Technical Note on Simplified Free Gingival Graft Using Tack Fixation (sFGG).

Free gingival graft (FGG) is the gold standard procedure for the reliable augmentation of lost keratinized mucosa (KM) around dental implants. This conventional surgical approach has its drawbacks, including limitations in manipulation, the requirement for suturing, postoperative discomfort, and pain. This case report aimed to evaluate the efficacy of a simplified free gingival graft (sFGG) in addressing the issue of inadequate keratinized mucosa around dental implants. Fixation tacks were used to perform the sFGG procedure. Initially, a partial-thickness flap was created and apically repositioned. The gingival graft was harvested from the palate with a narrow profile and securely affixed to the recipient site using 5 mm long fixation tacks. Significant gains in keratinized mucosa were achieved and successfully maintained within 1 year. Consequently, the sFGG technique emerges as a simple and reliable treatment approach for managing inadequate keratinized mucosa around dental implants.

Volumetric evaluation of effects of platelet-rich fibrin and concentrated growth factor on early bone healing after endodontic microsurgery: a randomized controlled trial.

BACKGROUND: This randomized controlled clinical trial compared the effects of platelet-rich fibrin (PRF) and concentrated growth factor (CGF) on early bone healing after endodontic microsurgery. METHODS: Eighteen patients with an isolated periapical lesion < 10 mm in the maxillary anterior region were randomly assigned to three groups: control, PRF, or CGF. Endodontic microsurgery was performed and PRF or CGF membranes were placed over the bone defects in the experimental groups. The volume of the bone defect at postoperative one week, three months, and six months was evaluated using cone-beam computed tomography and Mimics software. The results were statistically analyzed using the Kruskal-Wallis test and post-hoc Mann-Whitney U test with Bonferroni correction. RESULTS: At the three-month follow-up, the PRF and CGF groups showed significantly greater bone healing compared with the control group (p > 0.05). However, no significant difference was observed between the PRF and CGF groups. At the six-month follow-up, no significant differences were observed between the groups. CONCLUSIONS: These results suggested that PRF and CGF promote early bone healing after endodontic microsurgery.

DMP1 and IFITM5 Regulate Osteogenic Differentiation of MC3T3-E1 on PEO-Treated Ti-6Al-4V-Ca2+/Pi surface.

Despite numerous studies on various surface modifications on titanium and its alloys, it remains unclear what kind of titanium-based surface modifications are capable of controlling cell activity. This study aimed to understand the mechanism at the cellular and molecular levels and investigate the in vitro response of osteoblastic MC3T3-E1 cultured on the Ti-6Al-4V surface modified by plasma electrolytic oxidation (PEO) treatment. A Ti-6Al-4V surface was prepared by PEO at 180, 280, and 380 V for 3 or 10 min in an electrolyte containing Ca2+/Pi ions. Our results showed that PEO-treated Ti-6Al-4V-Ca2+/Pi surfaces enhanced the cell attachment and differentiation of MC3T3-E1 compared to the untreated Ti-6Al-4V control but did not affect cytotoxicity as shown by cell proliferation and cell death. Interestingly, on the Ti-6Al-4V-Ca2+/Pi surface treated by PEO at 280 V for 3 or 10 min, MC3T3-E1 showed a higher initial adhesion and mineralization. In addition, the alkaline phosphatase (ALP) activity significantly increased in MC3T3-E1 on the PEO-treated Ti-6Al-4V-Ca2+/Pi (280 V for 3 or 10 min). In RNA-seq analysis, the expression of dentin matrix protein 1 (DMP1), sortilin 1 (Sort1), signal-induced proliferation-associated 1 like 2 (SIPA1L2), and interferon-induced transmembrane protein 5 (IFITM5) was induced during the osteogenic differentiation of MC3T3-E1 on the PEO-treated Ti-6Al-4V-Ca2+/Pi. DMP1 and IFITM5 silencing decreased the expression of bone differentiation-related mRNAs and proteins and ALP activity in MC3T3-E1. These results suggest that the PEO-treated Ti-6Al-4V-Ca2+/Pi surface induces osteoblast differentiation by regulating the expression of DMP1 and IFITM5. Therefore, surface microstructure modification through PEO coatings with Ca2+/Pi ions could be used as a valuable method to improve biocompatibility properties of titanium alloys.

GPR183 Regulates 7α,25-Dihydroxycholesterol-Induced Oxiapoptophagy in L929 Mouse Fibroblast Cell.

