Utility of intraoral scanner imaging for dental plaque detection.

Purpose: Oral hygiene, maintained through plaque control, helps prevent periodontal disease and dental caries. This study was conducted to examine the accuracy of plaque detection with an intraoral scanner (IOS) compared to images captured with an optical camera. Materials and Methods: To examine the effect of color tone, artificial tooth resin samples were stained red, blue, and green, after which images were acquired with a digital single-lens reflex (DSLR) camera and an IOS device. Stained surface ratios were then determined and compared. Additionally, the deviation rate of the IOS relative to the DSLR camera was computed for each color. In the clinical study, following plaque staining with red disclosing solution, the staining was captured by the DSLR and IOS devices, and the stained area on each image was measured. Results: The stained surface ratios did not differ significantly between DSLR and IOS images for any color group. Additionally, the deviation rate did not vary significantly across colors. In the clinical test, the stained plaque appeared slightly lighter in color, and the delineation of the stained areas less distinct, on the IOS compared to the DSLR images. However, the stained surface ratio was significantly higher in the IOS than in the DSLR group. Conclusion: When employing IOS with dental plaque staining, the impact of color was minimal, suggesting that the traditional red stain remains suitable for plaque detection. IOS images appeared relatively blurred and enlarged relative to the true state of the teeth, due to inferior sharpness compared to camera images.

Comparison of plaque control record measurements obtained using intraoral scanner and direct visualization.

OBJECTIVE: Intraoral scanner (IOS) can acquire three-dimensional color images of teeth. Thus, the detection of areas with plaque adhesion stained by plaque-disclosing solutions using an IOS could be a potential oral hygiene evaluation method. This study aimed to verify the usefulness of obtaining O'Leary's plaque control record (PCR) measurements using an IOS in clinical practice. METHODS: Twenty patients with >20% PCR measurements who underwent oral prophylaxis were enrolled in this study. A plaque-disclosing gel was applied to stain the areas with plaque adhesion, and the dentition was scanned using the IOS. The PCR values obtained via the direct method and those obtained using the digital image were compared for the entire dentition, maxillary total area, the labial and palatal aspects of the maxillary anterior teeth, the buccal and palatal aspects of the maxillary posterior teeth, mandibular total area, the labial and lingual aspects of the mandibular anterior teeth, and the buccal and lingual aspects of the mandibular posterior teeth. RESULTS: The IOS group tended to have higher values than the direct observation group. The labial and palatal aspect of the maxillary anterior teeth, the labial and lingual aspects of the mandibular anterior teeth did not differ significantly between the groups. CONCLUSION: Plaque adhesion was visualized easily and conclusively using an IOS. As the large tip size often hinders its use, it is necessary to develop a smaller IOS tip in the future.

Mouse maternal odontogenic infection with Porphyromonas gingivalis induces cognitive decline in offspring.

Introduction: Porphyromonas gingivalis (P. gingivalis), a major periodontal pathogen, causes intrauterine infection/inflammation. Offspring exposed to intrauterine infection/inflammation have an increased risk of neurological disorders, regardless of gestational age. However, the relationship between maternal periodontitis and offspring functional/histological changes in the brain has not yet been elucidated. Methods: In this study, we used a gestational mouse model to investigate the effects of maternal odontogenic infection of P. gingivalis on offspring behavior and brain tissue. Results: The step-through passive avoidance test showed that the latency of the acquisition trial was significantly shorter in the P. gingivalis group (p < 0.05), but no difference in spontaneous motor/exploratory parameters by open-field test. P. gingivalis was diffusely distributed throughout the brain, especially in the hippocampus. In the hippocampus and amygdala, the numbers of neuron cells and cyclic adenosine monophosphate response element binding protein-positive cells were significantly reduced (p < 0.05), whereas the number of ionized calcium binding adapter protein 1-positive microglia was significantly increased (p < 0.05). In the hippocampus, the number of glial fibrillary acidic protein-positive astrocytes was also significantly increased (p < 0.05). Discussion: The offspring of P. gingivalis-infected mothers have reduced cognitive function. Neurodegeneration/neuroinflammation in the hippocampus and amygdala may be caused by P. gingivalis infection, which is maternally transmitted. The importance of eliminating maternal P. gingivalis-odontogenic infection before or during gestation in maintenance healthy brain function in offspring should be addressed in near future.

