[Healing of the dento-gingival junction following modified crown lengthening procedure in beagle dogs].

OBJECTIVE: To evaluate the type of wound healing following modified crown lengthening surgery in dog model to provide a biological basis for its clinical application. METHODS: Flap surgery, traditional crown lengthening procedure and modified crown lengthening procedure were performed on the right maxillary central incisor, the left maxillary central incisor and the left maxillary first lateral incisor respectively of five male beagle dogs. The right maxillary first lateral incisors with no surgical intervention were used as controls. Thirty-six weeks after the experimental procedure, tissue blocks were harvested and prepared for histological examination and analysis. RESULTS: Histometric examination of buccolingual sections stained with hematoxylin-eosin demonstrated that the type of wound healing in the flap surgery group was re-attachment, similar to the control group. For the traditional crown lengthening surgery group, all of the five beagle dogs had lamellar cementum defects on root surface, the wound healing of four beagle dogs was new attachment accompanied by new cementum formation at cementum defect areas and the suprac-restal connective tissue was functionally oriented perpendicular to the new cementum. The wound healing of the other beagle dog was long junctional epithelial attachment, in which the junctional epithelium extended to the apical terminus of the cementum defect. In the modified crown lengthening surgery group, four beagle dogs had cementum defects on root surface (two lamellar cementum defects and two shallow platform-like cementum defects), the wound healing of three beagle dogs was new attachment, however, the supracrestal connective tissue was parallel to the root surface. The type of wound healing of another one beagle dog was long junctional epithelial attachment. Wound healing of one beagle dog in this group could not be characterized due to incomplete dissection. CONCLUSION: Wound healing in the modified crown lengthening surgery group was similar to the traditional crown lengthening surgery group, and two types of wound healing were observed: new attachment and long junctional epithelium attachment. Neither type of root treatment procedure (root planing or root reshaping) nor root surface defect pattern (the lamellar cementum defect or shallow platform-like cementum defect) influenced the observed type of wound healing.

The Roles of FOXO1 in Periodontal Homeostasis and Disease.

Periodontitis is an oral chronic inflammatory disease that is initiated by periodontal microbial communities and requires disruption of the homeostatic responses. The prevalence of periodontal disease increases with age; more than 70% of adults 65 years and older have periodontal disease. A pathogenic microbial community is required for initiating periodontal disease. Dysbiotic immune-inflammatory response and bone remodeling are characteristics of periodontitis. The transcription factor forkhead box protein O1 (FOXO1) is a key regulator of a number of cellular processes, including cell survival and differentiation, immune status, reactive oxygen species (ROS) scavenging, and apoptosis. Although accumulating evidence indicates that FOXO1 activity can be induced by periodontal pathogens, the roles of FOXO1 in periodontal homeostasis and disease have not been well documented. The present review summarizes how the FOXO1 signaling axis can regulate periodontal bacteria-epithelial interactions, immune-inflammatory response, bone remodeling, and wound healing.

Aggregatibacter Actinomycetemcomitans Induces Autophagy in Human Junctional Epithelium Keratinocytes.

The adverse environmental conditions found in the periodontium during periodontitis pathogenesis stimulate local autophagy responses, mainly due to a continuous inflammatory response against the dysbiotic subgingival microbiome. The junctional epithelium represents the main site of the initial interaction between the host and the dysbiotic biofilm. Here, we investigated the role of autophagy in junctional epithelium keratinocytes (JEKs) in response to Aggregatibacter actinomycetemcomitans or its purified lipopolysaccharides (LPS). Immunofluorescence confocal analysis revealed an extensive nuclear translocation of transcription factor EB (TFEB) and consequently, an increase in autophagy markers and LC3-turnover assessed by immunoblotting and qRT-PCR. Correspondingly, challenged JEKs showed a punctuate cytosolic profile of LC3 protein contrasting with the diffuse distribution observed in untreated controls. Three-dimensional reconstructions of confocal images displayed a close association between intracellular bacteria and LC3-positive vesicles. Similarly, a close association between autophagic vesicles and the protein p62 was observed in challenged JEKs, indicating that p62 is the main adapter protein recruited during A. actinomycetemcomitans infection. Finally, the pharmacological inhibition of autophagy significantly increased the number of bacteria-infected cells as well as their death, similar to treatment with LPS. Our results indicate that A. actinomycetemcomitans infection induces autophagy in JEKs, and this homeostatic process has a cytoprotective effect on the host cells during the early stages of infection.

