Oral Health Interventions in Natural Disasters: A Scoping Review.

OBJECTIVES: This work aimed to identify, appraise, and summarize existing knowledge about oral health interventions in the context of natural disasters and verify the main research gaps. METHODS: We searched in PubMed (National Library of Medicine, Maryland, USA), EMBASE (Elsevier, Amsterdam, Netherlands) and Epistemonikos (Epistemonikos Foundation, Santiago, Chile) until 2021 for primary studies and systematic reviews, assessing any oral health intervention in the context of natural disasters. The interventions were classified according to Cochrane Effective Practice and Organization of Care (EPOC) categories, and the type of natural disaster was defined according to the classification by the Centre for Research on the Epidemiology of Disasters (CRED). RESULTS: We assessed a total of 19 studies (majorly in Japan, n = 8), all performed in the context of an earthquake or mixed natural disasters (earthquake and tsunami). Regarding interventions, 12 studies reported a promotional/ preventive intervention, with oral examination being the most frequent. 7 studies reported therapeutic interventions, mainly related to emergency management of fractures and injuries. CONCLUSIONS: The evidence accessed in our study was limited, highlighting the need for further research to focus on different oral health care interventions and outcomes in the context of different natural disasters, thus enhancing the formulation and implementation of recommendations and protocols worldwide.

A study of unfavorable splits in the sagittal ramus osteotomy with a short lingual cut.

In the bilateral sagittal split osteotomy, a short lingual cut is made on the medial side of the ramus; however, in some cases, a true fracture occurs on the buccal side of the ramus. The purpose of this study was to evaluate the relationship between the splitting pattern of the mandible and the form of the mandible, the surgical technique used, and the postoperative occurrence of relapse after 'unfavorable' splits. The investigation examined 143 patients in whom a short lingual cut was attempted. The rate of unfavorable split was 14.7% (42/286). A strong correlation was observed between the reach of the lateral bone cut to the inferior border of the mandible and an unfavorable split. According to multivariate regression, the factors leading to an insufficient lateral bone cut were the degree of inward curvature of the ramus (P=0.001) and the position of the lateral bone cut (P=0.002). There was no significant difference in relapse between cases of unfavorable and normal splits. An unfavorable split does not affect the prognosis of the occlusion, but it is important to confirm the inward curvature of the ramus and set the position of the lateral bone cut adequately to avoid unfavorable splits.

Treatment of refractory non-union after maxillary osteotomy: A case report.

Maxillary non-union is a rare complication that occurs after an orthognathic surgery such as Le Fort I osteotomy. Here, we report a case of refractory non-union after maxillary osteotomy, which required a second surgery with bone graft. A 33-year-old man who had undergone bimaxillary osteotomy complained of an abnormal sensation in the right alar part about 1 year after the surgery. The patient was diagnosed as having maxillary non-union. Although surgical stabilization was performed using titanium plates, the non-union remained. The re-fusion surgery was performed about 3 years after the bimaxillary osteotomy with autologous bone graft using a biodegradable fixation system. At the 1-year follow up, the maxillary non-union was healed both clinically and radiographically. Re-fusion surgery using bone graft with biodegradable fixation might be an effective treatment option in cases of prolonged non-union that becomes evident after a long period following the initial maxillary osteotomy.

Influence of the anatomical form of the posterior maxilla on the reliability of superior maxillary repositioning by Le Fort I osteotomy.

Certain patients with facial deformities require superior repositioning of the maxilla via Le Fort I osteotomy; however, the magnitude of superior repositioning of the maxilla is often less than expected. In this study, the correlation between the accuracy of superior repositioning of the maxilla and the anatomical form of the maxillary posterior region was examined. Seventy-five patients who underwent Le Fort I osteotomy without forward movement of the maxilla but with superior repositioning of the maxilla were included in this study. The bone volume around the descending palatine artery (DPA), the angle of the junction between the pterygoid process and the tuberosity, and the distance between the upper second molar and the pterygoid process were measured via three-dimensional analysis. A significant negative correlation (r=-0.566) was found between the bone volume around the DPA and the ratio of repositioning (actual movement divided by expected movement). It is possible that the superior repositioning of the maxilla expected prior to surgery was not sufficiently attained because of the large volume of bone around the DPA. The results of this study show that in some patients, superior repositioning was not achieved at the expected level because of bone interference attributable to the anatomical form of the maxillary posterior region.

