[Characteristics of the alveolar bone defects evaluated by cone-beam CT in periodontitis patients with orthodontic treatment history of Angle class â ¡ malocclusion].

Objective: To evaluate the levels of alveolar bone defects by using cone-beam CT in periodontitis patients with history of orthodontic treatment and to find the special tooth positions, sites and periodontitis stages of alveolar bone defects, so as to provide reference for the formulation of clinical personalized diagnosis and treatment plans. Methods: Thirty patients who were diagnosed as Angle class Ⅱ malocclusion, treated by using labial fixed orthodontic appliances and also diagnosed as periodontitis (orthodontic group) were recuited from January 2009 to June 2019 at the School and Hospital of Stomatology, China Medical University in the present study. They were aged (27.0±5.4) years old (ranged 18-41 years old). Another 60 periodontitis patients without a history of orthodontic treatment matched according to age, gender and severity of periodontitis were selected as control group (non-orthodontic group). They were aged (26.7±5.2) years old (ranged 18-41 years old). Cone-beam CT images were used to measure the heights of the alveolar bone defects at each tooth position of the patients. The difference in the heights of the alveolar bone defects between the orthodontic group and the non-orthodontic group at the same position of the maxillary and mandibular alveolar bones were compared. The specificities of the defect heights in different positions of the maxillary and mandibular alveolar bones and different sites of the same tooth position were analyzed among orthodontic group. The specificities of the different tooth positions of the maxillary and mandibular alveolar bones of the different periodontitis stages among orthodontic group were compared. Results: The heights of the alveolar bone defects in the maxillary canine area and molar area, the mandibular incisor area, the canine area and the premolar area in the orthodontic group were higher than that in the non-orthodontic group, and the differences were statistically significant (P<0.05). In orthodontic group, the most severe teeth in the maxillary and mandibular alveolar bone defects were the canine areas [(3.75±1.00), (3.83±1.10) mm]. Secondly, the more severe tooth positions of the maxillary alveolar bone height defects were the molar area [(3.67±0.84) mm] and the incisor area [(3.39±0.83) mm] and the more severe tooth positions of the mandibular alveolar bone defects were the incisor area [(3.73±1.42) mm] and the molar area [(3.54±0.81) mm]. The height of the alveolar bone defect in the mandibular incisor area was greater than that in the maxillary (P<0.05). The bone defect in the maxillary molar area was severer than that of the mandibular area (P<0.05). The alveolar bone defects in the buccal and lingual sides were mostly larger than that of the mesial and distal sides both in maxillary and mandibular positions except for the maxillary incisor area(P<0.05). The most severe alveolar bone defect position changed with the periodontitis stage. The most severe tooth position of the maxillary in stage Ⅰ periodontitis was in the molar area [(3.26±0.63) mm], whereas the incisor area was the most severe tooth of the mandible [(3.14±1.04) mm]. In addition, among maxillary incisor area, canine area, premolar area, molar area, the most severe alveolar bone defect height was the canine area in stage Ⅱ, Ⅲ, Ⅳ mandibular (P<0.05). Conclusions: In periodontitis patients with a history of orthodontic treatment, the height of the alveolar bone defect was specific to the tooth positions and sites. With the periodontitis stage changing, the most severe defect position changed in both maxillary and mandibular alveolar bones. It is recommended to pay more attention to the alteration of alveolar bone in periodontitis patients with a history of orthodontic treatment and give timely targeted treatment plans.

The rag locus of Porphyromonas gingivalis might arise from Bacteroides via horizontal gene transfer.

Porphyromonas gingivalis is regarded as one of the risk factors of periodontitis. P. gingivalis exhibits a wide variety of genotypes. Many insertion sequences (ISs), located in their chromosomes, made P. gingivalis differentiate into virulent and avirulent strains. In this research, we investigated the prevalence of P. gingivalis in the gingival crevicular fluid (GCF) among periodontitis patients from Zhenjiang, China, detected the P. gingivalis rag locus distributions by multiplex polymerase chain reaction (PCR), and analyzed the origin of the P. gingivalis rag locus based on evolution. There were three rag locus variants co-existing in Zhenjiang. The results showed that the rag locus may be associated with severe periodontitis. This work also firstly ascertained that the rag locus might arise, in theory, from Bacteroides sp. via horizontal gene transfer.