Topical application of glycyrrhetinic acid in the gingival sulcus inhibits attachment loss in lipopolysaccharide-induced experimental periodontitis in rats.

BACKGROUND AND OBJECTIVE: Attachment loss of the junctional epithelium and alveolar bone destruction are signs of periodontitis, which is mainly caused by an inflammatory response to dental plaque. Glycyrrhetinic acid (GA), a component of the licorice herb, has been shown to have important anti-inflammatory activities; however, there are no previous reports on the ability of its inhibitory effects to prevent periodontal diseases. Hence, in this study, using our experimental periodontitis model, we attempted to evaluate whether GA had an effect on the prevention of attachment loss and alveolar bone loss. MATERIAL AND METHODS: Rats were intraperitoneally immunized with Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 5) received 3 topical applications of 50 µg/µL of LPS followed by one application of the vehicle (propylene glycol:ethyl alcohol:phosphate-buffered saline [PBS] = 8:1:1) into the gingival sulcus. This protocol was repeated twice per day for 10 days. The low (n = 5) and high (n = 5) groups received topical application of LPS and 0.03% or 0.3% GA, respectively. The control group received topical application of PBS and vehicle. The rats were killed on the 10th day. Attachment loss, alveolar bone level and inflammatory cell infiltration were investigated histometrically. The formation of immune complexes and infiltration of LPS were evaluated immunohistologically. RESULTS: Attachment loss, formation of immune complexes and infiltration of inflammatory cells were increased in the LPS group compared with the control group, and were completely inhibited in the low and high groups compared with the LPS group. The LPS group showed greater alveolar bone destruction compared with the control group and GA-treated groups. In addition, invasion of LPS was detected in the LPS group, was absent in the control group and was weaker in the GA-treated groups than in the LPS group. CONCLUSION: In the present study, we showed that GA inhibits periodontal destruction in the rat experimental periodontitis model.

Polydopamine deposition with anodic oxidation for better connective tissue attachment to transmucosal implants.

BACKGROUND AND OBJECTIVE: Nowadays, most designs for the transmucosal surface of implants are machined-smooth. However, connective tissue adhered to the smooth surface of an implant has poor mechanical resistance, which can render separation of tissue from the implant interface and induce epithelial downgrowth. Modification of the transmucosal surface of implants, which can help form a good seal of connective tissue, is therefore desired. We hypothesized that anodic oxidation (AO) and polydopamine (PD) deposition could be used to enhance the attachment between an implant and peri-implant connective tissue. We tested this hypothesis in the mandibles of Beagle dogs. MATERIAL AND METHODS: AO and PD were used to modify the transmucosal region of transmucosal implants (implant neck). The surface microstructure, surface roughness and elemental composition were investigated in vitro. L929 mouse fibroblasts were cultured to test the effect of PD on cell adhesion. Six Beagle dogs were used for the in vivo experiment (n = 6 dogs per group). Three months after building the edentulous animal model, four groups of implants (control, AO, PD and AO + PD) were inserted. After 4 months of healing, samples were harvested for histometric analyses. RESULTS: The surfaces of anodized implant necks were overlaid with densely distributed pores, 2-7 µm in size. On the PD-modified surfaces, N1s, the chemical bond of nitrogen in PD, was detected using X-ray photoelectron spectroscopy. L929 developed pseudopods more quickly on the PD-modified surfaces than on the surfaces of the control group. The in vivo experiment showed a longer connective tissue seal and a more coronally located peri-implant soft-tissue attachment in the AO + PD group than in the control group (P < .05). CONCLUSION: The modification of AO + PD on the implant neck yielded better attachment between the implant and peri-implant connective tissue.