7α,25-dihydroxycholesterol (7α,25-DHC) is an oxysterol synthesized from 25-hydroxycholesterol by cytochrome P450 family 7 subfamily B member 1 (CYP7B1) and is a monooxygenase (oxysterol-7α-hydroxylase) expressed under inflammatory conditions in various cell types. In this study, we verified that 7α,25-DHC-induced oxiapoptophagy is mediated by apoptosis, oxidative stress, and autophagy in L929 mouse fibroblasts. MTT assays and live/dead cell staining revealed that cytotoxicity was increased by 7α,25-DHC in L929 cells. Consequentially, cells with condensed chromatin and altered morphology were enhanced in L929 cells incubated with 7α,25-DHC for 48 h. Furthermore, apoptotic population was increased by 7α,25-DHC exposure through the cascade activation of caspase-9, caspase-3, and poly (ADP-ribose) polymerase in the intrinsic pathway of apoptosis in these cells. 7α,25-DHC upregulated reactive oxygen species (ROS) in L929 cells. Expression of autophagy biomarkers, including beclin-1 and LC3, was significantly increased by 7α,25-DHC treatment in L929 cells. 7α,25-DHC inhibits the phosphorylation of Akt associated with autophagy and increases p53 expression in L929 cells. In addition, inhibition of G-protein-coupled receptor 183 (GPR183), a receptor of 7α,25-DHC, using GPR183 specific antagonist NIBR189 suppressed 7α,25-DHC-induced apoptosis, ROS production, and autophagy in L929 cells. Collectively, GPR183 regulates 7α,25-DHC-induced oxiapoptophagy in L929 cells.

Demethoxycurcumin induces apoptosis via inhibition of NF-κB pathway in FaDu human head and neck squamous cell carcinoma.

Background: Demethoxycurcumin (DMC) is a curcumin analog with antitumor properties. However, its effects have not been investigated in human head and neck squamous cell carcinoma (HNSCC). The aim of the present study was to verify the antitumor effect and cellular signaling pathways of DMC in FaDu HNSCC cells. Methods: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), cell Live/Dead staining, hematoxylin and eosin staining, DAPI staining, FACS, western blotting, caspase-3 activity assay, and nuclear translocation were performed to verify apoptosis and the cellular signaling pathway of DMC in FaDu cells. Results: DMC increased FaDu cell death, with cells presenting altered morphology and condensed nuclei. DMC increased significantly the apoptotic population of FaDu cells. Sequentially, DMC increased the expression of cleaved caspase-3 and PARP through the up-regulation of pro-apoptotic factors such as FasL, cleaved caspase-8, Bax, Bad, and cleaved caspase-9 and the suppression of anti-apoptotic factors including Bcl-xL and Bcl-2 in FaDu cells. Furthermore, DMC not only suppressed the phosphorylation of NF-κB, but also inhibited the translocation of NF-κB from cytosol to nucleus of FaDu cells. Conclusions: Present study demonstrates that DMC-induced cell death is mediated caspase-dependently by death receptor-mediated extrinsic and mitochondria-dependent intrinsic apoptosis through the inhibition of NF-κB translocation from the cytosol to the nucleus of FaDu cells. DMC is a curcuminoid with antitumor properties that modulates the NF-κB cellular signaling pathway in FaDu cells. Taken together, this study suggests that DMC has a considerable chemotherapeutic potential for HNSCC.

Comparison of Various Time-Related Modifications of Ultraviolet Photofunctionalization on SLA-Treated Titanium Surfaces.

PURPOSE: The purpose of this study was to compare changes in the physicochemical and biologic characteristics of titanium surfaces through short-term re-hydrophobization for 24 hours and ultraviolet (UV) re-irradiation for 24 hours. MATERIALS AND METHODS: Photofunctionalization was performed with four 15-W bactericidal lamps at an intensity of 5.0 mW/cm2 (wavelength = 254 ± 20 nm) on sandblasted, large-grit, acid-etched (SLA)-treated titanium surfaces, which were stored in a sterilized sealed container for 8 weeks to allow enough biologic aging. The duration of the UV irradiation was as follows: irradiation group-UV irradiated for 24 hours; re-hydrophobization group-UV irradiated for 24 hours and then stored in an ambient sterilized medium; and re-irradiation group-UV irradiated for 24 hours followed by storing for 24 hours in an ambient sterilized medium and then UV re-irradiated for 24 hours. The surface characteristics were evaluated with field emission scanning electron microscopy, x-ray photoelectron spectroscopy (XPS), and water contact angle. Cell viability and morphology were measured using fluorescence staining. Alkaline phosphatase (ALP) assay and alizarin red S staining were performed to evaluate the differentiation of osteogenic cells and the mineralization capability. RESULTS: Macroroughness and superimposed microroughness were observed on the disk surfaces in all groups as typically seen on SLA surfaces. The water contact angles were measured to be 1.85, 1.48, and 1.18 degrees for the irradiation group, re-hydrophobization group, and re-irradiation group, respectively, indicating superhydrophilicity. There was no difference in the surface elemental ratio or the spectra of XPS, cell viability, or ALP activity. Although the re-irradiation group had the highest total amount of calcium deposition, there was no statistical significance. CONCLUSION: Within the limitations of the study, improved superhydrophilicity and bioactivity after UV irradiation were maintained during short-term re-hydrophobization and repeated re-irradiation without changing the topography of SLA titanium surfaces.

