Fatal complications in a patient with severe multi-space infections in the oral and maxillofacial head and neck regions: A case report.

BACKGROUND: Odontogenic infection is one of the common infectious diseases in oral and maxillofacial head and neck regions. Clinically, if early odontogenic infections such as acute periapical periodontitis, alveolar abscess, and pericoronitis of wisdom teeth are not treated timely, effectively and correctly, the infected tissue may spread up to the skull and brain, down to the thoracic cavity, abdominal cavity and other areas through the natural potential fascial space in the oral and maxillofacial head and neck. Severe multi-space infections are formed and can eventually lead to life-threatening complications (LTCs), such as intracranial infection, pleural effusion, empyema, sepsis and even death. CASE SUMMARY: We report a rare case of death in a 41-year-old man with severe odontogenic multi-space infections in the oral and maxillofacial head and neck regions. One week before admission, due to pain in the right lower posterior teeth, the patient placed a cigarette butt dipped in the pesticide "Miehailin" into the "dental cavity" to relieve the pain. Within a week, the infection gradually spread bilaterally to the floor of the mouth, submandibular space, neck, chest, waist, back, temporal and other areas. The patient had difficulty breathing, swallowing and eating, and was transferred to our hospital as an emergency admission. Following admission, oral and maxillofacial surgeons immediately organized consultations with doctors in otolaryngology, thoracic surgery, general surgery, hematology, anesthesia and the intensive care unit to assist with treatment. The patient was treated with the highest level of antibiotics (vancomycin) and extensive abscess incision and drainage in the oral, maxillofacial, head and neck, chest and back regions. Unfortunately, the patient died of septic shock and multiple organ failure on the third day after admission. CONCLUSION: Odontogenic infection can cause serious multi-space infections in the oral and maxillofacial head and neck regions, which can result in multiple LTCs. The management and treatment of LTCs such as multi-space infections should be multidisciplinary led by oral and maxillofacial surgeons.

WoundCareLog APP - A new application to record wound diagnosis and healing.

The incidence of chronic wounds has been increasing over the past 20 years. However, the standardized diagnosis and treatment practice of chronic refractory wounds have not been established. In addition, the properties of the wound are characterized by morphology and thus correct description of the wound in medical history collection plays a vital role, which directly affects the definitive diagnosis. To develop more accurate format of clinical history record which can correctly reflect a patient's course and treatment progress, and to standardize the medical history record of chronic refractory wounds, at the national or regional level, we designed the WoundCareLog APP. It acts as a recording and communication tool for wound healing specialists at all levels of medical institutions in China. The WoundCareLog APP is fully compatible to meet the criteria and requirements of conventional medical records by embedding 9 modules. In addition, the demands for morphological description of wounds in wound healing diagnosis and treatment have been fulfilled by enroll of digital imaging technology to overcome the inadequacies of traditional medical history records.

Hypertrophic scar regression is linked to the occurrence of endothelial dysfunction.

Most microvessels have been shown to become stenosed or completely occluded during hypertrophic scar progression. Here, we examined the morphology of capillary endothelial cells (ECs) and fibroblasts using immunofluorescence staining for CD31 and alpha-smooth muscle actin (α-SMA) and electron microscopy. In addition, ECs and fibroblasts were isolated from scar tissues, and the levels of transforming growth factor beta 1 (TGF-ß1), platelet-derived growth factor (PDGF), endothelin 1 (ET-1), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) were assayed using ELISAs. Furthermore, we assessed cell viability, total collagen production, and cell apoptosis in hypertrophic scar-derived fibroblasts cultured with EC-conditioned medium. Then, anti-TGF-ß1, anti-PDGF, anti-ET-1, anti-VEGF, and anti-bFGF neutralising antibodies were individually added to the EC medium to identify which growth factor plays a more important role in inhibiting fibroblasts biology. Our results showed microvessel lumen occlusion and EC atrophy during scar development, particularly in regressive scars (RSs). Additionally, EC growth factor secretion decreased and reached the lowest levels in RSs. Furthermore, based on the culture results, RS EC medium inhibited fibroblast viability and collagen production and induced apoptosis. Moreover, TGF-ß1, PDGF, and bFGF played more important roles in these processes than VEGF and ET-1. The endothelial dysfunction occurring in hypertrophic scars contributes to fibroblast inhibition and scar regression, and reduced TGF-ß1, PDGF, and bFGF levels play key roles during this process.