Comparison of peri-implant and periodontal marginal soft tissues in health and disease.

The integrity of the peri-implant soft-tissue seal is crucial for maintaining peri-implant tissue health. Whilst the transmucosal component of the restored implant shares some common features with teeth, namely the presence of a junctional epithelium and a connective tissue component, there are some important differences. A key difference is the nature of the relationship of the connective tissue with the implant surface, whereby there is 'adaptation' of collagen fibers in a parallel orientation in relation to the implant, but insertion of fiber attachment perpendicularly into cementum in the case of teeth. This, combined with reduced cellularity and vascularity in the peri-implant connective tissue, may make implants more susceptible to disease initiation and progression. Furthermore, the presence of a subgingival connection between the implant and the abutment/restoration poses some specific challenges, and maintaining the integrity of this connection is important in preserving peri-implant tissue health. Implant design features, such as the nature of the connection between the implant and the abutment, as well as the surface characteristics of the abutment and implants, may influence the maintenance of the integrity of soft tissue around implants. Iatrogenic factors, such as incorrect seating of the abutment and/or the restoration, and the presence of residual subgingival cement, will lead to loss of soft-tissue integrity and hence predispose to peri-implant disease.

The periodontal pocket: pathogenesis, histopathology and consequences.

The conversion of junctional epithelium to pocket epithelium is regarded as a hallmark in the development of periodontitis. Knowledge of factors contributing to the initiation and progression of pocket formation is important and may result in the development of better preventive measures and improve healing outcomes after therapeutic interventions. The periodontal pocket is a pathologically deepened gingival sulcus. In healthy periodontal conditions, the defense mechanisms are generally sufficient to control the constant microbiological challenge through a normally functioning junctional epithelium and the concentrated powerful mass of inflammatory and immune cells and macromolecules transmigrating through this epithelium. In contrast, destruction of the structural integrity of the junctional epithelium, which includes disruption of cell-to-cell contacts and detachment from the tooth surface, consequently leading to pocket formation, disequilibrates this delicate defense system. Deepening of the pocket apically, and also horizontal expansion of the biofilm on the tooth root, puts this system to a grueling test. There is no more this powerful concentration of defense cells and macromolecules that are discharged at the sulcus bottom and that face a relatively small biofilm surface in the gingival sulcus. In a pocket situation, the defense cells and the macromolecules are directly discharged into the periodontal pocket and the majority of epithelial cells directly face the biofilm. The thinning of the epithelium and its ulceration increase the chance for invasion of microorganisms and their products into the soft connective tissue and this aggravates the situation. Depending on the severity and duration of disease, a vicious circle may develop in the pocket environment, which is difficult or impossible to break without therapeutic intervention.

Observation and determination of periodontal tissue profile using optical coherence tomography.

