Catálogo Taxonômico da Fauna do Brasil: setting the baseline knowledge on the animal diversity in Brazil

The limited temporal completeness and taxonomic accuracy of species lists, made available in a traditional manner in scientific publications, has always represented a problem. These lists are invariably limited to a few taxonomic groups and do not represent up-to-date knowledge of all species and classifications. In this context, the Brazilian megadiverse fauna is no exception, and the Catálogo Taxonômico da Fauna do Brasil (CTFB) (http://fauna.jbrj.gov.br/), made public in 2015, represents a database on biodiversity anchored on a list of valid and expertly recognized scientific names of animals in Brazil. The CTFB is updated in near real time by a team of more than 800 specialists. By January 1, 2024, the CTFB compiled 133,691 nominal species, with 125,138 that were considered valid. Most of the valid species were arthropods (82.3%, with more than 102,000 species) and chordates (7.69%, with over 11,000 species). These taxa were followed by a cluster composed of Mollusca (3,567 species), Platyhelminthes (2,292 species), Annelida (1,833 species), and Nematoda (1,447 species). All remaining groups had less than 1,000 species reported in Brazil, with Cnidaria (831 species), Porifera (628 species), Rotifera (606 species), and Bryozoa (520 species) representing those with more than 500 species. Analysis of the CTFB database can facilitate and direct efforts towards the discovery of new species in Brazil, but it is also fundamental in providing the best available list of valid nominal species to users, including those in science, health, conservation efforts, and any initiative involving animals. The importance of the CTFB is evidenced by the elevated number of citations in the scientific literature in diverse areas of biology, law, anthropology, education, forensic science, and veterinary science, among others

Smoking cessation may present a positive impact on mandibular bone quality and periodontitis-related bone loss: A study in rats

Background: It has been previously shown that cigarette smoke inhalation (CSI) enhances bone loss in ligature-induced periodontitis. In this study, the hypothesis that the interruption of smoke exposure would reverse the impact of CSI on mandibular bone quality and periodontitis-related bone loss was tested. Methods: Fifty-three Wistar rats were randomly assigned to one of the following groups: group 1: control, N = 16; group 2: 83 days of CSI prior to ligature placement, N = 17; or group 3: 90 days of CSI before and 60 days after ligature placement, N = 20. Animals were sacrificed 60 days after ligature placement, the jaws removed and immediately radiographed for photodensitometry analysis. Bone loss was histometrically evaluated. Results: CSI did not affect unligated sites in either condition (P > 0.05); however, smoke inhalation during the whole experimental period significantly enhanced bone loss in ligated teeth (P < 0.05). Moreover, similar levels of bone loss were observed for ligated teeth between the control and cessation groups (0.90 ± 0.33 mm(2); 0.96 ± 0.32 mm(2); 1.64 ± 0.65 mm(2); groups 1, 2 and 3, respectively). Radiographically, continuous exposure to cigarette smoke promoted a significantly reduced bone density (1.74 ± 0.38 aluminum equivalence [Al eq]; 1.74 ± 0.14 Al eq; and 0.68 ± 0.10 Al eq for groups 1, 2, and 3, respectively). Conclusions: Within the limits of the present investigation, it can be assumed that CSI may enhance bone loss in ligature-induced periodontitis, and negatively impact mandibular bone quality. Additionally, smoke exposure cessation seems to reverse its impact on mandibular bone, and, therefore, may be of clinical relevance.76452052

Bone density around titanium implants may benefit from smoking cessation: A histologic study in rats

Purpose: This study tested the hypothesis that interruption of cigarette smoke inhalation (CSI) would reverse its impact on bone quality around implants. Materials and Methods: Sixty-nine rats were assigned to 1 of 4 groups. Group 1 (n = 16) was the control group; group 2 experienced CSI for the duration of the study (150 days); group 3 experienced CSI for 83 days prior to implant placement, until 7 days prior to implant placement, when CSI ceased; and for group 4, CSI exposure was temporarily halted from 7 days before implantation to 21 days afterward. Bone density (the proportion of mineralized bone in a 500-mu m-wide zone lateral to the implant) was calculated for each specimen (mean +/- SD). Results: In the cortical bone, a slight difference in bone density was noted between the groups (97.66% +/- 3.69% for group 1, 98.30% +/- 0.95% for group 2, 98.83% +/- 0.73% for group 3, and 98.11% +/- 1.14 for group 4; P > .05). In contrast, continuous exposure to cigarette smoke (group 2) significantly decreased density in the cancellous bone in comparison to the other groups (25.69% +/- 9.41% for group 1, 18.08% +/- 6.0% for group 2, 25.46% +/- 5.42 for group 3, and 26.20% +/- 6.77% for group 4; P .05). Discussion: The results support the concept that the effects of cigarette consumption on dental implants may be reversible, and therefore suggest that smokers may realize satisfactory outcomes if they cease smoking, even temporarily. Conclusion: In conclusion, smoking may affect bone quality around titanium implants in cancellous bone, and cessation could result in a return toward to the levels of the control group.20571371