LRP1 in vascular mural cells modulates cerebrovascular integrity and function in the presence of APOE4.

Cerebrovasculature is critical in maintaining brain homeostasis; its dysregulation often leads to vascular cognitive impairment and dementia (VCID) during aging. VCID is the second most prevalent cause of dementia in the elderly, after Alzheimer's disease (AD), with frequent cooccurrence of VCID and AD. While multiple factors are involved in the pathogenesis of AD and VCID, APOE4 increases the risk for both diseases. A major apolipoprotein E (apoE) receptor, the low-density lipoprotein receptor-related protein 1 (LRP1), is abundantly expressed in vascular mural cells (pericytes and smooth muscle cells). Here, we investigated how deficiency of vascular mural cell LRP1 affects the cerebrovascular system and cognitive performance using vascular mural cell-specific Lrp1-KO mice (smLrp1-/-) in a human APOE3 or APOE4 background. We found that spatial memory was impaired in the 13- to 16-month-old APOE4 smLrp1-/- mice but not in the APOE3 smLrp1-/- mice, compared with their respective littermate control mice. These disruptions in the APOE4 smLrp1-/- mice were accompanied with excess paravascular glial activation and reduced cerebrovascular collagen IV. In addition, blood-brain barrier (BBB) integrity was disrupted in the APOE4 smLrp1-/- mice. Together, our results suggest that vascular mural cell LRP1 modulates cerebrovasculature integrity and function in an APOE genotype-dependent manner.

Experimental tooth loss affects spatial learning function and blood-brain barrier of mice.

OBJECTIVE: This study aims to investigate how experimental tooth loss affected learning, memory function, and brain pathophysiology in mice. MATERIALS AND METHODS: The mice (C57BL/6 J, 2-month-old, male) were divided into tooth loss and control groups. The behavioral test battery was performed at 6 and 12 months after tooth extraction. The protein levels of the tight junctions in the brains of the mice were analyzed. Hippocampal astrocyte was measured using immunohistochemical staining. RESULTS: The results of behavioral tests and biochemical analysis performed during the 6 months observation period did not show significant differences between the groups. However, the escape latency in the tooth loss group was significantly longer than that in the control group at the 12 months after tooth extraction. The level of claudin-5 decreased in the tooth loss group. Additionally, hippocampal astrogliosis was found in the tooth loss group. CONCLUSIONS: Experimental tooth loss reduced the level of claudin-5 and caused astrogliosis in the brains of mice, which was accompanied by deterioration of learning functions. This study may provide a new insight about the association between tooth loss and cognitive dysfunction.

Association between dietary hardness score and activities of daily living among individuals aged 90 years.

OBJECTIVES: With the rapidly aging world population, Japan has many older people with difficulties in maintaining oral health. This study aimed to investigate the relationship between dietary hardness score and performance of activities of daily living (ADL) of 90-year-old individuals in rural areas of Japan. MATERIAL AND METHODS: A total of 236 individuals (64 men and 172 women) aged 90 years in Mitsugi town, Hiroshima, Japan, were included. Assessment of oral status and survey of ADL were performed. The association of ADL with dietary hardness score and the number of remaining teeth was determined. RESULTS: The mean dietary hardness score was 8.3 ± 2.6. Eighty individuals showed independence in ADL, whereas 156 individuals showed dependence. Logistic regression analysis, adjusted for potential confounding factors, showed that dietary hardness score was associated with ADL status but not the number of remaining teeth. CONCLUSION: Our findings suggest that a low dietary hardness score is associated with dependence on ADL in 90-year-old individuals.

Vascular ApoE4 Impairs Behavior by Modulating Gliovascular Function.

The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and multiple vascular conditions. ApoE is abundantly expressed in multiple brain cell types, including astrocytes, microglia, and vascular mural cells (VMCs). Here, we show that VMC-specific expression of apoE4 in mice impairs behavior and cerebrovascular function. Expression of either apoE3 or apoE4 in VMCs was sufficient to rescue the hypercholesterolemia and atherosclerosis phenotypes seen in Apoe knockout mice. Intriguingly, vascular expression of apoE4, but not apoE3, reduced arteriole blood flow, impaired spatial learning, and increased anxiety-like phenotypes. Single-cell RNA sequencing of vascular and glial cells revealed that apoE4 in VMCs was associated with astrocyte activation, while apoE3 was linked to angiogenic signature in pericytes. Together, our data support cell-autonomous effects of vascular apoE on brain homeostasis in an isoform-dependent manner, suggesting a critical contribution of vascular apoE to AD pathogenesis.