Classification of postoperative edema based on the anatomic division with mandibular third molar extraction.

PURPOSE: Several investigations have been performed for a postoperative edema after extraction, but the results have been controversial due to low objectivity or poorly reproducible assessments of the edema. The aim of this study was to suggest a classification and patterns of postoperative edema according to the anatomical division associated with extraction of mandibular third molar as a qualitative evaluation method. METHODS: This study was conducted forty-four mandibular third molars extracted and MRI was taken within 48 h after extraction. The postoperative edema space was classified by MRI (one anatomic component-buccinator muscle-and four fascial spaces-supra-periosteum space, buccal space, parapharyngeal space, and lingual space), and evaluated independently by two examiners. The inter-examiner reliability was calculated using Kappa statistics. RESULTS: The evaluation of buccinator muscle edema showed good agreement and the fascial spaces showed constant high agreement. The incidence of postoperative edema was high in the following order: supra-periosteum space (75.00%), buccinator muscle (68.18%), parapharyngeal space (54.55%), buccal space (40.91%), and lingual space (25.00%). CONCLUSION: Postoperative edema could be assessed clearly by each space, which showed a different tendency between the anatomic and fascial spaces.

25-Hydroxycholesterol-Induced Oxiapoptophagy in L929 Mouse Fibroblast Cell Line.

25-hydroxycholesterol (25-HC) is an oxysterol synthesized from cholesterol by cholesterol-25-hydroxylase during cholesterol metabolism. The aim of this study was to verify whether 25-HC induces oxiapoptophagy in fibroblasts. 25-HC not only decreased the survival of L929 cells, but also increased the number of cells with condensed chromatin and altered morphology. Fluorescence-activated cell sorting results showed that there was a dose-dependent increase in the apoptotic populations of L929 cells upon treatment with 25-HC. 25-HC-induced apoptotic cell death was mediated by the death receptor-dependent extrinsic and mitochondria-dependent intrinsic apoptosis pathway, through the cascade activation of caspases including caspase-8, -9, and -3 in L929 cells. There was an increase in the levels of reactive oxygen species and inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in L929 cells treated with 25-HC. Moreover, 25-HC caused an increase in the expression of beclin-1 and microtubule-associated protein 1A/1B-light chain 3, an autophagy biomarker, in L929 cells. There was a significant decrease in the phosphorylation of protein kinase B (Akt) in L929 cells treated with 25-HC. Taken together, 25-HC induced oxiapoptophagy through the modulation of Akt and p53 cellular signaling pathways in L929 cells.

Oxysterol 25-hydroxycholesterol as a metabolic pathophysiological factors of osteoarthritis induces apoptosis in primary rat chondrocytes.

The aim of the present study was to investigate the pathophysiological etiology of osteoarthritis that is mediated by the apoptosis of chondrocytes exposed to 25-hydroxycholesterol (25-HC), an oxysterol synthesized by the expression of cholesterol-25-hydroxylase (CH25H) under inflammatory conditions. Interleukin-1ß induced the apoptosis of chondrocytes in a dose- dependent manner. Furthermore, the production of 25-HC increased in the chondrocytes treated with interleukin-1ß through the expression of CH25H. 25-HC decreased the viability of chondrocytes. Chondrocytes with condensed nucleus and apoptotic populations increased by 25-HC. Moreover, the activity and expression of caspase-3 were increased by the death ligand-mediated extrinsic and mitochondria-dependent intrinsic apoptotic pathways in the chondrocytes treated with 25-HC. Finally, 25-HC induced not only caspase-dependent apoptosis, but also induced proteoglycan loss in articular cartilage ex vivo cultured rat knee joints. These data indicate that 25-HC may act as a metabolic pathophysiological factor in osteoarthritis that is mediated by progressive chondrocyte death in the articular cartilage with inflammatory condition.