Effect of estrogen and calcitonin therapies on bone density in a lateral area adjacent to implants placed in the tibiae of ovariectomized rats

Background: This study evaluated the influence of estrogen and calcitonin administration on tibial bone density in a lateral area adjacent to implants placed in ovariectomized rats (OVX). Methods: One screw-type titanium implant was placed bilaterally in the ovariectomized rats, and the animals assigned to one of the following groups: group 1 (n = 15): sham surgeries; group 2 (n = 15): OVX; group 3 (n = 14): OVX subcutaneously administered with calcitonin (CT) 4 days/week (16 IU/kg); group 4 (n = 14): OVX administered daily with 17beta estradiol (20 mug/kg). After 60 days, the animals were sacrificed and undecalcified sections obtained. Blood samples were collected to measure serum levels of alkaline phosphatase and calcium at the time of sacrifice. Bone density was measured in a 500 mum wide mineralized zone lateral to the implant. Results: Alkaline phosphatase levels in groups 2 and 3 (P >0.05) were statistically higher than groups 1 and 4 (P 0.05). However, in zone B, the animals that received estrogen administration (group 4) presented a higher bone density than groups 2 and 3 (P <0.05). Conclusion: It appears that estrogen therapy may prevent the negative influence of endogenous estrogen deficiency on bone density around titanium implants placed in ovariectomized rats.74111618162

The influence of cigarette smoke inhalation and its cessation on the tooth-supporting alveolar bone: a histometric study in rats

Objective: It has been previously shown that smoking may enhance periodontal breakdown and impair bone healing around titanium implants. However, there is a lack of information concerning the effect of smoking on the tooth-supporting alveolar bone. Thus, the aim of this study was to histometrically evaluate the influence of cigarette smoke inhalation and its cessation on tooth-supporting alveolar bone. Methods: Sixty male Wistar rats were randomly assigned to one of the following groups: group 1 - control (n = 15), group 2 - 2 months of cigarette smoke inhalation (n = 13), group 3 - 3 months of cigarette smoke inhalation and 2 months without exposure to cigarette smoke inhalation (n = 16) and group 4 - 5 months of cigarette smoke inhalation (n = 16). Five months after the beginning of cigarette smoke inhalation regime (2 months for group 2), the animals were killed and the mandible was removed and prepared for histological sections. The proportion of mineralized tissue in the furcation area (i.e. a 1000 mu m zone under the furcation and between the roots) was obtained. Results: Data analysis demonstrated that the animals continuously exposed to cigarette smoke inhalation presented a decreased proportion of mineralized tissue (groups 2 and 4), when compared to control and cessation groups (groups 1 and 3) (p < 0.05). Similar levels of proportion of mineralized tissue were observed in groups 1 and 3, showing a beneficial effect of cigarette smoke inhalation cessation on proportion of mineralized tissue. Conclusion: Within the limits of the present study, it can be concluded that cigarette smoke inhalation may affect the tooth-supporting bone as early as 2 months after the initial exposure, and that smoke exposure cessation may revert its negative impact on the alveolar bone.41211812

Effect of intermittent PTH administration in the periodontitis-associated bone loss in ovariectomized rats

Objective: Parathyroid hormone intermittent administration has been considered to treat bone mass decrease in osteoporotic individuals. The present study evaluates whether PTH can affect alveolar bone loss in ovariectornized rats, since estrogen deficiency has been proposed as a risk factor for periodontal disease. Design and methods: Thirty female rats were set in groups: ovariectomized (Ovx) and Sham operated. Ovx were divided in two groups: Ovx-PTH (1-34) treated and Ovx, which received vehicle. After 1 week, cotton ligature was placed around one tower first molar of all animals to induce periodontal disease. Ovx treated received PTH doses of 40 mu g/kg, three times a week for 30 days. After that, the animals were sacrificed, the mandibles extracted, X-rayed and samples prepared for histological evaluation. Histomorphometry was performed using image analyzer software. Scanning electron microscopy (SEM) of the tibias was also performed in all animals to evaluate possible changes in bone structure caused by the estrogen deficiency. Optical densities of the radiographs were measured by aluminum step-wedge equivalent thickness. Results: Histomorphomery indicated the anabolic PTH effect in ovariectomized rats with significant inhibition of periodontitis manifestation (p < 0.05) thus neutralizing the periodontitis inductor effects. The photo densitometry showed a lower mandibular optical density in the ovariectomized group that did not receive PTH (p < 0.05). SEM image confirmed the early effect of estrogen deficiency in osseous tissue and PTH anabolic effect. Conclusion: PTH systemic intermittent administration was able to reduce alveolar bone toss in ovariectomized rats, despite the presence of a periodontal disease inductor and estrogen deficiency. (c) 2004 Elsevier Ltd. All rights reserved.50442142

Histometric evaluation of bone around titanium implants with different surface treatments in rats exposed to cigarette smoke inhalation