Two-photon fluorescence and fluorescence imaging of two styryl heterocyclic dyes combined with DNA.

Two new styryl heterocyclic two-photon (TP) materials, 4-[4-(N-methyl)styrene]-imidazo [4,5-f][1,10] phenanthroline-benzene iodated salt (probe-1) and 4,4-[4-(N-methyl)styrene]-benzene iodated salt (probe-2) were successfully synthesized and studied as potential fluorescent probes of DNA detection. The linear and nonlinear photophysical properties of two compounds in different solvents were investigated. The absorption, one- and two-photon fluorescent spectra of the free dye and dye-DNA complex were also examined to evaluate their photophysical properties. The binding constants of dye-DNA were obtained according to Scatchard equation with good values. The results showed that two probes could be used as fluorescent DNA probes by two-photon excitation, and TP fluorescent properties of probe-1 are superior to that of probe-2. The fluorescent method date indicated that the mechanisms of dye-DNA complex interaction may be groove binding for probe-1 and electrostatic interaction for probe-2, respectively. The MTT assay experiments showed two probes are low toxicity. Moreover, the TP fluorescence imaging of DNA detection in living cells at 800 nm indicated that the ability to locate in cell nuclei of probe-1 is better than that of probe-2.

Fluorescent detection and imaging of Hg(2+) using a novel phenanthroline derivative based single- and two-photon excitation.

A novel phenanthroline derivative, 4-[4-(N-methyl)styrene]-imidazo[4,5-f][1,10]phenanthroline-benzene iodated salt (MSIPBI), was synthesized, and the linear absorption and fluorescent spectra of MSIPBI in different solvents were investigated. The photophysical properties in unbound and in ligand-metal complexes were evaluated by UV absorption and one- and two-photon fluorescent spectra, and the quantum yields, two-photon active cross-sections and the binding constant of dye-metal were calculated. The results indicated that MSIPBI has a large Stokes shift (more than 167nm), and the dye was selective and sensitive for the detection of Hg(2+) with a two-photon active cross-section of 55.5GM in tris-HCl buffer solution at 800nm. Furthermore, the results of the fluorescence microscopy imaging indicated that MSIPBI is an efficient fluorescent probe for the detection of Hg(2+) in living cells by one- and two-photon excitation. Moreover, the experiments of determination Hg(2+) in river water and tap water were finished.

A review of the effectiveness of antimitotic drug injections for hypertrophic scars and keloids.

Hypertrophic scars and keloids are common problems after injury and cause functional and cosmetic deformities. A wide variety of treatments have been advocated for hypertrophic scars and keloids regression. Unfortunately, the reported efficacy has been variable. This article explores antimitotic drugs described in the literature such as steroid injection, 5-FU, mitomycin C, and bleomycin, which mainly target the fibroblasts in scar tissue, have been proposed as the effective modalities for scar treatment and scar prevention after surgery, but restricted due to possible side effects. The current accepted treatment for hypertrophic scar and keloid are combination therapy and the early treatment which could achieve better efficacy and less adverse effect.

[The effect of focal-adhesion micromanipulation in trauma and wound healing].

OBJECTIVE: To explore the effect of focal-adhesion micromanipulation on the biological behavior of fibroblast. METHODS: Micro-pot was made by microcontact printing. The molecules of constitutive protein was adhered on micro-pot by self-assemble of peptides. Skin fibroblasts were cultured on the membrane by self-made biomechanical cell culture for 2 weeks. Morphology observation and cell immunohistochemistry analysis was performed. RESULTS: After 2 weeks, the morphology of the fibroblasts was diverse and more compliant. Cell immunohistochemistry analysis found that the expression of integrinbeta1, alpha5 and tensin was dramatically reduced. CONCLUSIONS: The morphology and the biological behaviour of the fibroblasts in hypertrophic scar can be changed after micromanipulation of focal adhesion.

Antimitotic drug injections and radiotherapy: a review of the effectiveness of treatment for hypertrophic scars and keloids.

Scars are a common complication of surgery or burn wound management. Scars occur over the body, affecting people of both sexes and all ages. Scar therapy is a constant clinical challenge; antimitotic drugs and radiotherapy are used with varying degrees of success. This article examines the success of both these types of treatment modalities.

Isolation, culture and characterization of endothelial cells from human hypertrophic scar.