BACKGROUND AND OBJECTIVE: Diagnosis is a crucial step in periodontal treatment. The aim of this study was to evaluate the effectiveness of optical coherence tomography (OCT) for observation and determination of periodontal tissue profiles in vivo. MATERIAL AND METHODS: In experiment 1, refractive indices of purified water, porcine gingiva and human gingiva at 1330 nm were determined for the analysis of OCT images of periodontal tissues. In experiment 2, OCT examination was performed in the midlabial apico-coronal plane of mandibular anteriors in 30 Asian volunteers with healthy gingiva. Sulcus depth was measured on intra-oral photographs taken during probing. In the OCT images, the gingival, epithelial and connective tissue thickness, and the position of alveolar bone crest were determined and finally, the biologic width was measured. RESULTS: Refractive indices of purified water, porcine gingiva and human gingiva were 1.335, 1.393 and 1.397, respectively. Cross-sectional images of gingival epithelium, connective tissue and alveolar bone were depicted in real-time. The sulcular and junctional epithelium could be visualized occasionally. Laser penetration and reflection were limited to a certain depth with an approximate maximal imaging depth capability of 1.5 mm and OCT images of the periodontal structure were not clear in some cases. The average maximal thickness of gingiva and epithelium and biologic width at the mandibular anteriors were 1.06 ± 0.21, 0.49 ± 0.15 and 2.09 ± 0.60 mm, respectively. CONCLUSION: OCT has promise for non-invasive observation of the periodontal tissue profile in detail and measurement of internal periodontal structures including biologic width in the anterior region.

Biodegradable gelatin/beta-tricalcium phosphate sponges incorporating recombinant human fibroblast growth factor-2 for treatment of recession-type defects: A split-mouth study in dogs.

BACKGROUND AND OBJECTIVE: Tissue engineering by using recombinant human (rh) growth factor technology may offer a promising therapeutic approach for treatment of gingival recession. Fibroblast growth factor-2 (FGF-2) has shown the ability to promote periodontal regeneration. Gelatin/beta-tricalcium phosphate (gelatin/ß-TCP) sponges have been developed to control the release of growth factors. The present study evaluated the periodontal regenerative efficacy of rhFGF-2 by comparing gelatin/ß-TCP sponges incorporated with rhFGF-2 to the scaffolds alone in artificially created recession-type defects in dogs. MATERIAL AND METHODS: Critically sized buccal gingival recession defects were surgically created on maxillary canine teeth of five dogs. In each animal, defects were randomized to receive either a gelatin/ß-TCP sponge soaked with rhFGF-2 (gelatin/ß-TCP/rhFGF-2) or phosphate-buffered saline (gelatin/ß-TCP). Eight weeks after surgery, biopsy specimens were obtained and subjected to microcomputed tomography and histological analyses. RESULTS: Complete root coverage was achieved in both groups. Microcomputed tomography revealed significantly greater new bone volume in the gelatin/ß-TCP/rhFGF-2 group. Histologically, both groups achieved periodontal regeneration; however, gelatin/ß-TCP/rhFGF-2 sites exhibited more tissue regeneration, characterized by significantly larger amounts of new cementum and new bone. Gelatin/ß-TCP sites featured increased long junctional epithelium and connective tissue attachment. In the gelatin/ß-TCP/rhFGF-2 sites, new bone exhibited many haversian canals and circumferential lamellae as well as remarkably thick periosteum with blood vascularization and hypercellularity. CONCLUSION: Within the limitations of this study, rhFGF-2 in gelatin/ß-TCP sponges exhibits an increased potential to support periodontal wound healing/regeneration in canine recession-type defects.

The histopathological comparison on the destruction of the periodontal tissue between normal junctional epithelium and long junctional epithelium.