IL-6 Induced by Periodontal Inflammation Causes Neuroinflammation and Disrupts the Blood-Brain Barrier.

Background: Periodontal disease (PD) is a risk factor for systemic diseases, including neurodegenerative diseases. The role of the local and systemic inflammation induced by PD in neuroinflammation currently remains unclear. The present study investigated the involvement of periodontal inflammation in neuroinflammation and blood-brain barrier (BBB) disruption. Methods: To induce PD in mice (c57/BL6), a ligature was placed around the second maxillary molar. Periodontal, systemic, and neuroinflammation were assessed based on the inflammatory cytokine mRNA or protein levels using qPCR and ELISA. The BBB permeability was evaluated by the mRNA levels and protein levels of tight junction-related proteins in the hippocampus using qPCR and immunofluorescence. Dextran tracing in the hippocampus was also conducted to examine the role of periodontal inflammation in BBB disruption. Results: The TNF-α, IL-1ß, and IL-6 levels markedly increased in gingival tissue 1 week after ligation. The IL-6 serum levels were also increased by ligature-induced PD. In the hippocampus, the IL-1ß mRNA expression levels were significantly increased by ligature-induced PD through serum IL-6. The ligature-induced PD decreased the claudin 5 expression levels in the hippocampus, and the neutralization of IL-6 restored its levels. The extravascular 3-kDa dextran levels were increased by ligature-induced PD. Conclusions: These results suggest that the periodontal inflammation-induced expression of IL-6 is related to neuroinflammation and BBB disruption in the hippocampus, ultimately leading to cognitive impairment. Periodontal therapy may protect against neurodegenerative diseases.

Tau and apolipoprotein E modulate cerebrovascular tight junction integrity independent of cerebral amyloid angiopathy in Alzheimer's disease.

INTRODUCTION: Cerebrovascular pathologies including cerebral amyloid angiopathy (CAA) and blood-brain barrier (BBB) dysregulation are prominent features in the majority of Alzheimer's disease (AD) cases. METHODS: We performed neuropathologic and biochemical studies on a large, neuropathologically confirmed human AD cohort (N = 469). Amounts of endothelial tight junction proteins claudin-5 (CLDN5) and occludin (OCLN), and major AD-related molecules (amyloid beta [Aß40], Aß42, tau, p-tau, and apolipoprotein E) in the temporal cortex were assessed by ELISA. RESULTS: Higher levels of soluble tau, insoluble p-tau, and apolipoprotein E (apoE) were independently correlated with lower levels of endothelial tight junction proteins CLDN5 and OCLN in AD brains. Although high Aß40 levels, APOE ε4, and male sex were predominantly associated with exacerbated CAA severity, those factors did not influence tight junction protein levels. DISCUSSION: Refining the molecular mechanisms connecting tau, Aß, and apoE with cerebrovascular pathologies is critical for greater understanding of AD pathogenesis and establishing effective therapeutic interventions for the disease.

Alzheimer's Risk Factors Age, APOE Genotype, and Sex Drive Distinct Molecular Pathways.

Evidence suggests interplay among the three major risk factors for Alzheimer's disease (AD): age, APOE genotype, and sex. Here, we present comprehensive datasets and analyses of brain transcriptomes and blood metabolomes from human apoE2-, apoE3-, and apoE4-targeted replacement mice across young, middle, and old ages with both sexes. We found that age had the greatest impact on brain transcriptomes highlighted by an immune module led by Trem2 and Tyrobp, whereas APOE4 was associated with upregulation of multiple Serpina3 genes. Importantly, these networks and gene expression changes were mostly conserved in human brains. Finally, we observed a significant interaction between age, APOE genotype, and sex on unfolded protein response pathway. In the periphery, APOE2 drove distinct blood metabolome profile highlighted by the upregulation of lipid metabolites. Our work identifies unique and interactive molecular pathways underlying AD risk factors providing valuable resources for discovery and validation research in model systems and humans.

APOE4-mediated amyloid-ß pathology depends on its neuronal receptor LRP1.

