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Healing Response (healing + response)
Kinds of Healing Response Selected AbstractsPeriodontal response to two intracanal medicaments in replanted monkey incisorsDENTAL TRAUMATOLOGY, Issue 6 2001Y. L. Thong Abstract , Intracanal medicaments are recommended for use in replanted teeth to inhibit inflammatory root resorption. This study compared the effect of calcium hydroxide (Pulpdent®) and a corticosteroid-antibiotic paste (Ledermix®) on periodontal healing and root resorption following replantation. Incisors of eight Macaca fascicularis monkeys were extracted, stored dry for 15 min and replanted. After 11 days, root canals in two adjacent maxillary incisors were treated with one medicament and contralateral incisors with the other medicament, or left as untreated controls. Animals were sacrificed 8 weeks later and the teeth prepared for histomorphometric evaluation of periodontal ligament inflammation and root resorption. Periodontal ligament inflammation and inflammatory root resorption were markedly inhibited by both calcium hydroxide and corticosteroid-antibiotic relative to untreated controls. Replacement resorption was lowest in the corticosteroid-antibiotic group, and significantly (P<0.05) more normal periodontal ligament was present in this group (79.6%) than in calcium hydroxide and control groups (64.6% and 62.7%, respectively). Treatment with the corticosteroid-antibiotic inhibited inflammatory resorption and was slightly more effective than calcium hydroxide in producing a periodontal healing response. [source] Review of Fractional Photothermolysis: Treatment Indications and EfficacyDERMATOLOGIC SURGERY, Issue 10 2009EMILY P. TIERNEY MD BACKGROUND Fractional photothermolysis (FP) is one of the most significant milestones in laser technology and resurfacing. METHODS Review of the Medline English literature and recent international conferences regarding FP technology, applications, and indications. RESULTS Successful conditions treated with nonablative FP reported in the literature include acne scarring; dyschromia and fine wrinkling of photoaging on the face, chest, neck, and hands; melasma; poikiloderma of Civatte; nevus of Ota; scars; minocycline hyperpigmentation; telangiectatic matting; residual hemangioma; granuloma annulare; colloid milium; and disseminated superficial actinic porokeratosis. An advance in 2007 was the introduction of ablative FP (AFP), which results in significantly greater improvement in skin laxity and textural abnormalities. Most recently, AFP has demonstrated significantly greater improvement than nonablative FP in reducing acne scarring and skin redundancy and laxity associated with photoaging. CONCLUSIONS Through the induction of microthermal zones of injury, FP technology stimulates a robust and rapid wound healing response resulting in improvement in a diversity of aesthetic, inflammatory, and preneoplastic skin disorders. Further investigation into the technology and diverse array of cutaneous conditions that can benefit from FP is highly needed. [source] Therapeutic angiogenesis and vasculogenesis for tissue regenerationEXPERIMENTAL PHYSIOLOGY, Issue 3 2005Paolo Madeddu Therapeutic angiogenesis/vasculogenesis holds promise for the cure of ischaemic disease. The approach postulates the manipulation of spontaneous healing response by supplementation of growth factors or transplantation of vascular progenitor cells. These supplements are intended to foster the formation of arterial collaterals and promote the regeneration of damaged tissues. Angiogenic factors are generally delivered in the form of recombinant proteins or by gene transfer using viral vectors. In addition, new non-viral methods are gaining importance for their safer profile. The association of growth factors with different biological activity might offer distinct advantages in terms of efficacy, yet combined approaches require further optimization. Alternatively, substances with pleiotropic activity might be considered, by virtue of their ability to target multiple mechanisms. For instance, some angiogenic factors not only stimulate the growth of arterioles and capillaries, but also inhibit vascular destabilization triggered by metabolic and oxidative stress. Transplantation of endothelial progenitor cells was recently proposed for the treatment of peripheral and myocardial ischaemia. Progenitor cells can be transplanted either without any preliminary conditioning or after ex vivo genetic manipulation. Delivery of genetically modified progenitor cells eliminates the drawback of immune response against viral vectors and makes feasible repeating the therapeutic procedure in case of injury recurrence. It is envisioned that these new approaches of regenerative medicine will open unprecedented opportunities for the care of life-threatening diseases. [source] Fibroblast activation protein increases apoptosis, cell adhesion, and migration by the LX-2 human stellate cell line,HEPATOLOGY, Issue 4 2005Xin Maggie Wang Injury and repair in chronic liver disease involve cell adhesion, migration, apoptosis, proliferation, and a wound healing response. In liver, fibroblast activation protein (FAP) has both collagenase and dipeptidyl peptidase IV (DPIV) activities and is expressed only by activated hepatic stellate cells (HSC) and myofibroblasts, which produce and degrade extracellular matrix (ECM). FAP was colocalized with collagen fibers, fibronectin, and collagen type I in human liver. FAP function was examined in vitro by expressing green fluorescent protein FAP fusion protein in cell lines cultured on collagen-I, fibronectin, and Matrigel. Glutamates at 203 and 204 as well as serine624 of FAP were essential for peptidase activity. Human embryonic kidney 293T cells overexpressing FAP showed reduced adhesion and migration. FAP overexpression in the human HSC line LX-2 caused increased cell adhesion and migration on ECM proteins as well as invasion across transwells in the absence or presence of transforming growth factor beta-1. FAP overexpression enhanced staurosporine streptomyces,stimulated apoptosis in both cell lines. Interestingly, the enzyme activity of FAP was not