Long circulating liposomes encapsulating organophosphorus acid anhydrolase in diisopropylfluorophosphate antagonism.

These studies are focused on antagonizing organophosphorous (OP) intoxications by a new conceptual approach using recombinant enzymes encapsulated within sterically stabilized liposomes to enhance diisopropylfluorophosphate (DFP) degradation. The OP hydrolyzing enzyme, organophosphorous acid anhydrolase (OPAA), encapsulated within the liposomes, was employed either alone or in combination with pralidoxime (2-PAM) and/or atropine. The recombinant OPAA enzyme, from the ALTEROMONAS: strain JD6, has high substrate specificity toward a wide range of OP compounds, e.g., DFP, soman, and sarin. The rate of DFP hydrolysis by liposomes containing OPAA (SL)* was measured by determining the changes in fluoride-ion concentration using a fluoride ion-selective electrode. This enzyme carrier system serves as a biodegradable protective environment for the OP-metabolizing enzyme (OPAA), resulting in an enhanced antidotal protection against the lethal effects of DFP. Free OPAA alone showed some antidotal protection; however, the protection with 2-PAM and/or atropine was greatly enhanced when combined with (SL)*.

In vitro studies on sterically stabilized liposomes (SL) as enzyme carriers in organophosphorus (OP) antagonism.

This study describes a new approach for organophosphorous (OP) antidotal treatment by encapsulating an OP hydrolyzing enzyme, OPA anhydrolase (OPAA), within sterically stabilized liposomes. The recombinant OPAA enzyme was derived from Alteromonas strain JD6. It has broad substrate specificity to a wide range of OP compounds: DFP and the nerve agents, soman and sarin. Liposomes encapsulating OPAA (SL)* were made by mechanical dispersion method. Hydrolysis of DFP by (SL)* was measured by following an increase of fluoride ion concentration using a fluoride ion selective electrode. OPAA entrapped in the carrier liposomes rapidly hydrolyze DFP, with the rate of DFP hydrolysis directly proportional to the amount of (SL)* added to the solution. Liposomal carriers containing no enzyme did not hydrolyze DFP. The reaction was linear and the rate of hydrolysis was first order in the substrate. This enzyme carrier system serves as a biodegradable protective environment for the recombinant OP-metabolizing enzyme, OPAA, resulting in prolongation of enzymatic concentration in the body. These studies suggest that the protection of OP intoxication can be strikingly enhanced by adding OPAA encapsulated within (SL)* to pralidoxime and atropine.

Inhibition of viral adhesion and infection by sialic-acid-conjugated dendritic polymers.

Multiple sialic acid (SA) residues conjugated to a linear polyacrylamide backbone are more effective than monomeric SA at inhibiting influenza-induced agglutination of red blood cells. However, "polymeric inhibitors" based on polyacrylamide backbones are cytotoxic. Dendritic polymers offer a nontoxic alternative to polyacrylamide and may provide a variety of potential synthetic inhibitors of influenza virus adhesion due to the wide range of available polymer structures. We evaluated several dendritic polymeric inhibitors, including spheroidal, linear, linear-dendron copolymers, comb-branched, and dendrigraft polymers, for the ability to inhibit virus hemagglutination (HA) and to block infection of mammalian cells in vitro. Four viruses were tested: influenza A H2N2 (selectively propagated two ways), X-31 influenza A H3N2, and sendai. The most potent of the linear and spheroidal inhibitors were 32-256-fold more effective than monomeric SA at inhibiting HA by the H2N2 influenza virus. Linear-dendron copolymers were 1025-8200-fold more effective against H2N2 influenza, X-31 influenza, and sendai viruses. The most effective were the comb-branched and dendrigraft inhibitors, which showed up to 50000-fold increased activity against these viruses. We were able to demonstrate significant (p < 0.001) dose-dependent reduction of influenza infection in mammalian cells by polymeric inhibitors, the first such demonstration for multivalent SA inhibitors. Effective dendrimer polymers were not cytotoxic to mammalian cells at therapeutic levels. Of additional interest, variation in the inhibitory effect was observed with different viruses, suggesting possible differences due to specific growth conditions of virus. SA-conjugated dendritic polymers may provide a new therapeutic modality for viruses that employ SA as their target receptor.