Colorimetric analysis of unstained lesions surrounding oral squamous cell carcinomas and oral potentially malignant disorders using iodine.

To determine whether the measurement of staining with 3% Lugol's solution provided efficient criteria for determining the area of resection for oral carcinomas and oral potentially malignant disorders, the authors analyzed the color of unstained lesions (USLs) in relation to histopathological findings. After vital iodine staining, USLs were seen in 48 of 54 patients (88.9%). A significant difference was seen in the value of lightness between stained lesions (SLs) and USLs for patients with moderate and severe epithelial dysplasia (P<0.001). The deviation between the macroscopically observable and the histopathological boundaries was -0.65+/-1.26 mm (range: -4.36 to 1.52). Color charts prepared on the basis of values for lightness and hue reproduced the macroscopic color differences in USLs, suggesting that it may become possible to diagnose USLs histologically on the basis of the measured color values and use of color charts to help determine the resection area in surgery.

Amphiregulin induces proliferative activities in osseous dysplasia.

Human osseous dysplasia (OD) is a benign fibro-osseous neoplasm of periodontal ligament origin in which normal bone is replaced with fibrous connective tissue containing abnormal bone or cementum. However, cellular differentiation and proliferation in OD have not been fully elucidated. In vitro culture systems have distinct advantages for analytical studies. Therefore, we established immortalized cell lines (OD-1) from OD lesions of the jaw from an individual with gnathodiaphyseal dysplasia (GDD). We hypothesized that OD-1 had a characteristic growth mechanism different from that of mineralized-associated cells such as osteoblasts. To clarify the difference of gene expression patterns between OD-1 and osteoblasts, we compared the profiles of genes expressed in the 2 cell types by microarray analysis. We identified amphiregulin to be highly expressed in OD-1 compared with osteoblasts and gingival fibroblasts. OD-1 showed proliferative activities regulated in an autocrine manner by amphiregulin, and amphiregulin may play a significant role in the proliferation of OD.

Metastatic tumor thrombus attached to a pacemaker electrode.

We present a patient with a large tumor embolus attached to a pacemaker electrode leading to multiple pulmonary emboli. At postmortem examination, this thrombus was composed of clusters of well-differentiated squamous cell carcinoma intermingled with fibrin. Tumor involvement was not evident in the myocardium, endocardium, or epicardium. The primary tumor was discovered in the lower intrathoracic esophagus. Tumor microemboli from the esophageal primary lesions may have accumulated around the pacemaker electrode due to turbulent flow in this region, producing a large and friable tumor embolus.

Differences in the extent of inflammation caused by intratracheal exposure to three ultrafine metals: role of free radicals.

Nickel and cobalt, which belong to the same elemental group, are known to cause interstitial lung disease and bronchial asthma. The ability of these metals to injure lung cells and cause inflammation is likely to be important in their pathogenicity but comparative studies are rare. Additionally, ultrafine (uf) forms of these metals are used increasingly and there is little available information on their toxicity. Thus the inflammatory response following intratracheal instillation of ultrafine particles of Co, Ni, and TiO2 was compared. Physiological saline (PS) was used as a vehicle control and DQ12 quartz as a positive control. Male Wistar rats were intratracheally instilled with the 3 particle types at a dose of 1 mg suspended in physiological saline. At 1, 3, 7, 15, and 30 d after the injection, lung weight and the cellular and biochemical changes in bronchoalveolar lavage fluid (BALF) were determined. By all of the indices, Uf-Ni appeared to be the most injurious to the lung, causing severe and sustained inflammation, cytotoxicity and increased epithelial permeability. The next most toxic material was DQ12 quartz, with Uf-Co being closely similar in ability to cause inflammation. Uf-TiO2 was more active than the saline control in all of the indices, but was the least toxic of the particles studied. The present study reveals that three ultrafine particles of the same diameter are dramatically different in their ability to cause inflammation. The three ultrafines were compared as to their ability to cause free-radical damage to supercoiled plasmid DNA, and the result of free-radical activity was found to be Uf-TiO2 << Uf-Co = Uf-Ni. Difference in free-radical-generation activity therefore could underlie the difference in inflammation of these three ultrafine particle types.

Apolipoprotein E and antioxidants have different mechanisms of inhibiting Alzheimer's beta-amyloid fibril formation in vitro.

