLANT MICROBIOLOGY CONTENTS Oral implants pierce through the mucosa, thus establishing the connection between the oral environment and the underlying tissues.
The soft tissue connection to the transmucosal part is of crucial importance as it relates to the stability of the peri implant tissues and the prevention of the peri implant infection with subsequent destruction of the peri implant structures.
Hermetic closure of the gingival tissues is important to minimize the risk of infection and prevent the apical down growth of the epithelium.
REGENERATION OF THE ATTACHED GINGIVA AND ITS ABILITY TO FORM A GINGIVAL SULCUS LINED BY CREVICULAR EPITHELIUM McKinney et al 1984 SYSTEMATIC SCIENTIFIC STUDY TO INVESTIGATE THE SEAL PHENOMENON James and Kelln1974, 1981 NECESSITY FOR ATTACHED GINGIVA TO APPROPRIATELY ADAPT TO THE IMPLANT Lavelle 1981 CONCEPT OF A SEAL AROUND THE DENTAL IMPLANTS Weinmann 1956 EARLY CIVILIZATIONS LATE 19 th and EARLY 20 th CENTURIES Gramm CT (1898) Lewis (1889) The concept of the gingival epithelium in forming a biological seal is one of great importance in implant dentistry PERMUCOSAL PASSAGE A WEAK LINK A zone where initial tissue breakdown begins that can result in eventual tissue necrosis and destruction around implants. The seal is a physiological barrier to prevent ingress of bacterial plaque,toxins, oral debris.. 1 INFLAMMATION OF SOFT TISSUES 2 OSTEOCLASTIC ACTIVITY 3 CHRONIC RESORPTION OF SUPPORTING BONE 4 FILL WITH GRANULATION TISSUE 5 IMPLANT MOBILITY 6 PERCOLATION OF BACTERIAL TOXINS AND DEGENERATIVE AGENTS FURTHER INTO THE INTERNAL ENVIRONMENT SURROUNDING THE IMPLANT 7 ACUTE SUPPURATIVE INFLAMMATION 8 EXTENSIVE MOBILITY 9 RENDERING SUPPORT TO PROSTHESIS IMPRACTICAL 10 IMPLANT TO BE REMOVED PERIIMPLANT MUCOSA EPITHELIAL COMPONENT PERIIMPLANT MUCOSA CONNECTIVE TISSUE
The interface between the epithelial cells and the titanium surface is characterized by the presence of hemidesmosomes and a basal lamina.
EA: Epithelial Attachment, LBI: Lamina Basalis Interna, LBE: Lamina Basalis Externa, BC: Basal Complex, a junctional epithelium, b sulcular epithelium, c oral epithelium; T/I : Titanium Implant, LL: Lamina Lucida, LD: Lamina Densa, HD: Hemidesmosomes, D: Desmosomes a junctional epithelium, b sulcular epithelium, c oral epithelium; Im : Implant, Ab: Abutment, MR: Margin of gingiva, Bo: Bone, A/I : Abutment/ Implant junction, aAE : apical point of attached epithelium 1. Implant Crown 2. Vertical alveologingival ct fibers 3. Circular gingival fibers 4. Circular gingival fibers 5. Periosteal gingival ct fibers
The connective tissue appears to be in direct contact with the surface (TiO) of the implant. The collagen fibers in this connective tissue form bundles which run PARALLEL to the implant surface. They can also have a cuff like circular orientation. Higher amounts of collagen type V and VI were noticed. Capillary loops under JE and SE
Moon et al (1999) reported that the attachment tissue close to the implant contains only few blood vessels but a large number of fibroblasts that were oriented with their long axes parallel with the implant surface. In more lateral compartments, there were fewer fibroblasts but more collagen fibers and more vascular structures.
Berglundh et al (1994) observed that the vascular system of the peri implant mucosa originates SOLELY from the LARGE SUPRAPERIOSTEAL BLOOD VESSEL on the outside of the alveolar ridge.