BACKGROUND AND OBJECTIVE: The barrier function of long junctional epithelium is thought to be important after periodontal initial therapy and periodontal surgery. Although the difference between long junctional epithelium and normal junctional epithelium regarding their resistance to destruction of periodontal tissue has been investigated, the mechanism still remains unclear. Using our rat experimental periodontitis model in which loss of attachment and resorption of alveolar bone is induced by the formation of immune complexes, we investigated the resistance of periodontal tissue containing long junctional epithelium and normal junctional epithelium to destruction. MATERIAL AND METHODS: Rats were divided into four groups. In the immunized long junctional epithelium (I-LJE) group, rats were immunized with lipopolysaccharide (LPS), and curettage and root planing procedures were performed on the palatal gingiva of the maxillary first molars to obtain reattachment by long junctional epithelium. In the immunized normal junctional epithelium (I-JE) group, rats were immunized without curettage and root planing procedures. In the nonimmunized long junctional epithelium (nI-LJE) group, rats were not immunized but curettage and root-planing procedures were performed. In the control group, neither immunization nor curettage and root-planing was performed. In all rats, periodontal inflammation was induced by topical application of LPS into the palatal gingival sulcus of maxillary first molars. The rats were killed at baseline and after the third and fifth applications of LPS. Attachment loss and the number of inflammatory cells and osteoclasts in the four groups were compared histopathologically and histometrically. RESULTS: After the third application of LPS in the I-LJE group, attachment loss showed a greater increase than in control and nI-LJE groups, and inflammatory cell infiltration and osteoclasts were increased more than in the other groups. After the fifth application of LPS, attachment loss was greater and there was a higher degree of inflammatory cell infiltration in nI-LJE and I-LJE groups than in control and I-JE groups. CONCLUSION: Our findings suggest that the destruction of periodontal tissue is increased in tissue containing long junctional epithelium compared with normal junctional epithelium and that the immunized condition accelerates the destruction by forming immune complexes.

Influence of Four Different Abutment Materials and the Adhesive Joint of Two-Piece Abutments on Cervical Implant Bone and Soft Tissue.

PURPOSE: The main aim of this study was to evaluate the influence of four different abutment materials and the adhesive joint of two-piece abutments on the cervical implant bone and soft tissue. MATERIALS AND METHODS: Sixty-four titanium implants (Camlog Conelog; 4.3 ± 9 mm) were placed bone level into the edentulous arches of four minipigs. Four different types of abutments were placed at implant exposure: zirconium dioxide, lithium disilicate, and titanium bonded to a titanium luting base with resin cement; one-piece titanium abutments served as the control. The animals were sacrificed 6 months after implant exposure, and the bone-to-implant contact (BIC) area, sulcus depth, the length of the junctional epithelium and the connective tissue, the biologic width, and first cervical BIC-implant shoulder distance were measured using histomorphometry and light and fluorescence microscopy. RESULTS: Overall, 14 implants were lost (22%). At exposure, the implant shoulder-bone distance was 0.6 ± 0.7 mm. Six months later, the bone loss was 2.1 ± 1.2 mm measured histomorphometrically. There was a significant difference between the two measurements (P ≤ .0001). No significant influence could be found between any of the abutment materials with regard to bone loss or soft tissue anatomy (P > .05), with the exception of zirconium dioxide and onepiece titanium abutments when measuring the length of the junctional epithelium (P ≤ .01). The maxilla provided significantly more soft tissue and less bone loss compared with the mandible (P ≤ .02). CONCLUSION: All tested abutment materials and techniques seem to be comparable with regard to soft tissue properties and the cervical bone level.

Localized juvenile spongiotic gingival hyperplasia possibly originates from the junctional gingival epithelium-an immunohistochemical study.

AIMS: To immunohistochemically evaluate the cytokeratin (CK) pattern of expression in localized juvenile spongiotic gingival hyperplasia (LJSGH) as compared with the gingival epithelium (GE). METHODS AND RESULTS: Ten cases of LJSGH were semiquantitatively evaluated for the immunohistochemical pattern of CK1/10, CK4, CK8/18, and CK19. GE controls were taken from 10 cases of reactive gingival fibroepithelial hyperplasia. GEs showed mean positivity rates of 80% for both CK1/10 and CK4, and 5% for both CK8/18 and CK19. LJSGHs showed mean positivity rates of 65% for CK19, 60% for CK8/18, 30% for CK4, and 5% for CK1/10. The differences between LJSGHs and GEs were statistically significant (P < 0.01). CONCLUSIONS: The LJSGH pattern of CK expression is reminiscent of the profile described in the literature for the junctional epithelium (JE). Possibly, JE exteriorized from the gingival sulcus would be more prone to irritation from a variety of sources, resulting in inflammation and hyperplasia, with the subsequent development of LJSGH.