We compared the mechanisms of apolipoprotein E- (apoE-) and antioxidant- (AO-) mediated inhibition of beta-amyloid fibril (fA beta) formation in vitro, based on a nucleation-dependent polymerization model using fluorescence spectroscopy with thioflavin T. We first applied a kinetic plot to transform a sigmoidal time-course curve of fA beta formation from freshly prepared amyloid beta-peptides (A beta) into a straight line. Mathematical treatment of this plot demonstrated that the above-described sigmoidal curve is a logistic curve and provided us with a kinetic parameter t(1/2), the time when the rate of fA beta formation is maximum. t(1/2) of beta-amyloids (A beta) (1-42) and (1-40) were 18.7 +/- 1.7 min and 6.3 +/- 0.2 h, respectively (mean +/- SD, n = 3) and were independent of the initial A beta concentration examined. Although apoE extended t(1/2) of both A betas in a dose-dependent manner, AO did not. On the other hand, the final amount of fA beta formed was decreased by both apoE and AO dose-dependently. We then analyzed the effect of apoE and AO on the extension reaction of fA beta, based on a first-order kinetic model. Although apoE extended the time to proceed to equilibrium in a dose-dependent manner, AO did not. On the other hand, both apoE and AO dose-dependently decreased the final amount of fA beta formed. These results indicate that apoE and AO inhibit fA beta formation in vitro by different mechanisms and suggest the existence of multiple pharmacological targets for the prevention of fA beta formation.

Apolipoprotein E and alpha 1-antichymotrypsin in dialysis-related amyloidosis.

Dialysis-related amyloidosis as represented by carpal tunnel syndrome is a serious complication of long-term dialysis treatment of patients with chronic renal failure. beta 2-microglobulin has been identified as a structural component of the amyloid deposits, but other factors also are associated with amyloid formation. We recently demonstrated the presence of apolipoprotein E and alpha 1-antichymotrypsin in the amyloid deposits. We therefore analyzed how polymorphic variants of both genes were related to the onset of amyloidosis. Among the apolipoprotein E genotypes, allele epsilon 2 represented a protective factor that delayed the onset of disease. In contrast, polymorphic alpha 1-antichymotrypsin alleles had no effect on the onset of amyloidosis. Thus, the apolipoprotein E epsilon 2 allele can be added to the list of factors that determine the onset of dialysis-related amyloidosis, which include patient age at initiation of dialysis therapy, dialysis duration, and the dialysis membrane used.

Citrate uptake by isolated rat renal brush border membrane vesicles in cadmium-intoxicated rats.

Epidemiological Studies have reported that the formation of renal stones is often observed in workers exposed to cadmium (Cd). Citrate is known to be a protective factor against renal stone formation. We previously reported that direct exposure to high-level cadmium impaired the citrate uptake by the brush border membrane vesicles (BBMV), which may mean that the formation of renal stones from exposure to Cd could be prevented. In the present study, to clarify the mechanism of Cd-induced renal stone formation, the characteristics of BBMV-induced citrate uptake were determined in Cd-intoxicated rats. Cd intoxication was induced by daily subcutaneous injections of CdCl2 at a dose of 2 mg Cd/kg body wt per day for 17 to 20 days. The BBMV were prepared by the divalent cation precipitation method. Citrate uptake was measured by the Millipore rapid membrane filtration technique. The citrate uptake per mg protein was not significantly different between the two groups. The volume of BBMV was significantly reduced (50%) in Cd-intoxicated rats compared with that of control rats. Percentages of the equilibrium value were also significantly inhibited in Cd-intoxicated rats.

Concentration-dependent inhibitory effects of apolipoprotein E on Alzheimer's beta-amyloid fibril formation in vitro.

