Bimaxillary protrusion with an atrophic alveolar defect: orthodontics, autogenous chin-block graft, soft tissue augmentation, and an implant.

Bimaxillary protrusion in a 28-year-old woman was complicated by multiple missing, restoratively compromised, or hopeless teeth. The maxillary right central incisor had a history of avulsion and replantation that subsequently evolved into generalized external root resorption with Class III mobility and severe loss of the supporting periodontium. This complex malocclusion had a discrepancy index of 21, and 8 additional points were scored for the atrophic dental implant site (maxillary right central incisor). The comprehensive treatment plan included extraction of 4 teeth (both maxillary first premolars, the maxillary right central incisor, and the mandibular right first molar), orthodontic closure of all spaces except for the future implant site (maxillary right central incisor), augmentation of the alveolar defect with an autogenous chin-block graft, enhancement of the gingival biotype with a connective tissue graft, and an implant-supported prosthesis. Orthodontists must understand the limitations of bone grafts. Augmented alveolar defects are slow to completely turn over to living bone, so they are usually good sites for implants but respond poorly to orthodontic space closure. However, postsurgical orthodontic treatment is often indicated to optimally finish the esthetic zone before placing the final prosthesis. The latter was effectively performed for this patient, resulting in a total treatment time of about 36 months for comprehensive interdisciplinary care. An excellent functional and esthetic result was achieved.

Combustion products of 1,3-butadiene are cytotoxic and genotoxic to human bronchial epithelial cells.

Adverse health effects of airborne toxicants, especially small respirable particles and their associated adsorbed chemicals, are of growing concern to health professionals, governmental agencies, and the general public. Areas rich in petrochemical processing facilities (e.g., eastern Texas and southern California) chronically have poor air quality. Atmospheric releases of products of incomplete combustion (e.g., soot) from these facilities are not subject to rigorous regulatory enforcement. Although soot can include respirable particles and carcinogens, the toxicologic and epidemiologic consequences of exposure to environmentally relevant complex soots have not been well investigated. Here we continue our physico-chemical analysis of butadiene soot and report effects of exposure to this soot on putative targets, normal human bronchial epithelial (NHBE) cells. We examined organic extracts of butadiene soot by gas chromatography-mass spectrometry (GC-MS), probe distillation MS, and liquid chromatography (LC)-MS-MS. Hundreds of aromatic hydrocarbons and polycyclic aromatic hydrocarbons with molecular mass as high as 1,000 atomic mass units were detected, including known and suspected human carcinogens (e.g., benzo(a)pyrene). Butadiene soot particles also had strong, solid-state free-radical character in electron spin resonance analysis. Spin-trapping studies indicated that fresh butadiene soot in a buffered aqueous solution containing dimethylsulfoxide (DMSO) oxidized the DMSO, leading to CH(3)* radical formation. Butadiene soot DMSO extract (BSDE)-exposed NHBE cells displayed extranuclear fluorescence within 4 hr of exposure. BSDE was cytotoxic to > 20% of the cells at 72 hr. Morphologic alterations, including cell swelling and membrane blebbing, were apparent within 24 hr of exposure. These alterations are characteristic of oncosis, an ischemia-induced form of cell death. BSDE treatment also produced significant genotoxicity, as indicated by binucleated cell formation. The combination of moderate cytotoxicity and genotoxicity, as occurred here, can be pro-carcinogenic.

Energy dissipation and radical scavenging by the plant phenylpropanoid pathway.