Effect of Platform Shift/Switch on Crestal Bone Levels and Mucosal Profile Following Flapless Surgery and Crestal/Subcrestal Implant Placement.

BACKGROUND: Crestal remodeling/bone loss appears a common sequel to dental implant placement. Several hypotheses and clinical strategies have been advanced to explain and avert crestal remodeling; however, causative mechanisms remain unclear and the efficacy of clinical protocol uncertain. OBJECTIVE: The objective of the present study was to provide a histologic record of crestal versus subcrestal implant placement on crestal remodeling and mucosal profile comparing platform shift/switch and standard abutments following flapless implant surgery using a dog model. METHODS: Four dental implants each were placed into the left and right edentulated posterior mandibles in five adult male hound-Labrador mongrel dogs using a flapless approach including crestal versus subcrestal placement and using platform shift versus standard abutments. Block biopsies were collected for histological/histometric analysis following an 8-week healing interval. RESULTS: Both crestal and subcrestal implant installation resulted in significant crestal remodeling and bone loss, in particular at buccal sites, without significant differences between platform shift/switch and standard abutments. Implants installed subcrestally exhibited a significantly taller mucosal profile over crestal-level implants without significant differences between platform shift/switch and standard abutments; the epithelial attachment at all times arrested on the abutment surface. CONCLUSIONS: Comparing platform shift/switch versus standard abutments using a minimally invasive flapless approach including crestal or subcrestal implant placement, the platform shift/switch abutments offer no selective advantage over standard abutments.

Odontogenic Ameloblast-associated Protein (ODAM) Mediates Junctional Epithelium Attachment to Teeth via Integrin-ODAM-Rho Guanine Nucleotide Exchange Factor 5 (ARHGEF5)-RhoA Signaling.

Adhesion of the junctional epithelium (JE) to the tooth surface is crucial for maintaining periodontal health. Although odontogenic ameloblast-associated protein (ODAM) is expressed in the JE, its molecular functions remain unknown. We investigated ODAM function during JE development and regeneration and its functional significance in the initiation and progression of periodontitis and peri-implantitis. ODAM was expressed in the normal JE of healthy teeth but absent in the pathologic pocket epithelium of diseased periodontium. In periodontitis and peri-implantitis, ODAM was extruded from the JE following onset with JE attachment loss and detected in gingival crevicular fluid. ODAM induced RhoA activity and the expression of downstream factors, including ROCK (Rho-associated kinase), by interacting with Rho guanine nucleotide exchange factor 5 (ARHGEF5). ODAM-mediated RhoA signaling resulted in actin filament rearrangement. Reduced ODAM and RhoA expression in integrin ß3- and ß6-knockout mice revealed that cytoskeleton reorganization in the JE occurred via integrin-ODAM-ARHGEF5-RhoA signaling. Fibronectin and laminin activated RhoA signaling via the integrin-ODAM pathway. Finally, ODAM was re-expressed with RhoA in regenerating JE after gingivectomy in vivo. These results suggest that ODAM expression in the JE reflects a healthy periodontium and that JE adhesion to the tooth surface is regulated via fibronectin/laminin-integrin-ODAM-ARHGEF5-RhoA signaling. We also propose that ODAM could be used as a biomarker of periodontitis and peri-implantitis.

Periodontal regeneration employing gingival margin-derived stem/progenitor cells in conjunction with IL-1ra-hydrogel synthetic extracellular matrix.