Recently, many research groups have examined the effect of apolipoprotein E (apoE) on beta-amyloid fibril (betaAf) formation in vitro. However, their data were somewhat controversial and no exact kinetic assessment of the role of apoE has thus far been available. We examined the effect of human apoE on betaAf formation in vitro, starting with various concentrations of freshly prepared beta-amyloid(1-40) (beta1-40) and using fluorescence spectroscopy with thioflavine T. When 50 microM of beta1-40 was incubated with a 1:1000 to 1:100 molar ratio of apoE, a dose-dependent inhibitory effect of apoE was observed. Both the nucleation and extension phases of betaAf formation in vitro were inhibited by apoE. On the other hand, when 300 microM of beta1-40 was incubated with a 1:100 molar ratio of apoE, the inhibitory effect of apoE was completely abolished. We then focused our study on the kinetics of the inhibitory effect of apoE on the extension phase of betaAf formation in vitro, utilizing the recently established first-order kinetic model of betaAf extension in vitro [Naiki, H., & Nakakuki, K. (1996) Lab. Invest. 74, 374-383]. The mathematical treatment of the data suggests that apoE inhibits the extension of betaAf in vitro, by making a complex with beta1-40, thus eliminating free beta1-40 from the reaction mixture. The equilibrium association constant with beta1-40 was practically the same among the three major recombinant apoE isoforms. These results indicate that the effects of apoE on betaAf formation in vitro is differential and could settle some of the controversy about beta-amyloid-apoE interaction in vitro.

Direct effect of inorganic mercury on citrate uptake by isolated rat renal brush border membrane vesicles.

Occupational exposure to mercury has long been associated with renal proximal injury and an increased incidence of proteinuria, as has such exposure to cadmium. Renal citrate excretion is very important with respect to acid-base balance since the metabolism of citrate generates three bicarbonate ions. In this study, we exposed isolated rat renal brush border membrane vesicles (BBMV) to mercury (Hg2+) and examined their citrate uptake characteristics. BBMV were prepared by the divalent cation precipitation method. Citrate uptake was measured by the Millipore rapid membrane filtration method. The preincubation of BBMV with 0.5 and 2 mM HgCl2 for 1 min significantly inhibited citrate uptake compared with that of BBMV without Hg preincubation. The analysis of the time course of citrate uptake during a 30-min preincubation of BBMV with 0.1 mM Hg2+ also revealed a significant reduction in the uptake compared with that of the control BBMV without preincubation. These findings indicate that the preincubation of BBMV with mercury results in a time- and concentration-dependent inhibition of citrate uptake.

Infection of human papillomavirus (HPV) and p53 over-expression in human female genital tract carcinoma.

Inactivation of p53 gene products either by mutation or by complex formation with E6 oncoprotein encoded by high risk HPV appears to be a common event in cervical carcinogenesis. This study was designed to clarify this association in 41 primary cervical, 15 endometrial, 3 ovarian and one rectal carcinomas. Polymerase chain reaction analysis revealed presence of high risk HPV in 36 (88%) cervical, 5 (33%) endometrial and none of ovarian and rectal carcinomas. HPV 16 was found in 14 cervical carcinomas, HPV 18 in 19 cervical and 2 endometrial carcinomas and HPV 33 in 28 cervical and 5 endometrial carcinomas. Expression of tumor suppressor protein p53 by using polyclonal antibody CM-1, was detected in 28 (68%) cervical, 7 (47%) endometrial, 2 (66%) ovarian and one (100%) rectal carcinoma. Twenty six cervical and 3 endometrial carcinoma cases were positive for both high risk HPV and p53. We conclude that beside cervical carcinoma HPV infection is not uncommon in endometrial carcinoma and in our experimental design there is no inverse correlation between HPV infection and p53 over-expression in a variety of the tumors analysed in the present study.

Temperature-sensitive parainfluenza type 1 vaccine virus directly accesses the central nervous system by infecting olfactory neurons.

Immunohistochemical investigation showed that intranasal inoculation of mice with a temperature-sensitive (ts) mutant of parainfluenza type 1 vaccine virus resulted in infection of some olfactory neurons as well as respiratory epithelial cells. It also disclosed the presence of viral antigens in glomeruli of the olfactory bulb but not in the secondary neurons (mitral and tufted cells). Polymerase chain reaction demonstrated the persistence of virus-specific nucleic acids in the olfactory bulb. These observations lead to the conclusion that parainfluenza virus, even with a ts phenotype, gains access to the central nervous system by infecting olfactory neurons.

First-order kinetic model of Alzheimer's beta-amyloid fibril extension in vitro.