Carrying the ε4 allele of the APOE gene encoding apolipoprotein E (APOE4) markedly increases the risk for late-onset Alzheimer's disease (AD), in which APOE4 exacerbates the brain accumulation and subsequent deposition of amyloid-ß (Aß) peptides. While the LDL receptor-related protein 1 (LRP1) is a major apoE receptor in the brain, we found that its levels are associated with those of insoluble Aß depending on APOE genotype status in postmortem AD brains. Thus, to determine the functional interaction of apoE4 and LRP1 in brain Aß metabolism, we crossed neuronal LRP1-knockout mice with amyloid model APP/PS1 mice and APOE3-targeted replacement (APO3-TR) or APOE4-TR mice. Consistent with previous findings, mice expressing apoE4 had increased Aß deposition and insoluble amounts of Aß40 and Aß42 in the hippocampus of APP/PS1 mice compared with those expressing apoE3. Intriguingly, such effects were reversed in the absence of neuronal LRP1. Neuronal LRP1 deficiency also increased detergent-soluble apoE4 levels, which may contribute to the inhibition of Aß deposition. Together, our results suggest that apoE4 exacerbates Aß pathology through a mechanism that depends on neuronal LRP1. A better understanding of apoE isoform-specific interaction with their metabolic receptor LRP1 on Aß metabolism is crucial for defining APOE4-related risk for AD.

Dual functionalized liposome-mediated gene delivery across triple co-culture blood brain barrier model and specific in vivo neuronal transfection.

Gene therapy has become a promising approach for neurodegenerative disease treatment, however there is an urgent need to develop an efficient gene carrier to transport gene across the blood brain barrier (BBB). In this study, we strategically designed dual functionalized liposomes for efficient neuronal transfection by combining transferrin (Tf) receptor targeting and enhanced cell penetration utilizing penetratin (Pen). A triple cell co-culture model of BBB confirmed the ability of the liposomes to cross the barrier layer and transfect primary neuronal cells. In vivo quantification of PenTf-liposomes demonstrated expressive accumulation in the brain (12%), without any detectable cellular damage or morphological change. The efficacy of these nanoparticles containing plasmid ß-galactosidase in modulating transfection was assessed by ß-galactosidase expression in vivo. As a consequence of accumulation in the brain, PenTf-liposomes significantly induced gene expression in mice. Immunofluorescence studies of brain sections of mice after tail vein injection of liposomes encapsulating pDNA encoding GFP (pGFP) illustrate the superior ability of dual-functionalized liposomes to accumulate in the brain and transfect neurons. Taken together, the multifunctional liposomes provide an excellent gene delivery platform for neurodegenerative diseases.

A stability evaluation of a novel titanium dental implant/interconnected porous hydroxyapatite complex under functional loading conditions.

The aim of this study was to evaluate the stability of implant/interconnected porous calcium hydroxyapatite complex (implant/IPCHA-complex) under functional loading. Implant/IP-CHA-complexes were placed into the mandibles of four Beagle-Labrador hybrid dogs (complex-group). On the other side, an implant was placed directly (control-group). To subject the loading, the animals were fed a hard diet throughout the loading phase of 5 months. The implant stability quotients (ISQs) and bone implant contact (BIC), and histological evaluations were performed. The ISQs of implant/IP-CHA-complex was significantly lower at placement than that of the control-implant. On the other hand, there was no significant difference between in the groups during loading. The BIC measurements, there was no significantly difference between in both groups. Histologically, newly formed bone was observed in contact with most of the implant surface in the complex-group. An IP-CHA/implant-complex would be able to achieve both bone reconstruction and implant stability under functional loading conditions.

Preoperative evaluation of bone quality for dental implantation using an ultrasound axial transmission device in an ex vivo model.