Environmental stresses such as high light, low temperatures, pathogen infection and nutrient deficiency can lead to increased production of free radicals and other oxidative species in plants. A growing body of evidence suggests that plants respond to these biotic and abiotic stress factors by increasing their capacity to scavenge reactive oxygen species. Efforts to understand this acclimatory process have focused on the components of the 'classical' antioxidant system, i.e. superoxide dismutase, ascorbate peroxidase, catalase, monodehydroascorbate reductase, glutathione reductase and the low molecular weight antioxidants ascorbate and glutathione. However, relatively few studies have explored the role of secondary metabolic pathways in plant response to oxidative stress. A case in point is the phenylpropanoid pathway which is responsible for the synthesis of a diverse array of phenolic metabolites such as flavonoids, tannins, hydroxycinnamate esters and the structural polymer lignin. These compounds are often induced by stress and serve specific roles in plant protection, i.e. pathogen defence, ultraviolet screening, antiherbivory, or structural components of the cell wall. This review will highlight a novel antioxidant function for the taxonomically widespread phenylpropanoid metabolite chlorogenic acid (CGA; 5-O-caffeoylquinic acid) and assess its possible role in abiotic stress tolerance. The relationship between CGA biosynthesis and photosynthetic carbon metabolism will also be discussed. Based on the properties of this model phenolic metabolite, we propose that under stress conditions phenylpropanoid biosynthesis may represent an alternative pathway for photochemical energy dissipation that has the added benefit of enhancing the antioxidant capacity of the cell.

Voltammetric detection of superoxide production by photosystem II.

Oxygen radicals play both pathological and physiological roles in biological systems. The detection of such radicals is difficult due to their transient nature and the presence of highly efficient antioxidant mechanisms. In plants the physiological role of oxygen is twofold, oxygen is produced by the oxidation of water and consumed as an electron acceptor. The direct involvement of oxygen in photosynthetic events exposes the photosynthetic apparatus to a high probability of damage by oxygen radicals. We report here a direct, simple and rapid method for the measurement of superoxide in vitro based on voltammetric detection. It has potential applications for other in vitro systems investigating superoxide production. We show that in addition to the well established production of superoxide from photosystem I, under reducing conditions superoxide is also produced by photosystem II, probably from the Q(A) site.

Effects of viral lower respiratory tract infection on lung function in infants with cystic fibrosis.

OBJECTIVE: To determine the effect of respiratory viral infections on pulmonary function in infants with cystic fibrosis (CF) after the respiratory virus season (October through March). METHODS: Recruitment was for one respiratory virus season during a 3-year span, 1988 to 1991, with reenrollment allowed; 22 infants <2 years of age with CF (30 patient-seasons) and 27 age-matched controls (28 patient-seasons) participated. Primary outcome variables were preseason and postseason pulmonary function tests and serology for viral antibodies. Twice-weekly telephone calls screened for respiratory symptoms. The presence of respiratory symptoms triggered a home visit and an evaluation for upper or lower (LRTI) respiratory tract infection. A nasopharyngeal sample for viral culture was performed with each visit. RESULTS: Controls and CF infants each had a mean of 5.3 acute respiratory illnesses; CF infants were four times more likely to develop an LRTI compared with controls (odds ratio, 4.6; 95% confidence interval, 1.3 and 16.5). Three of 7 (43%) CF infants with respiratory syncytial virus infection (documented by culture) required hospitalization. Controls had no association between respiratory illness and postseason pulmonary function. For CF infants, reduced postseason maximal flow at functional residual capacity (V'maxFRC) was associated with two interactions, ie, respiratory syncytial virus infection and LRTI, and male sex and LRTI; increased gas trapping (FRC) was associated with an interaction between respiratory syncytial virus and LRTI and day care. Postseason pulmonary function tests were obtained a mean of 3. 2 months after final LRTI. CONCLUSIONS: Infants with CF incurring respiratory virus infection are at significant risk for LRTI, for hospitalization, and for deterioration in lung function that persists months after the acute illness.

Scavenging of peroxynitrite by a phenolic/peroxidase system prevents oxidative damage to DNA.

We examined the ability of horseradish peroxidase (HRP), an analog of human myeloperoxidase, to protect DNA against oxidative damage caused by peroxynitrite in the presence of chlorogenic acid (CGA), a naturally occurring polyphenol. Chlorogenic acid inhibits the formation of single strand breaks in supercoiled pBR322 DNA by acting as a scavenger of peroxynitrite. Horseradish peroxidase markedly enhances the extent of DNA protection by catalyzing the decomposition of peroxynitrite in the presence of CGA. Horseradish peroxidase alone does not inhibit peroxynitrite-induced DNA strand breaks, indicating that CGA is required as an electron donor to regenerate the active enzyme. The apparent second order rate constant for the HRP-mediated oxidation of CGA in the presence of peroxynitrite at pH 6.9 is 3.4 x 10(7) M(-1) s(-1). This high rate suggests that CGA and other dietary polyphenols might efficiently scavenge peroxynitrite in peroxidase-containing systems in vivo.