25-Hydroxycholesterol Induces Death Receptor-mediated Extrinsic and Mitochondria-dependent Intrinsic Apoptosis in Head and Neck Squamous Cell Carcinoma Cells.

BACKGROUND/AIM: Oxysterol plays important physiological roles in diverse biological processes including apoptosis. However, the mechanisms underlying oxysterol-induced apoptosis remain unknown. 25-hydroxycholesterol (25-HC) is an oxysterol synthesized by cholesterol 25-hydroxylase from cholesterol during sterol metabolism. The aim of present study was to investigate 25-HC-induced apoptosis and associated signalling pathways in FaDu cells, which is originated form human head and neck squamous cell carcinoma cells. MATERIALS AND METHODS: 25-HC-induced apoptosis was investigated by cell cytotoxicity assay using MTT, cell viability assay using cell LIVE/DEAD cell viability assay, haematoxylin & eosin staining, nuclear staining, fluorescence-activated cell sorting, western blotting using specific antibodies associated with extrinsic and intrinsic apoptosis pathways, and caspase-3/-7 activity assay in FaDu cells. RESULTS: 25-HC dose-dependently decreased the viability of FaDu cells and up-regulated apoptotic events, such as alteration in morphology, and nuclear condensation. Flow cytometric analysis showed an increase in apoptotic population upon 25-HC treatment, suggesting that 25-HC induces apoptosis in FaDu cells. Moreover, 25-HC-induced apoptosis in FaDu cells was dependent on the activation of caspases by Fas antigen ligand-triggered death receptor-mediated extrinsic pathway and mitochondria-dependent intrinsic pathway via mitogen activated protein kinases. CONCLUSION: Cholesterol-derived oxysterol, 25-HC has potential anti-cancer function in FaDu cells and may have potential properties for the discovery of anti-cancer agents.

Formononetin induces apoptotic cell death through the suppression of mitogen­activated protein kinase and nuclear factor­κB phosphorylation in FaDu human head and neck squamous cell carcinoma cells.

Formononetin, a phytoestrogen extracted from various herbal plants, has been investigated as an anticancer agent against diverse types of cancer. The aim of the present study was to investigate the induction of apoptotic cell death by formononetin in the FaDu pharyngeal squamous cell carcinoma cell line. Formononetin significantly increased FaDu cell death, with an estimated IC50 value of 50 µM; however, it did not affect the viability of normal L929 mouse fibroblasts used as normal control at 5­25 µM. Typical characteristics of apoptosis, such as morphological alterations, chromatin condensation, DNA fragmentation and the size of the apoptotic cell population, were increased in FaDu cells treated with formononetin for 24 h. Furthermore, formononetin­induced FaDu cell death involved the death receptor­mediated extrinsic and the mitochondria­dependent intrinsic apoptotic pathways by activating the caspase cascade. The chemotherapeutic effects of formononetin were mediated by the suppression of mitogen­activated protein kinases, including extracellular signal­regulated kinase 1/2 and p38, and nuclear factor­κB phosphorylation in FaDu cells. Finally, the oral administration of formononetin decelerated tumor growth through the expression of cleaved caspase­3 in a FaDu cell xenograft animal model. Taken together, these findings indicate that formononetin holds promise as a chemotherapeutic agent and may be of value in the treatment of human head and neck squamous cell carcinoma.

Phenformin Induces Caspase-dependent Apoptosis of FaDu Head and Neck Squamous Cell Carcinoma Cells.

BACKGROUND/AIM: The present study aimed to investigate the apoptotic effects of phenformin, a therapeutic agent for diabetes, on head and neck squamous cell carcinoma (HNSCC). MATERIALS AND METHODS: Cytotoxicity was measured by the MTT and live/dead cell assay. Phenformin-induced apoptotic FaDu cell death and its associated cellular signaling pathways were investigated by hematoxylin and eosin staining, 4',6-diamidino-2-phenylindole staining, caspase-3 activity assay, fluorescence-activated cell sorting analysis, and western blotting. RESULTS: Phenformin promoted death of and apoptotic processes in FaDu cells, including morphological alterations and nuclear condensation. Furthermore, treatment with phenformin increased caspase-3 activity and apoptotic populations via the caspase cascade through cleavage of capspase-8, -9, and -3 and poly(ADP-ribose) polymerase in FaDu cells. Moreover, phosphorylation levels of mitogen-activated protein kinases, nuclear factor-κB, and AKT were down-regulated in FaDu cells by phenformin. CONCLUSION: Phenformin induced death of FaDu cells via caspase-dependent extrinsic and intrinsic apoptosis pathways and is a promising novel therapeutic agent for HNSCC.

