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.

Increased crown-to-implant ratio may not be a risk factor for dental implant failure under appropriate plaque control.

OBJECTIVE: The aim of this study was to evaluate whether increased crown-to-implant (C/I) ratio influences implant stability or not under proper healthy control of peri-implant mucosa. The hypothesis of this study is that implant stability can be maintained despite High C/I, under appropriate plaque control. MATERIALS AND METHODS: Five male Beagle-Labrador hybrid dogs (2 years old) were used. Their bilateral mandibular premolar extraction was performed. After allowing 12 weeks for bone healing, 3 types of vertical marginal bone loss were simultaneously prepared randomly. Then, 30 titanium implants were placed in the edentulous areas and defined as High C/I, Mid C/I and Low C/I groups. This time point was designated as the baseline (0 Week). Twelve weeks after implant placement, metal superstructures were cemented to the implants and an occlusal plate was set at the opposite side. At the same time, Calcein green was injected for remodeling evaluation. Implants were loaded by feeding the dogs a hard pellet diet. Tooth brushing was performed 5 days per week during the study to maintain healthy peri-implant mucosa. Twenty-four weeks following implant placement, the interface structure was evaluated clinically, radiologically, and histologically. RESULT: Implant stability quotient (ISQ) increased with time in all 3 groups, without any significant correlation with the C/I value (p >0.05). Moreover, mean marginal bone loss adjacent around implants in all 3 groups ranged between 0.11 and 0.19 mm, with no significant difference (p >0.05). Many fluorescence-labeled bones are shown in the High C/I group. It is considered that high remodeling activity prevent marginal bone loss in the High C/I group and this may provide favorable implant stability under proper plaque control. CONCLUSION: These findings suggest that increased C/I may not be a risk factor for implant failure if the peri-implant mucosa is kept healthy, as was the case in this animal model.

Tooth loss induces memory impairment and neuronal cell loss in APP transgenic mice.

Tooth loss is a known risk factor of Alzheimer's disease (AD). However, the association of tooth loss with the molecular pathogenesis of AD is still unknown. The hypothesis that the molecular pathogenesis of AD is enhanced by molar tooth loss was tested. Seventeen female transgenic mice (J20) were divided into the experimental (EX, n=10) and control (C, n=7) groups. In the EX group, maxillary bilateral molar teeth were extracted at the age of 6 months. In the C group, however, these teeth remained intact. Passive avoidance test was performed to evaluate learning and memory abilities right after tooth extraction (6 months old) and 4 months later (10 months old). After the test at 10 months, amyloid beta (Aß) deposition and changes of neuronal cell number and area in the hippocampus were investigated using half of the brains. The other half was homogenized and used to determine Aß40 and Aß42 levels by ELISA. At the 10 months of age, learning and memory abilities were significantly impaired in the EX group compared to the C group (P<0.05). The neuronal cell number in the CA1 and CA3 regions was significantly lower in the EX group than in the C group (P<0.05). Total Aß, Aß40, and Aß42 levels showed no significant intergroup difference. Molar tooth loss may cause neuronal cell loss in the hippocampus, leading to memory impairment; this process may be independent of the amyloid cascade.

Influence of static overload on the bony interface around implants in dogs.

PURPOSE: The aim of this study was to investigate bony changes around selectively overloaded implants in dogs. MATERIALS AND METHODS: Twelve adult male beagles were used: 4 animals each for control, 4-week-load, and 12-week-load groups. Three implants were placed on the right side of each of the 12 animals and the time point designated as the study's baseline. Superstructures were then fabricated and attached only in the 2 implant-loaded groups 12 and 20 weeks following implant placement. Each lower distal implant was then fit with a cantilever-type superstructure extending in a mesial direction so as to be able to generate a controlled overload. The mesial and central implants were attached via superstructures equipped with a stainless steel screw, which could be tightened to create a controlled overload force. The force was induced by a controlled static 250-microm submerging of the cantilever of the distal implant. After 24 weeks, tissue specimens including implants were evaluated histologically and histomorphometrically. RESULTS: Numerous fluorescence-labeled bone areas were noted in the 4-week-load group, showing a high remodeling activity. Marginal bone loss was significantly greater in the 12-week-load group than in the 4-week-load group. The ratio of fluorescence-labeled bone area in the inner thread region was significantly higher in the 4-week-load group than in the 12-week-load group. CONCLUSIONS: These findings demonstrate that static overload-induced forces can elicit changes in peri-implant bone in experimental animals.