There is a lack of histological information about the influence of cigarette smoke on bone around surface-treated implants. The aim of the present study was to test the influence of titanium surface treatment on osseointegration in animals that were exposed to intermittent cigarette smoke inhalation. Twenty-two male Wistar rats were used. One tibia, chosen at random, received a machined titanium implant (MI) while the other received an aluminum oxide-blasted surface implant (ABI). The animals were randomly assigned to one of the following groups: Group 1 - control (n=11) and Group 2 - intermittent cigarette smoke inhalation (n=11). Sixty days after surgery, the animals were sacrificed. The degree of bone-to-implant contact (BIC), bone filling (BF) within the limits of the threads of the implants and bone density (proportion of mineralized bone in a 500-mu m-wide zone lateral to the implant - BD) were measured in the cortical (zone A) and cancellous bone (zone B) areas. Data analysis showed significant differences when comparing the groups and implant surfaces in both zones for BIC (two-way ANOVA - P < 0.05). The two groups presented higher BIC mean values for ABI, when compared with MI (P < 0.05). In group 2, cigarette smoke inhalation negatively affected BF in both zones (P < 0.05). Group 2 presented a significantly decreased BD in both zones (P < 0.05). No statistically significant differences were observed between surfaces in any of the groups for BD. Within the limits of the present study, it can be concluded that the aluminum oxide blast surface treatment may increase the degree of BIC but cannot overcome the detrimental effect of tobacco smoke on bone around titanium implants. To cite this article:Correa MG, Campos MLG, CEsar-Neto JB, Casati MZ, Nociti FH, Sallum EA. Histometric evaluation of bone around titanium implants with different surface treatments in rats exposed to cigarette smoke inhalation.Clin. Oral Impl. Res. 20, 2009; 588-593.doi: 10.1111/j.1600-0501.2008.01695.x.20658859

Effect of cigarette smoke inhalation and estrogen deficiency on bone healing around titanium implants: A histometric study in rats

Background: It has been shown that cigarette smoke inhalation (CSI) and estrogen deficiency (OVX) may affect bone quality around titanium implants; however, their association has not been evaluated. Therefore, this study aimed to verify the effects of CSI associated with OVX on bone healing around titanium implants. Methods: The tibia surface of 45 female Wistar rats was surgically exposed, and screw-shaped titanium implants were placed. The animals were randomly assigned to OVX (ovariectomized rats; n = 15), SHAM (sham-operated rats; n = 15), and CSI + OVX (4 months of intermittent cigarette smoke inhalation, starting 2 months before implant placement in ovariectomized rats; n = 15). The implants were placed at the time of OVX or SHAM surgery. After 60 days, the animals were sacrificed and undecalcified sections obtained. The percentages of mineralized tissue (bone density [BD]) in a 500-mu m-wide zone lateral to the implant, bone filling (BF) within the limits of the threads, and bone-to-implant contact (BIC) were measured in cortical (zone A) and cancellous (zone B) bone. Results: In zone A, the CSI + OVX group showed a significant difference regarding BIC and BD (P < 0.05) compared to the other groups. In zone B, data analysis showed that the CSI + OVX group presented the lowest percentage of BD and BIC, followed by the OVX and SHAM groups, respectively (P < 0.05). Conclusion: Within the limits of the present study, it can be concluded that cigarette smoke inhalation amplified the deleterious effects of estrogen deficiency, affecting both preexisting and newly formed bone in the cortical and cancellous bone around titanium implants.77459960

Smoking modulates interleukin-6 : interleukin-10 and RANKL : osteoprotegerin ratios in the periodontal tissues

Background and Objective: This study evaluated the effect of smoking on the gene expression of interleukin-1 alpha, -1ra, -6, -8 and -10, tumor necrosis factor-alpha, matrix metalloproteinase (MMP)-2 and -8, receptor activator of NF-kappa B ligand (RANKL) and osteoprotegerin, in sites with periodontitis. Material and Methods: Gingival biopsies were divided into three groups: the healthy group (periodontally healthy subjects; n = 10); the periodontitis group [subjects with severe chronic periodontitis who never smoked (probing depth >= 7 mm) (n = 25)]; and the smoking group (subjects diagnosed with severe chronic periodontitis who smoked >= 1 pack per day for at least 10 years; n = 25). Gene and protein expressions were analyzed by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Results: Data analysis demonstrated that, except for MMP-8 and osteoprotegerin, the levels of all factors were increased by inflammation (p < 0.001). The levels of interleukin-1 alpha, -1ra, -6 and -8, and RANKL, were higher in smokers with periodontitis compared with controls, whereas the levels of interleukin-10, MMP-8 and osteoprotegerin were lower (p < 0.001). Smoking lowered the levels of interleukin-1 alpha, -8, -10, tumor necrosis factor-alpha, MMP-8 and osteoprotegerin, and increased the levels of interleukin-6 and -1ra in sites with a comparable type of periodontitis (p < 0.001). Conclusion: In conclusion, smoking modulates gene expression in the periodontium, and the influence of smoking on periodontal disease may involve effects of interleukin-6:interleukin-10 and RANKL:osteoprotegerin ratios.42218419