Anticatabolic Effects of Morin through the Counteraction of Interleukin-1ß-Induced Inflammation in Rat Primary Chondrocytes.

Morin, a flavonoid isolated from various medicinal herbal plants, has an anti-inflammatory effect. This study aimed to elucidate the anticatabolic effects and cellular mechanism of morin against interleukin-1ß (IL-1ß) in rat primary chondrocytes. Morin at 10-100 µM did not affect the viability of rat primary chondrocytes. Treatment with morin for 21 days ameliorated the IL-1ß-induced decrease in extracellular matrix. Furthermore, treatment with morin attenuated IL-1ß-induced proteoglycan loss in the articular cartilage through suppression of catabolic factors, such as matrix metalloproteinases, inflammatory mediators, and pro-inflammatory cytokines. These data indicated that morin exerted anticatabolic effects that can prevent and reduce progressive degeneration of the articular cartilage, and thus may be a potential candidate treatment for osteoarthritis.

Effects of Platelet-Derived Material (Platelet-Rich Fibrin) on Bone Regeneration.

PURPOSE: The purpose of this study was to evaluate the effects of the growth factor within platelet-rich fibrin (PRF) in proliferation and differentiation of osteoblast and to observe the effectiveness of PRF. MATERIALS AND METHODS: The colorimetric MTT assay, cell live and dead assay, alkaline phosphatase staining and activity assay, alizarine red S, and von Kossa staining were performed. Finally, the alterations of biomarkers associated with bone formation were verified at the mRNA level by quantitative polymerase chain reaction (PCR) and quantitative real-time PCR. In in vivo study, 6 adult mongrel dogs were used. The defect was performed and divided into 3 groups: (1) defect left unfilled, (2) defect filled with only 0.25-g Bio-Oss, and (3) defect filled with 0.25-g Bio-Oss mixed with PRF. RESULTS: MTT and cell live and dead assay showed that PRF did not affect the cell viability in MG-63 cells. The alkaline phosphatase activity, calcification, and mineralization were gradually increased in the MG-63 cells treated with PRF. Furthermore, the mRNA levels of biomarker gene in the MG-63 cells treated with PRF were significantly higher than those of control. In in vivo study, both radiographical and histological evaluations showed that the new bone formations were significantly increased in the defecting bone region transplanted with Bio-Oss and PRF compared with Bio-Oss only at 2 weeks after transplantation. CONCLUSION: PRF can promote the bone regeneration without any complications.

A Comparative Study with Biphasic Calcium Phosphate to Deproteinized Bovine Bone in Maxillary Sinus Augmentation: A Prospective Randomized and Controlled Clinical Trial.

PURPOSE: The purpose of this study was to evaluate a new graft material, biphasic calcium phosphate, composed of 60% hydroxyapatite and 40% ß-Tricalcium phosphate and deproteinized bovine bone mineral, which is established as a predictable graft material for maxillary sinus augmentation. MATERIALS AND METHODS: Maxillary sinus augmentation was performed with different bone materials. Bone biopsies were performed on tissue harvested from the future implant bed using a trephine bur at 6 months after maxillary sinus augmentation. Resonance frequency analysis was performed immediately and at 6 months after the implant placement. Microcomputed tomography and histomorphometric analysis were performed in all patients. RESULTS: Fifty-six patients (60 sinuses) were included in the study. At 6 months postoperative, 31 biopsies were performed on tissues harvested from the calcium phosphate, and 29 biopsies on tissues from the bovine bone grafts. There was no implant failure during the 21-month mean follow-up period. The overall implant stability quotient values were higher than 60, and gradually increased for 6 months. Higher new bone volume fraction and new bone surface density were observed in the calcium phosphate group compared with the bovine bone group. In contrast, residual bone graft volume in the bovine bone group was higher than that in the calcium phosphate group. Nevertheless, there was no significant difference between groups in the microcomputed tomography and histomorphometric parameters. CONCLUSION: Within the study's limitations, both graft materials demonstrated similar biocompatibility and osteoconductivity in the maxillary sinus augmentation.