This study investigated the clinical utility of an ultrasound axial transmission device in preoperative evaluation of bone quality for dental implantation, by clarifying the relationship between cortical bone speed of sound (cSOS), insertion torque values (ITV), and implant stability quotient (ISQ) in porcine femur bone. Eleven fresh porcine femurs, without soft tissue, were prepared. The cSOS of these bones were measured using the axial transmission device. Bone mineral density (BMD) and porosity (Po) were measured in cortical bone samples obtained from the region of ultrasound measurements by X-ray microcomputed tomography. Thirty-three implants were inserted into these samples (three implants per bone sample), and ITV and ISQ were measured for all implants. Then, cortical bone thickness (CbTh) of the area for implantation was measured for all implants using a micrometer. The mean cSOS was 3962 m/s; mean BMD and Po were 0.822 g/cm2 and 0.185%, respectively. cSOS and BMD values were positively correlated, and cSOS values and Po values were negatively correlated. Mean ITV, ISQ, and CbTh were 37.95 Ncm, 71.172, and 2.869 mm, respectively. There was a positive correlation between cSOS values and ISQ values. The cSOS of each bone did not correlate with ITV for all of the bone samples. However, when the CbTh ranges from 3.0 to 3.5 mm, ITV are correlated with cSOS. These findings suggest that cSOS, which reflects the cortical bone quality, may be clinical utility as a preoperative diagnosis of the implant.

Molar loss and powder diet leads to memory deficit and modifies the mRNA expression of brain-derived neurotrophic factor in the hippocampus of adult mice.

BACKGROUND: It is known that tooth loss is known to be a risk factor for Alzheimer's disease and soft diet feeding induces memory impairment. Recent studies have shown that brain-derived neurotrophic factor (BDNF) is associated with tooth loss or soft diet in young animal model, and that BDNF expression is decreased in patients with Alzheimer's disease. However, single or combined effect of tooth loss and/or soft diet on brain function has not fully understood. Here we examined the effect of molar loss and powder diet on memory ability and the expression of BDNF mRNA in the hippocampus of adult C57BL/6J mice. Twenty eight-weeks-old C57BL/6J mice were divided into intact molar group and extracted molar group. They were randomly divided into the I/S group (Intact upper molar teeth/Solid diet feeding), the E/S group (Extracted upper molar teeth/Solid diet feeding), the I/P group (Intact upper molar teeth/Powder diet feeding), and the E/P group (Extracted upper molar teeth/Powder diet feeding). The observation periods were 4 and 16-week. To analyze the memory ability, the step-through passive avoidance test was conducted. BDNF-related mRNA in the hippocampus was analyzed by real-time polymerase chain reaction (RT-PCR). RESULTS: At 4 weeks later, we performed memory test and isolated brains to analyze. There were no differences in memory function and BDNF mRNA level between these four groups. However, at 16 weeks later, E/S and E/P group showed memory impairment, and decreased level of BDNF mRNA. Whereas, the powder diet had no effect on memory function and BDNF mRNA level even at 16 weeks later. CONCLUSIONS: These results suggest that the effect of molar loss and powder diet on memory function and BDNF mRNA levels were different, molar loss may have a greater long-term effect on memory ability than powder diet does.

Osseointegration aspects of placed implant in bone reconstruction with newly developed block-type interconnected porous calcium hydroxyapatite.

OBJECTIVES: The purpose of this study was to evaluate the osseointegration of dental implant in bone reconstructions with interconnected porous calcium hydroxyapatite (IP-CHA). MATERIAL AND METHODS: The IP-CHA cylinders (D; 4.3 mm, H; 10.0 mm) were placed into bone sockets in each side of the femurs of four male dogs. The IP-CHA on the right side was a 24-week sample. Twelve weeks after placement, a titanium implant was placed into a socket that was prepared in half of the placed IP-CHA cylinder on the right side. On the left side, another IP-CHA cylinder was placed as a 12-week sample. After another 12 weeks, the samples were harvested, and the bone regeneration and bone-implant contact (BIC) ratios were measured. RESULTS: New bone formation area was superior in the 24-week IP-CHA compared with the 12-week IP-CHA. BIC was not significantly different between IP-CHA and the parent sites. Osseointegration was detected around the implant in IP-CHA-reconstructed bone. CONCLUSION: Our preliminary results suggest that IP-CHA may be a suitable bone graft material for reconstructing bones that require implant placement.