AIM: This study investigated the periodontal regenerative potential of gingival margin-derived stem/progenitor cells (G-MSCs) in conjunction with IL-1ra-releasing hyaluronic acid synthetic extracellular matrix (HA-sECM). MATERIALS AND METHODS: Periodontal defects were induced at four sites in eight miniature pigs in the premolar/molar area (-4 weeks). Autologus G-MSCs were isolated from the free gingival margin and magnetically sorted, using anti-STRO-1 antibodies. Colony formation and multilineage differentiation potential were tested. The G-MSCs were expanded and incorporated into IL-1ra-loaded/unloaded HA-sECM. Within every miniature pig, four periodontal defects were randomly treated with IL-1ra/G-MSCs/HA-sECM (test group), G-MSCs/HA-sECM (positive-control), scaling and root planing (SRP; negative control-1) or left untreated (no-treatment group; negative control 2). Differences in clinical attachment level (ΔCAL), probing depth (ΔPD), gingival recession (ΔGR), radiographic defect volume (ΔRDV), and changes in bleeding on probing (BOP) between baseline and 16 weeks post-transplantation, as well as periodontal attachment level (PAL), junctional epithelium length (JE), connective tissue adhesion (CTA), cementum regeneration (CR) and bone regeneration (BR) at 16 weeks post-transplantation were evaluated. RESULTS: Isolated G-MSCs showed stem/progenitor cell characteristics. IL-1ra loaded and unloaded G-MSCs/HA-sECM showed higher ΔCAL, ΔPD, ΔGR, PAL, CR and BR as well as a lower JE compared to their negative controls and improved BOP. CONCLUSION: G-MSCs in conjunction with IL-1ra-loaded/unloaded HA-sECM show a significant periodontal regenerative potential.

Non-Invasive Periodontal Probing Through Fourier-Domain Optical Coherence Tomography.

BACKGROUND: Periodontitis is a multifactorial and infectious disease that may result in significant debilitation. The aim of this study is to exploit two optical coherence tomography (OCT) systems operating in the Fourier domain at different wavelengths, 930 and 1,325 nm, for structural analysis of periodontal tissue in porcine jaws. METHODS: Five fresh porcine jaws were sectioned and stored in formalin before OCT analysis. Two- and three-dimensional OCT images of the tooth/gingiva interface were performed, and measurements of the gingival structures were obtained. The 930-nm OCT system operates in the spectral domain, whereas the 1,325-nm system is a swept-source model. Stereomicroscope images, the gold standard, were used for direct comparison. RESULTS: Through image analysis, it is possible to identify the free gingiva and the attached gingiva, the calculus deposition over tooth surfaces, and the subgingival calculus that enables the enlargement of the gingival sulcus. In addition, the gingival thickness and the gingival sulcus depth can be non-invasively measured, varying from 0.8 to 4 mm. CONCLUSIONS: Regarding the ability of the two OCT systems to visualize periodontal structures, the system operating at 1,325 nm shows a better performance, owing to a longer central wavelength that allows deeper tissue penetration. The results with the system at 930 nm can also be used, but some features could not be observed due to its lower penetration depth in the tissue.

Periodontal considerations in veneer cases.

Porcelain veneers are a minimally invasive technique to enhance patients' smiles. A crucial component in these cases is the supporting periodontal apparatus and its interaction with the restorations. This article addresses basic concepts such as biologic width, altered eruption patterns, appropriate gingival contouring and smile design to give practitioners the tools to diagnose, evaluate and treat cases successfully and predictably.

Enamel Hypomineralization and Structural Defects in Amelotin-deficient Mice.