B.W. Epithelial attachment Supracrestal connective tissue zone 3 to 4mm 2mm 1mm A MINIMUM DIMENSION OF THE BIOLOGICAL WIDTH IS NEEDED IN ORDER TO ACCOMMODATE FOR THE SOFT TISSUE HEALING PROCESS; WHEN THIS DIMENSION IS NOT PRESENT, BONE RESORPTION MAY OCCUR TO ALLOW FOR AN APPROPRIATE BIOLOGICAL DIMENSION
DAY 0: COAGULUM OCCUPIES SPACE BETWEEN MUCOSA AND IMPLANT SURFACE DAY 4: GRANULOCYTES INFILTRATE CLOT; INITIAL SEAL 1 WEEK: FIBROBLASTS AND COLLAGEN FIBERS 2 WEEKS: CONNECTIVE TISSUE RICH IN CELLS AND VASCULARITY; JUNCTIONAL EPI STARTS TO FORM 4 WEEKS: JUNCTIONAL EPITHELIUM FORMS; MATURE CT MORPHOGENESIS OF PERI IMPLANT MUCOSA (BERGLUNDH et al 2007) I n case of an implant probe goes beyond the sulcus and reaches closer to the bone Ericsson and Lindhe (1993) Probing caused both compression and lateral dislocation of the peri implant mucosa, and the average histologic probing depth was markedly deeper than at the tooth site: 2mm vs 0.7 mm. The tip of the probe was consistently positioned deep in the connective tissue/ abutment interface and apical of the barrier epithelium. Distance between probe tip and the bone crest was 0.2 mm.
The depth of the probe penetration reveals the thickness of the mucoperiosteum through which the abutment/ restoration is emerging rather than a loss of attachment. FLEXIBLE PLASTIC PROBE FOR PROBING AROUND IMPLANTS Recommended to not probe the implant for at least 3 months following abutment attachment to avoid disrupting the permucosal seal COMPARISON OF TOOTH AND IMPLANT SUPPORT STRUCTURES STRUCTURE TOOTH IMPLANT Connection Cementum, bone , periodontium Osseointegration , bone functional ankylosis Junctional epithelium Hemidesmosomes and basal lamina ( lamina lucida and lucida , lamina densa zones ) Hemidesmosomes and basal lamina ( lamina , lamina densa and sublamina lucida zones ) Connective tissue 13 groups : perpendicular to tooth surfaces Decreased collagen, increased fibroblasts Only 2 groups : parallel and circular fibers . No attachment to the implant surface and bone Increased collagen and decreased fibroblasts Biological width 2.04 to 2.91 mm 3.08 mm
Vascularity Greater ; supraperiosteal and periodontal ligament Less ; periosteal Probing depth 3mm in health
2.5 to 5.0mm ( depending on soft tissue depth ) Bleeding on probing More reliable Less reliable Attachment between the periodontal tissue and the root surface Attachment between the peri-implant tissue and an implant surface Periotest was originally devised by Dr. Schulte to measure tooth mobility. Teerlinck, et al.(1991) used this method to overcome destructive methods in measuring the implant stability. Periotest evaluates the damping capacity of the periodontium. It is designed to identify the damping capacity and the stiffness of the natural tooth or implant by measuring the contact time of an electronically driven and electronically monitored rod after percussing the test surface. Periotest value(PTV) is marked from -8(low mobility) to +50(high mobility). PTV of -8 to -6 is considered good stability. Control Box +Probe PROBE APPLI ED HORI ZONTALLY MUCOSAL THICKNESS SURGICAL PROCEDURE LOADING TITANIUM SURFACES AND ABUTMENT MATERIALS
IMPLANT STRUCTURE AND POSITION
IMMEDIATE POST EXTRACTIVE INSERTION
THIN BIOTYPE OCHSENBEIN &ROSS THICK BIOTYPE DELICATE AND FRIABLE REACTS TO INJURY BY RECESSION AMOUNT OF KERATINIZED MUCOSA USUALLY QUITE SMALL DENSER AND MORE FIBROTIC GINGIVA MIMICKING THE FLATTER AND THICKER UNDERLYING OSSEOUS ARCHITECTURE MORE RESISTANT TO INJURY
PROBE VISIBLE THROUGH THE THIN GINGIVA THIN BIOTYPE MORE PRONE TO CRESTAL BONE RESORPTION AVOID SUPRACRESTAL PLACEMENT THICK BIOTYPE LESS CRESTAL BONE RESORPTION SUPRACRESTAL PLACEMENT MINIMIZES BONE LOSS A minimum of 3 mm of peri implant mucosa is required for a stable epithelial connective tissue attachment to form.
Linkevicious et al in a human study done to compare the effects of tissue thickness at the time of surgery on crestal bone changes around non submerged implants after one year follow up found that positioning an implant 2mm supra crestally did not prevent crestal bone loss, if THIN GINGIVAL TISSUES are present at the time of implant placement. Implants with thin tissue underwent additional bone loss interproximally than the group with thick tissue pattern which had significantly less bone loss.