Clinical and histomorphometric evaluation of decompression followed by enucleation in the treatment of odontogenic keratocyst.

BACKGROUND/PURPOSE: The classification and treatment of odontogenic keratocyst (OKC) are controversial. The objective of this study was to present the efficiency of decompression followed by enucleation by clinical and histomorphometric evaluation for the treatment of OKC. MATERIALS AND METHODS: Thirty four OKCs of 27 patients who underwent decompression followed by enucleation were included in this study. Clinical and histomorphometric analysis were performed. RESULTS: The average decreasing rate was 59% in maximum diameter, 66% in the amount of the volume for the average of period of the decompression was 9.8 months. The mean of increasing rate of the thickness of the epithelial lining was 921.16%. There were no recurrences for a mean follow-up period of 5.8 years. The thin and friable cyst wall of the OKC was changed to thickened, hard type. CONCLUSION: The decompression was found to be effective and reliable as a treatment of the OKC to decrease the recurrence tendency, even for Gorlin-Goltz syndrome.

Removal of a fractured needle during inferior alveolar nerve block: two case reports.

The inferior alveolar nerve block is the most common method of local anesthesia for intraoral surgery at the posterior mandibular region. However, unexpected complications may occur when administering the local anesthesia. One of these uncommon complications is the fracture of the needle. If the injection needle is broken during the surgery, it should be removed immediately. However, this is one of the most difficult procedures. In this report, we present two cases of needle fracture during the procedure, and its successful removal under general/local anesthesia administration.

Biochanin-A induces apoptosis and suppresses migration in FaDu human pharynx squamous carcinoma cells.

The aim of the present study was to investigate biochanin-A-induced anticancer effects and their cellular signaling pathway in FaDu pharyngeal squamous carcinoma cells. Biochanin-A induced cell death through increased cytotoxicity of FaDu cells in a dose- and time-dependent manner. The number of cells with nucleus condensation and the apoptotic population were increased in the FaDu cells stimulated with biochanin-A for 24 h. Furthermore, extrinsic apoptotic factors such as FasL and their downstream target caspase-8 were increased and activated in the FaDu cells treated with biochanin-A in a dose-dependent manner. Moreover, biochanin-A decreased the expression of intrinsic anti-apoptotic factors such as Bcl-2 and Bcl-xL, and increased the level and activation of intrinsic apoptotic factors such as Bad and caspase-9. Finally, biochanin-A induced the activation of caspase-3 and Poly(ADP ribose) polymerase (PARP) in FaDu cells. Our results suggest that biochanin-A-induced apoptosis was mediated by death receptor mediated-extrinsic and mitochondria-dependent intrinsic apoptotic signaling pathways. Biochanin-A also inhibited wound healing migration and proliferation of FaDu cells via the downregulation and inactivation of matrix metalloproteinase-2 and -9 that are mediated by the suppression of p38, mitogen activated protein kinase (MAPK), NF-κB and Akt cellular signaling pathways. Therefore, these data suggest that the biochanin-A may act as a potential chemotherapeutic compound to treat head and neck cancer.

Comparative Study on Osseointegration of Implants After Flap and Flapless Surgery in the Mandible of Dogs.

PURPOSE: The objective of this study was to compare the implant stability and osseointegration of implants using a flap or flapless technique. MATERIAL AND METHODS: Mandibular premolars and molars were extracted from both sides in 6 dogs. After 8 weeks, 4 fixtures were implanted using either a flap or flapless technique. Implant stability quotient was measured on insertion and at 2, 4, and 8 weeks later. The animals were killed while the tissues were histologically analyzed. RESULTS: Implant stability increased for 8 weeks, and no statistically significant differences were observed between the surgical protocols. Bone-implant contact showed 60.27% ± 30.99% for flapless surgery and 59.73% ± 17.12% for flap surgery. And the results of new bone formation area from total area showed 56.07% ± 27.78% for flapless surgery and 57.00% ± 14.66% for flap surgery. There were no statistically significant differences. CONCLUSION: This study showed no significant difference in implant stability as well as osseointegration regardless of flap or flapless technique.

Incidence and Management of Fractured Dental Implants: Case Reports.

The fracture of dental implants is a rare occurrence in clinical settings. Possible causes of implant fracture include design or production flaws, overloaded occlusion force, implant location, metal fatigue, and bone resorption around the implant. This study reports on the successful removal and reimplantation of fractured implants.