Amelotin (AMTN) is a relatively recently discovered enamel protein that is predominantly expressed by ameloblasts during the maturation stage of amelogenesis and is present at lower levels in the junctional epithelium of erupted teeth. Previous studies have suggested a function of this protein in enamel mineralization and cell attachment. Genetic mouse models have been instrumental in defining the role of many enamel-related proteins, but a genetic mouse model lacking the Amtn gene has not been reported. Here, we describe the generation of amelotin-deficient mice and the analysis of their enamel phenotype in comparison with that of wild-type animals. Ablation of AMTN expression resulted in mechanically inferior enamel of mandibular incisors that showed chipping and fractures at the incisal edge. Enamel mineralization was delayed, resulting in hypomineralized inner enamel and structural defects in the outer enamel. Erupted enamel close to the gingival margin showed increased surface roughness. The expression levels of the enamel matrix proteins AMEL, AMBN, ENAM, and ODAM and the enamel proteases MMP-20 and KLK-4 were not significantly altered, although the expression of KLK-4 was delayed. The morphology of ameloblasts showing prominent Tomes' processes during the secretory stage was not altered, and there was no indication of disruption of cell structures or activities, but a residual layer, presumably consisting of organic material, remained at the enamel surface close to the gingival margin. The integrity of the dentogingival attachment at the junctional epithelium appeared unaffected by AMTN deficiency. These observations indicate that AMTN plays a subtle yet critical role in enamel biomineralization, particularly during the establishment of the outer and surface enamel layers. This role appears to be largely independent of other enamel proteins.

Histomorphometric evaluation of maxillary molar roots and surrounding periodontium following molar intrusion in rats.

OBJECTIVES: To investigate periodontal tissue changes during and after molar intrusion in rats. SETTING AND SAMPLE POPULATION: The Department of Orthodontics at Yonsei University. Thirty 12-week-old male rats were assigned to 1 control and 5 experimental groups (n = 5 each). MATERIALS AND METHODS: In the experimental groups, two maxillary molars were intruded for 2 weeks; the control group underwent the same procedures without the intrusion force. After 2 weeks of intrusion, rats in one of the experimental groups and in the control group were killed. In the other four experimental groups, the new molar positions were either retained or not retained with an occlusal bite block for 1 or 2 weeks prior to euthanization. Histomorphometric analysis was performed for sulcus depth, osteoclast number per unit alveolar bone length, and root resorption area per unit root surface length. RESULTS: Sulcus depth increased during intrusion (P < 0.05), but decreased after 2 weeks of retention (P < 0.05). The number of osteoclasts increased during intrusion (P < 0.05), but subsequently decreased regardless of the retention regime (P < 0.05). Root resorption area increased after molar intrusion, irrespective of the retention regimen, relative to that of the control group (P < 0.05) and was the greatest after 2 weeks of retention. CONCLUSION: These results indicated that root resorption occurred during and after molar intrusion and that the surrounding periodontium remodeled accordingly as tooth positions were altered, regardless of retention regime.

Green tea extract inhibits the onset of periodontal destruction in rat experimental periodontitis.

BACKGROUND AND OBJECTIVE: Green tea extract exerts a variety of biological effects, including anti-inflammatory activities. However, there has been no report on the effect of green tea extract on loss of attachment, which is an important characteristic of periodontitis. Here, we examined the inhibitory effects of green tea extract on the onset of periodontitis in a rat model. MATERIAL AND METHODS: Rats were immunized intraperitoneally with Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 12) received a topical application of LPS onto the palatal gingival sulcus every 24 h. The green tea extract group (n = 12) received a topical application of LPS mixed with green tea extract, sunphenon BG, every 24 h. The phosphate-buffered saline (PBS) group (n = 6) received a topical application of PBS every 24 h. The levels of anti-LPS immunoglobulin G (IgG) in serum were determined using ELISA. Rats in the LPS and green tea extract groups were killed after the 10th and 20th applications. Rats in the PBS group were killed after the 20th application. Loss of attachment, level of alveolar bone and inflammatory cell infiltration were investigated histopathologically and histometrically. RANKL-positive cells and the formation of immune complexes were evaluated immunohistologically. RESULTS: There was no significant difference in the serum levels of anti-LPS IgG between the LPS group and the green tea extract group. In contrast, loss of attachment, level of alveolar bone, inflammatory cell infiltration and RANKL expression in the green tea extract group were significantly decreased compared with those in the LPS group. CONCLUSION: These findings demonstrate that green tea extract suppresses the onset of loss of attachment and alveolar bone resorption in a rat model of experimental periodontitis.