Initial tissue thickness if less than 2.5 mm leads to an expected bone loss of 1.45 mm within the first year of function.
In thick tissues, >2.5 mm or more, marginal bone recession can be avoided if the implant abutment junction is 2mm or above the bone level, minimal 0.2 mm
Thin Biotypes Thick maintain papillary height GINGIVAL RECESSION Apical and lingual direction Facial plate loss GRAYISH COLOR ALVEOLAR BONE RESORPTION
ESTHETIC MANAGEMENT TRIAD Abrahamsson et al 1996 : Evaluated the influence of the surgical protocol (one stage vs. two stage) on the soft tissue healing around 3 different implant systems. Histological results demonstrated similar dimensions and composition of the epithelial and connective tissue components.
Abrahamsson et al 1999 THE SURGICAL PROTOCOL (i.e. one or two stage surgical protocol) do not influence the dimensions and composition of the biological width. It was observed that the mucosa that formed at implants placed in a submerged or a non submerged procedure had many features in common THE DEEPER THE IMPLANT SHOULDER POSITION IN BONE THE LONGER THE BIOLOGICAL WIDTH.
Cochran et al. 1997 Evaluated the dimensions of the implanto gingival junction around non submerged loaded and not loaded implants at 3 and 12 months after implant placement.
SD: 0.50 mm JE: 1.44 mm CT: 1.01 mm LOADED SD: 0.49mm JE: 1.16 mm CT: 1.36 mm UNLOADED Abrahamsson et al. Analyzed soft tissue healing to abutments made of titanium, gold alloy, dental porcelain and AlO ceramic
Failed to form an attachment Gold alloy and porcelains Formed attachment with similar dimensions and tissue structures Titanium and ceramic Abrahamsson et al. 2002 Demonstrated that surface characteristics (smooth vs rough titanium surfaces) do not influence the biologic width dimension.
ABUTMENT IMPLANT INTERFACE MICROGAP LEVEL BONE CREST LEVEL OF THE INTERFACE SUBMERGED AND NON SUBMERGED CRESTAL BONE LOSS IN VARIOUS CASES SUBMERGED Implant placed into the bone and the top of the implant placed at or below the bone crest Soft tissues are closed over the bone and implant thereby submerging it NON SUBMERGED Implant extends coronally beyond the alveolar crest where the soft tissue flap is placed around the implant body Second intervention not needed Hermann et al 2000 Study on 6 types of implants A C NON SUBMERGED D F SUBMERGED A : 6mm R/S at bone crest B: 5mm; R/S 1mm below A,B: ONE PIECE; No interface C, D: 4.5 mm interface at bone crest E,F : 4.5 mm interface 1 mm above and 1mm below the crest
MEASUREMENTS: 1. Distance between the top of the implant (top) and first bone to implant contact (fBIC) for A and B. 2. Distance between interface (microgap) of the implant (IF) and fBIC 3. Top and R/S for A and B. 4. IF R/S (for C F).
TYPE TOP - fBIC R/S - fBIC MICROGAP - fBIC A 2.98 mm 0.19 mm B 3.88 mm 0.01 mm C 1.68 mm 0.39 mm D 0.28 mm 1.57 mm E 0.06 mm 2.64 mm F 0.89 mm 1.25 mm GREATEST BONE LOSS WAS OBSERVED AROUND TYPE F (2.25mm) TYPES C, D F: SEVERE SIGNS OF CLINICAL INFLAMMATION TYPE A AND B : SLIGHT INFLAMMATION R/S fBIC
IN ALL 2 PIECE IMPLANTS, THE LOCATION OF THE INTERFACE (MICROGAP) WHEN LOCATED AT OR BELOW THE ALVEOLAR CREST DETERMINES THE AMOUNT OF BONE RESORPTION
A and B showed minimal signs of clinical inflammation C, D F Moderate to Severe signs of disease
2 piece implants Abutment implant junction: Microgap Crestal bone resorption FURTHER BIOLOGICAL WIDTH CHANGES, INCREASED SUBGINGIVAL BACTERIAL COLONIZATION LEADING TO FURTHER BONE LOSS INEVITABLE 1.5 mm during first year 0.1 mm in subsequent years The greatest crestal bone loss occurs with 2 piece implants when the interface located below the crest rather than at or above the crestal bone level. Osseous changes influence the location of the gingival margin and the dimensions of the biologic width.