EPR detection of phytophenoxyl radicals stabilized by zinc ions: evidence for the redox coupling of plant phenolics with ascorbate in the H2O2-peroxidase system.

Chlorogenic acid (CGA; 3-o-caffeoylquinic acid), a phenylpropanoid metabolite of plants, was oxidized by H2O2 in the presence of horseradish peroxidase. The primary and secondary oxidized products both were free radicals which gave EPR multiline signals at g = 2.0044 and 2.0042 in the presence of zinc as a spin stabilizing agent. The EPR kinetics showed that ascorbate functioned as a cooperative reductant by regenerating CGA from its corresponding radicals. These results provide evidence to support the idea that the ascorbate-phenolic redox couple in conjunction with guaiacol peroxidase is an efficient H2O2 scavenging mechanism in higher plants.

Acclimation of Foliar Antioxidant Systems to Growth Irradiance in Three Broad-Leaved Evergreen Species.

The protective role of leaf antioxidant systems in the mechanism of plant acclimation to growth irradiance was studied in Vinca major, Schefflera arboricola, and Mahonia repens, which were grown for several months at 20, 100, and 1200 [mu]mol photons m-2 s-1. As growth irradiance increased, several constituents of the "Mehler-peroxidase" pathway also increased: superoxide dismutase, ascorbate peroxidase, glutathione reductase, ascorbate, and glutathione. This occurred concomitantly with increases in the xanthophyll cycle pool size and in the rate of nonphotochemical energy dissipation under steady-state conditions. There was no evidence for photosystem II overreduction in plants grown at high irradiance, although the reduction state of the stromal NADP pool, estimated from measurements of NADP-malate dehydrogenase activity, was greater than 60% in V. major and S. arboricola. Ascorbate, which removes reactive O2 species generated by O2 photoreduction in the chloroplast and serves as a reductant for the conversion of the xanthophyll cycle pigments to the de-epoxidized forms A plus Z, generally exhibited the most dramatic increases in response to growth irradiance. We conclude from these results that O2 photoreduction occurs at higher rates in leaves acclimated to high irradiance, despite increases in xanthophyll cycle-dependent energy dissipation, and that increases in leaf antioxidants protect against this potential oxidative stress.

Phylogenetic distribution of superoxide dismutase supports an endosymbiotic origin for chloroplasts and mitochondria.

Three isozymes of superoxide dismutase (SOD) have been identified and characterized. The iron and manganese isozymes (Fe-SOD and Mn-SOD, respectively) show extensive primary sequence and structural homology, suggesting a common evolutionary ancestor. In contrast, the copper/zinc isozyme (CuZn-SOD) shows no homology with Fe-SOD or Mn-SOD, suggesting an independent origin for this enzyme. The three isozymes are unequally distributed throughout the biological kingdoms and are located in different subcellular compartments. Obligate anaerobes and aerobic diazotrophs contain Fe-SOD exclusively. Facultative aerobes contain either Fe-SOD or Mn-SOD or both. Fe-SOD is found in the cytosol of cyanobacteria while the thylakoid membranes of these organisms contain a tightly bound Mn-SOD. Similarly, most eukaryotic algae contain Fe-SOD in the chloroplast stroma and Mn-SOD bound to the thylakoids. Most higher plants contain a cytosol-specific and a chloroplast-specific CuZn-SOD, and possibly a thylakoid-bound Mn-SOD as well. Plants also contain Mn-SOD in their mitochondria. Likewise, animals and fungi contain a cytosolic CuZn-SOD and a mitochondrial Mn-SOD. The Mn-SOD found in the mitochondria of eukaryotes shows strong homology to the prokaryotic form of the enzyme. Taken together, the phylogenetic distribution and subcellular localization of the SOD isozymes provide strong support for the hypothesis that the chloroplasts and mitochondria of eukaryotic cells arose from prokaryotic endosymbionts.