Recently, several studies have proposed models describing the mechanisms of Alzheimer's beta-amyloid fibril formation in vitro. However, these models are somewhat controversial and no exact kinetic analyses measuring the polymerization velocity as an indicator of the reaction, have thus far been available. We first formed beta-amyloid fibrils from a synthetic peptide, beta-amyloid(1-40), and determined the optimum conditions for quantitative fluorometry of these beta-amyloid fibrils with thioflavine T. Optimum fluorescence measurements of beta-amyloid fibrils were obtained at the excitation and emission wavelengths of 446 and 490 nm, respectively, with the reaction mixture containing 5 microM thioflavine T and 50 mM of glycine-NaOH buffer, pH 8.5. We then focused our study on the extension phase of beta-amyloid fibril formation in vitro. When beta-amyloid fibrils were incubated with monomeric beta-amyloid(1-40) in conditions where de novo seed formation does not occur, the extension of beta-amyloid fibrils was observed with electron microscopy. Quantitative fluorometry revealed that: (a) extension of amyloid fibrils proceeded by a pseudo-first-order exponential increase as measured by the fluorescence of thioflavine T; (b) the rate of extension was maximum around pH 7.5, and was dependent on the incubation temperature. Between 20 and 37 degrees C, good linearity was observed between the common logarithm of the initial rate and the reciprocal of the absolute temperature; (c) the rate of polymerization was found to be proportional to the product of beta-amyloid fibrils number concentration and the beta-amyloid(1-40) concentration; (d) the net rate of extension was the sum of the rates of polymerization and depolymerization. These results show that beta-amyloid fibril formation can be explained by a first-order kinetic model: i.e., the extension of beta-amyloid fibrils proceeds via the consecutive association of beta-amyloid(1-40) onto the ends of existing fibrils.

In vivo induction of apoptosis by influenza virus.

Intranasal exposure of mice to influenza virus led to cell death in bronchial/bronchiolar epithelial cells, alveolar cells and lymphoid cells. These cells displayed fragmentation of nuclei and chromatin condensation. Nick end-labelling of DNA in situ confirmed that such apoptotic cells had fragmented DNA. These results suggest that the influenza virus induces apoptosis in vivo.

Viremia induced by influenza virus.

A mouse model of influenza A/PR/8 virus infection was adopted to investigate the blood and various tissues of intranasally infected mice for the presence of viral RNA by using the nested polymerase chain reaction. The nucleoprotein gene was detected in the red blood cell fraction from 1 to 5 days post-inoculation, while it was found in the lung and brain up to 14 days and in the liver, spleen, kidney, heart, and skeletal muscle up to 7 days. The virus-specific messenger RNA was transiently found in these organs. When mice received the uv-inactivated virus, viremia did not occur. The prior transfer of the hyperimmune serum prevented pneumonia but not bronchitis, and viremia was totally abolished. These results suggest: (1) viremia occurs during the acute phase of infection, (2) the virus is present in various organs and there the virus gene is transiently expressed, and (3) the virus enters the blood stream possibly through capillaries of the infected alveolar wall. Viremia may influence the pathogenesis of influenza.

Efficacy of a temperature-sensitive Sendai virus vaccine in hamsters.

A temperature-sensitive HVJ-pB strain of parainfluenza type 1 (Sendai) virus was obtained from a persistently virus-infected cell culture. Intranasal inoculation of Syrian hamsters with the HVJ-pB temperature-sensitive mutant resulted in an abortive infection but induced a specific antibody response against Sendai virus without appreciable lesions in the respiratory tract. Prior exposure to the temperature-sensitive mutant protected hamsters from subsequent challenge with virulent wild-type virus. The efficacy of protection became apparent at 5 days after vaccination and lasted for at least 720 days. For practical use of the HVJ-pB vaccine, a single intranasal administration to newborn babies aged over 15 days is recommended.

Parainfluenza virus type 1 infects olfactory neurons and establishes long-term persistence in the nerve tissue.

A mouse model of Sendai virus infection was adopted to examine the in vivo neurovirulence of parainfluenza viruses. A nested polymerase chain reaction detected the Sendai virus nucleoprotein gene in the olfactory bulbs of intranasally infected mice for at least 168 days post-infection (p.i.) and virus-specific messenger RNAs for 28 days p.i. Viral proteins were histochemically detected in some olfactory neurons for 7 days p.i. They were also found in glomeruli of the olfactory bulbs but not in the mitral cells and the tufted cells. No virus was detected in the whole brain not including the olfactory bulbs. When mice were inoculated with UV-inactivated virus, the viral RNA was present in the olfactory bulbs for a short period of 14 days, with no demonstrable viraemia. These results demonstrate that the parainfluenza virus directly accesses the central nervous system via olfactory neurons and establishes long-term persistence in the nerve tissue.