Although the etiology underlying scar formation is not well understood, previous studies revealed that endothelial cells play a role in the pathogenesis of scar development. Recently, the authors developed a reliable technique to obtain endothelial cells from hypertrophic scars that involved separation of cells from the scar tissue matrix and isolation from other cell types. Using phase-contract and electron microscopy, the cells were observed to have a characteristic morphology consistent with cells of endothelial origin. The cells were further characterized as endothelial cells by assessment of endothelin (ET)-1 and intercellular adhesion molecule (ICAM) mRNA expression, and the presence of factor VIII antigen, CD34, CD31, and VE-cadherin. This isolation method provides a simple method for culturing endothelial cells from hypertrophic scar tissue and should prove useful for studying the role of endothelial cell involvement in scar formation.

[Study on the biological function of vascular endothelial cells in the hypertrophic scar].

OBJECTIVE: To explore the biological function of vascular endothelial cells from hypertrophic scar, and to analyze the relationship between them. METHODS: The samples from human hypertrophic scar and normal skin tissue were harvested for histological examination. Then vascular endothelial cells were purified and isolated from the samples, and the level of transforming growth factor (TGF) beta1, platelet derived growth factor (PDGF), endothelin1 (ET)-1, fibroblast growth factor (FGF)2 and vascular endothelial growth factor (VEGF) were determined in a single cell with ELISA. RESULTS: Few capillary vessels were observed in normal skin under microscope, while an increased number of them were present in hypertrophic scar, with slender, tortuous in morphology and even occluded. The diameter of blood capillary in hypertrophic scar was tiny under electron microscope, and the exfoliation of endothelial cells was observed. The levels of TGF-beta1, PDGF, ET-1, bFGF and VEGF from vascular endothelial cells from hypertrophic scar were 60 +/- 8, 30 +/- 4, 0.12 +/- 0.03, 52 +/- 5, 18.1 +/- 1.2 microg/cell, respectively, which were obviously lower than those in normal skin (P < 0.05). CONCLUSION: The biological function of vascular endothelial cells was attenuated in the hypertrophic scar, which mightbe the result of the production of large amounts of collagen in the scar tissue, as well as hypoxia.

[Study on the mechanism of scar formation: epidermis template defect theory].

Dermal defection and the degree of its loss determine the natural process of wound healing, which is the key reason leading to excess scar hyperplasia. The function of tri-dimensional structure in dermis acts as a template to regulate the properties of reparative cells. The template structure induces the reparative cells to grow into the structure which changes the skin mechanic status on wound area. Also, the component of extracellular matrix can affect behaviours of fibroblasts negatively or positively, for the reason that the structure of dermal tissue has a permissive effect on the dermal components in regulating behaviours of reparative cells. Therefore, the behaviors of cells depend on the structure of the template. The suitable tri-dimensional structure of dermis facilitates normal cell cycling. The more the structure of dermis closed to its physiological status, the better the biological behaviors of cells act. Moreover, the integrity as well as the continuity of dermal tissue is the prerequisite for serving as a template. The damage to the integrity and the continuity of dermal tissue may be one of the key reasons to lead abnormal tissue repair and scar formation. Thus, we hypothesize that the loss of dermal template may be one of the mechanism of abnormal scar formation and propose the theory of extracellular matrix framework deficiency or destruction.

[Influence of dermal template on the biomechanical compliance of wound tissue].

OBJECTIVE: To investigate the influence of dermal template on the biomechanical compliance of wound tissue during wound repair. METHODS: One hundred and forty-four SD rats subjected to full-thickness skin loss on the dorsum were enrolled in the study, and they were randomly divided into A (n = 6, without grafting on wound), B (n = 6, with full thickness skin grafting on wound), C (n = 6, with razor thin skin grafting on wound) and D [n = 6, with acellular dermal matrix (ADM) and razor thin skin grafting on wound] groups. The tissue samples from the wounds were harvested 1, 2, 4, 6, 12 and 20 weeks after the operation. The biomechanical compliance of the wound was assessed by Instron biomechanics tensiometer. The expression of alpha-SMA in the dermal fibroblasts of each group was determined by immunohistochemistry (ABC) method. RESULTS: The biomechanical compliance of the wound in D group was higher than that in A and C groups (P < 0.05), but lower than that in B group during 4 to 20 weeks after operation (P < 0.05). The expression of alpha-SMA in D group (7.53 +/- 0.98)% was lower than that in A (26.99 +/- 2.90)% and C (2.18 +/- 2.79)% groups (P < 0.01), but higher than that in B group at 4 weeks after operation (P < 0.05). CONCLUSION: Dermal template might affect the scar formation during wound healing, in improving wound healing quality by enhancing the biomechanical compliance of wound tissue.