SIGNIFICANT CRESTAL BONE LOSS OCCURS IN 2 PIECE IMPLANT CONFIGURATIONS EVEN WITH THE SMALLEST SIZE OF THE MICROGAP (<10m) IN COMBINATION WITH POSSIBLE MOVEMENTS BETWEEN IMPLANT COMPONENTS
Schultes and Gaggl 2001 Compared healing at implants placed in a healed ridge and implants immediately placed in fresh extraction sockets at 8 months have reported a LARGER DIMENSION OF SOFT TISSUE BARRIER IN IMPLANTS PLACED IMMEDIATELY
Both of these are characterized by an inflammatory reaction in the tissues surrounding an implant.
Peri-implant mucositis has been described as a disease in which the presence of inflammation is confined to the soft tissues surrounding a dental implant with no signs of loss of supporting bone following initial bone remodeling during healing.
Peri-implantitis has been characterized by an inflammatory process around an implant, which includes both soft tissue inflammation and progressive loss of supporting bone beyond biological bone remodeling Peri-implant diseases present in two forms PERI-IMPLANT MUCOSITIS PERI-IMPLANTITIS The term peri-implantitis was introduced in the 1980s (Mombelli A,1987)
Formerly used terms as implant histoclasia and peri implantoclasia accepted in the 1963 edition of Current Clinical Dental Terminology.
Peri implantitis was defined as an inflammatory reaction with loss of supporting bone in tissues surrounding a functioning implant Albrektsson T et al, Proceedings of the 1 st European Workshop on Periodontology, 1994
While peri-implant mucositis is a reversible inflammatory condition confined to the peri-implant soft-tissue unit, peri-implantitis is characterised by progressive inflammatory destruction of the crest of the alveolar bone supporting the implant, by increased peri- implant probing depths, and by bleeding and/or suppuration on probing.
Additionally, peri-implant mucositis may be successfully treated using non-surgical efforts if detected early, whereas peri-implantitis usually requires surgical treatment.
Main Diagnostic Differences Between Peri-implant Mucositis And Peri- implantitis
Increased probing depth +/- + BOP + + Suppuration +/- + Mobility - +/- Radiographic bone loss - + (a)Peri-implant mucositis presenting with changes in color, form, and texture
(b)Peri-implant mucositis presents radiographically with no change in crestal bone (a) Peri-implantitis presenting with changes in color, form, texture, and associated bone loss resulting in increased probing depth
(b) Peri implantitis radiographically demonstrates crestal bone resorption
Saucer shaped destruction of the crestal bone or wedge-shaped defects along the implant. Bone destruction may proceed without any notable signs of implant mobility until osseointegration is completely lost. Vertical bone destruction is associated with the formation of a peri-implant pocket. Bleeding after gentle probing with a blunt instrument There may be suppuration from the pocket. Tissues may or may not be swollen. Hyperplasia is frequently seen Pain is not a typical feature of peri-implantitis.
MICROBIOLOGY OF PERI- IMPLANT AREA
INITIAL COLONIZATION The microflora associated with stable osseointegrated implants serving successfully as abutments for overdentures was investigated in 18 edentulous patients. 50% FACULTATI VELY ANAEROBI C COCCI 17% FACULTATI VELY ANAEROBI C RODS 7% GRAM NEGATI VE ANAEROBI C RODS 9% F.nucleatum, P.intermedia Porphyromonas gingivalis and Spirochetes not found
PARTIALLY EDENTULOUS RIDGES Higher percentages of black pigmenting Gram negative anaerobes and wet spreaders (Capnocytophaga) MI CROBI AL STATUS OF THE REMAINI NG TEETH I NFLUENCES THE FATE OF NEWLY I NCORPORATED I MPLANTS
Thus the teeth microbiota are the primary source of putative pathogens.
MICROBIOLOGY OF DISEASED IMPLANTS Microbiology plays important role in etiology of peri- implantitis
The main cause of peri- implantitis is dental plaque (Meffert R.M.)
Aggretebacter actinomycetemcomitans Porphyromonas gingivalis Bacteroides forsythus Fusobacterium nucleatum Campylobacter Peptostreptococcus micros Prevotella intermedia ( Tanner A et al, 1997) From an experimental study it was reported that: For teeth, 3 weeks to 3 months of undisturbed plaque accumulation resulted in no further extension of the inflammatory lesion. However, for implants, under identical experimental conditions, a further spread in apical direction of the inflammatory cell infiltrate was consistently observed.
This implies that the defense mechanism of the gingiva may be more effective than that of the peri-implant mucosa in preventing further apical propagation of the pocket microbiota.