Osseointegration aspects of placed implant in bone reconstruction with newly developed block-type interconnected porous calcium hydroxyapatite

ABSTRACT Artificial bone has been employed to reconstruct bone defects. However, only few reports on implant placement after block bone grafting exist. Objectives The purpose of this study was to evaluate the osseointegration of dental implant in bone reconstructions with interconnected porous calcium hydroxyapatite (IP-CHA). Material and Methods The IP-CHA cylinders (D; 4.3 mm, H; 10.0 mm) were placed into bone sockets in each side of the femurs of four male dogs. The IP-CHA on the right side was a 24-week sample. Twelve weeks after placement, a titanium implant was placed into a socket that was prepared in half of the placed IP-CHA cylinder on the right side. On the left side, another IP-CHA cylinder was placed as a 12-week sample. After another 12 weeks, the samples were harvested, and the bone regeneration and bone-implant contact (BIC) ratios were measured. Results New bone formation area was superior in the 24-week IP-CHA compared with the 12-week IP-CHA. BIC was not significantly different between IP-CHA and the parent sites. Osseointegration was detected around the implant in IP-CHA-reconstructed bone. Conclusion Our preliminary results suggest that IP-CHA may be a suitable bone graft material for reconstructing bones that require implant placement.

Intermittent administration of parathyroid hormone enhances primary stability of dental implants in a bone-reduced rabbit model.

The aim of the study was to investigate the effect of parathyroid hormone (PTH) on primary stability of dental implants in a bone-reduced model. Ten female New Zealand white rabbits underwent ovariectomy and were administered glucocorticoid to induce osteoporosis. One group was administered PTH intermittently by subcutaneous injection for 4 weeks (PTH-group) and the other group was given injections of saline for 4 weeks (Osteoporosis; OP-group). After the administration period, implants were inserted into the distal femoral epiphyses of each animal. At implant placement, insertion torque (IT) and implant stability quotient (ISQ) were measured. Histological examination revealed newly formed trabecular bone around the implant socket in the PTH-group but not in the OP-group. The trabecular bone structures in the PTH-group appeared thicker than those in the OP-group. In the PTH-group, the mean IT value was significantly greater than that in the OP-group (29.8 ± 6.2 Ncm and 10.0 ± 2.1 Ncm, respectively; P < 0.05). The ISQ value in the PTH-group was significantly higher than that in the OP-group (74.7 ± 11.2 and 55.9 ± 13.5, respectively; P < 0.05). Intermittent PTH administration could be an effective treatment for achieving favorable primary stability of dental implants in patients with osteoporosis. (J Oral Sci 58, 241-246, 2016).

Tooth loss might not alter molecular pathogenesis in an aged transgenic Alzheimer's disease model mouse.

BACKGROUND AND OBJECTIVE: Previous studies have reported that tooth loss is a risk factor of Alzheimer's disease (AD). However, the association between tooth loss and cognition and the impact of tooth loss on the molecular pathogenesis of AD remain elusive. In this study, we tested the effect of tooth loss on learning and memory and on the molecular pathogenesis of AD in an aged AD model mice. MATERIALS AND METHODS: We divided 14-month-old amyloid precursor protein (APP) transgenic mice, an AD model mouse line, into upper molar extracted group (experimental) and molar intact group (control). At 18 months old, we analysed not only the changes of amyloid-beta (Aß), pyramidal cells in the brain but also the learning and memory ability with step-through passive avoidance test. RESULTS: The amount of Aß and the number of pyramidal cells in the hippocampus were not significantly different between the experimental and control group. Similarly, the difference of learning and memory ability could not be distinguished between the groups. CONCLUSION: Neither molecular pathogenesis of AD nor associated learning and memory were aggravated by tooth loss in these mice. The limited results of this study which used the aged mice may help the dental profession to plan and explain treatments to patients with AD, which must be designed while taking into account the severity of the AD symptoms.

The Effect of Superstructures Connected to Implants with Different Surface Properties on the Surrounding Bone.

The objective of this study was to investigate how the connection of superstructures to implants with different surface properties affects the surrounding bone. The right and left mandibular premolars and molars of 5 dogs were extracted. After 12 weeks, a machined implant was placed mesially and an anodized implant was placed distally on one side of the edentulous jaw, with the positions reversed on the opposite side. Twelve weeks after implantation, splinted superstructures were set to the implants. At 24 weeks after implantation, the implant stability quotient (ISQ) was measured, radiographs were obtained. Removal torque values were measured and histologic observation was performed. The ISQ values at 24 weeks after implantation were not significantly different between the groups. The removal torque values were significantly different between the distal anodized and distal machined implants (p < 0.05). From 12 to 24 weeks, marginal bone losses were not significantly different between the groups. Fluorescent observation of tissue samples revealed bone-remodeling activity around all of the implants. The results of this study suggest that when implants with different surface properties are connected, machined implants at the most distal sites might be a potential risk factor for implant-bone binding.