[Proliferation-inhibiting effect of advanced glycation end products modified human serum albumin to vascular endothelial cell ECV304].

OBJECTIVE: To study the proliferation-inhibiting and apoptosis-inducing effects of advanced glycation end products (AGE) modified human serum albumin (AGE-HSA) on human vein endothelial cells. METHODS: Human umbilical vein endothelial cells ECV304 were cultured in vitro with AGE-HSA of the concentrations of 12.5, 25, 50, 100, and 200 micro g/ml for 6, 12, 24, or 48 hour, then 20 micro l of 5 mg/ml MTT were added and the optical density (OD) at each time point was determined. Another ECV304 cells were cultured with AGE-HAS for 2, 4, or 8 days and then were stained with trypan blue to calculate the number of dead cells so as to calculate the proliferation-inhibiting rate. Another ECV304 cells were cultured with AGE-HAS for 6, 12, 24, or 48 hours and then stained with annexin V Fitc and propidium iodide (PI). Flow cytometry was used to calculate the annexin V Fitc positive cells (early and middle stage apoptotic cells) and Annexin V Fitc/PL positive cells (late apoptotic cells). Inverted microscope, transmission electron microscope, and fluorescence microscope were used to observe the histological changes of apoptotic cells. FCV304 cells incubated with HSA of the above-mentioned and without addition of the other agents concentrations were used as controls. RESULTS: The OD values of ECV304 cells cultured for 48 h with low concentrations (12.5, 25, and 50 micro g/ml) of AGE-HSA were not significantly different from those of the control (1.104 +/- 0.080, 1.098 +/- 0.097 and 1.059 +/- 0.122 VS. 1.159 +/- 0.088, all P > 0.05). The OD values of ECV304 cells cultured with low concentrations of AGE-HSA for 4 days and 6 days were significantly lower than those in the control group. The OD values of ECV304 cells cultured with high concentrations (100 and 200 micro g/ml) of AGE-HSA for 6 - 48 hours decreased to 0.117 +/- 0.033 and 0.081 +/- 0.020 in comparison with that of the control group (P < 0.01). Flow cytometry and fluorescence microscopy showed higher proportions of apoptotic cells among the ECV304 cells cultured with high concentrations of AGE-HAS than among the control cells at each time point (P < 0.01). The numbers of cells in the control group exponentially increased after culture for 2, 4, and 6 days. The number of cells cultured with low concentrations of AGE-HAS for 2 days was not significantly different from that of the control group (P > 0.05), however, the numbers of cells cultured with low concentrations of AGE-HAS for 4 and 6 days were significantly lower than those of the control group (both P < 0.01). The numbers of cells cultured with 100 or 200 micro g/ml AGE-HAS for 2 days were significantly lower than those of the control group (both P < 0.01) with a proliferation-inhibiting rate of 39.56% +/- 2.82% and 60.32% +/- 4.51% respectively. The apoptotic rates in cells cultured with low concentrations of AGE-HAS for 48 hours were not significantly different from those in the control group. The apoptotic rates in cells cultured with 100 or 200 micro g/ml AGE-HAS for 6, 12, 24, or 48 hours were significantly higher than those in the control group (all P < 0.01). The apoptotic rates in 200 micro g/ml group at different time points were significantly higher than those in the 100 micro g/ml group (P < 0.05 or 0.01). The apoptotic rate and number of apoptotic cells increased along with the increase of culture time and concentration of AGE-HAS. Microscopy showed morphological changes among the cells cultured with 100 micro g/ml AGE-HAS for 6, 12, 24, and 48 hours and the numbers of apoptotic cells, mainly late apoptotic cells, and dead cells increased remarkably since the cells were cultured for 48 hours. CONCLUSION: AGE-HSA inhibits the proliferation of vascular endothelial cells and induces apoptosis in dose and time dependent manner. AGE modification-induced pathobiological cascade may be involved in the pathogenesis of impaired wound healing in diabetes by the mechanism of angiogenesis retardation.