required for these functions. Overexpressing FAP increased the expression of matrix metalloproteinase-2 and CD44 and reduced integrin-,1 expression in 293T cells, suggesting potential pathways of FAP-mediated impairment of cell adhesion and migration in this epithelial cell line. In conclusion, these findings further support a pro-fibrogenic role for FAP by indicating that, in addition to its enzymatic functions, FAP has important nonenzymatic functions that in chronic liver injury may facilitate tissue remodeling through FAP-mediated enhancement of HSC cell adhesion, migration, and apoptosis. Supplementary material for this article can be found on the HEPATOLOGY website (http://www.interscience.wiley.com/jpages/0270-9139/suppmat/index.html). (HEPATOLOGY 2005;42:935,945.) [source] Complex endodontic treatment of an immature type III dens invaginatus.INTERNATIONAL ENDODONTIC JOURNAL, Issue 10 2008A case report Abstract Aim, To report the endodontic treatment of an immature maxillary central incisor with dens invaginatus. Summary, Dens invaginatus is a rare malformation of teeth, probably resulting from an infolding of the dental papilla during tooth development. The present case describes the complex endodontic treatment of a type III dens invaginatus in an immature maxillary central incisor with a necrotic pulp and abscess formation. The initial treatment goal was to achieve apexification of the pseudocanal root and conservative root canal treatment in the main canal. Following 1-year of treatment with calcium hydroxide dressings, radiography revealed a healing response, but no sign of a hard tissue barrier at the apex. Periapical surgery with the placement of a zinc oxide cement (IRM) root-end filling was considered successful at the 4-year follow-up. Key learning points ,,The complexity of the canal system and open apex in dens invaginatus present a challenge to endodontic treatment. ,,Correct diagnosis and treatment planning are fundamental to treatment of dens invaginatus. ,,Periapical surgery is indicated in cases of unsuccessful apexification in immature teeth with dens invaginatus and nonvital pulp. [source] Regenerative treatment with platelet-rich plasma combined with a bovine-derived xenograft in smokers and non-smokers: 12-month clinical and radiographic resultsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 1 2010Selcuk Yilmaz Abstract Aim: The purpose of this study was to assess the healing response of intrabony defects following regenerative treatment with platelet-rich plasma (PRP) combined with a bovine-derived xenograft (BDX) in smokers and non-smokers. Materials and Methods: A total of 24 advanced chronic periodontitis patients, 12 smokers and 12 non-smokers, with 113 intrabony defects with an intrabony component of 3 mm were included in this study. Defects were surgically treated with PRP/BDX. At baseline and 12 months after surgery, the following parameters were recorded: plaque and sulcus bleeding indices, probing depth (PD), relative attachment level, marginal recession, probing and radiographic bone levels. Results: Considering the soft tissue measurements, smokers and non-smokers presented a mean PD reduction of 3.97 ± 0.76 and 4.63 ± 0.52 mm, recession of 0.76 ± 0.44 and 0.50 ± 0.12 mm and attachment gain of 3.26 ± 0.42 and 4.06 ± 0.40 mm, respectively. Evaluation of the hard tissue findings revealed that the mean clinical and radiographic bone gains in smokers and non-smokers were 2.83 ± 0.47 and 3.63 ± 0.38 mm, 2.98 ± 0.38 and 3.67 ± 0.48 mm, respectively. Inter-group differences for PD reduction (p<0.05), attachment (p<0.001), clinical (p<0.001) and radiographic bone gains (p<0.001) were found to be significant between smokers and non-smokers. Conclusions: Within the limits of this study, the results indicate that treatment outcome following PRP/BDX application in intrabony defects is impaired with smoking. [source] Impaired healing response of periodontal furcation defects following flap debridement surgery in smokersJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 1 2003A controlled clinical trial Abstract Objectives: The purpose of the present parallel-design, controlled clinical trial was to evaluate the treatment outcome of periodontal furcation defects following flap debridement surgery (FDS) procedure in cigarette smokers compared to non-smokers. Materials and Methods: After initial therapy, 31 systemically healthy subjects with moderate to advanced periodontitis, who presented at least one Class I or II molar furcation defect, were selected. Nineteen patients (mean age: 40.3 years, 15 males) were smokers (,10 cigarettes/day) and 12 patients (mean age: 44.8 years, 3 males) were non-smokers. Full-mouth plaque score (FMPS) and full-mouth bleeding score (FMBS), probing pocket depth (PPD), vertical clinical attachment level (v-CAL), and horizontal clinical attachment level (h-CAL) were assessed immediately before and 6 months following surgery. Results: Overall, statistically significant v-CAL gain was observed in smokers (1.0 ± 1.3 mm) and non-smokers (1.3±1.1 mm), the difference between groups being statistically significant (p=0.0003). In proximal furcation defects, v-CAL gain amounted to 2.3±0.7 mm in non-smokers as compared to 1.0±1.1 mm in smokers (p=0.0013). At 6 months postsurgery, non-smokers presented a greater h-CAL gain (1.3±1.1 mm) than smokers (0.6±1.0 mm), with a statistically significant difference between groups (p=0.0089). This trend was confirmed in both facial/lingual (1.4±1.0 versus 0.8±0.8 mm) and proximal furcation defects (1.2±1.3 versus 0.5±1.2 mm). The proportion of Class II furcations showing improvement to postsurgery Class I was 27.6% in smokers and 38.5% in non-smokers. After 6 months, 3.4% of presurgery Class I furcation defects in smokers showed complete closure, as compared to 27.8% in non-smokers. Conclusions: The results of the present study indicated that (1) FDS produced clinically and statistically significant PPD reduction, v-CAL gain, and h-CAL gain in Class I/II molar furcation defects, and (2) cigarette smokers exhibited a less favorable healing outcome following surgery in terms of both v-CAL and h-CAL gain. Zusammenfassung Ziele: Der Zweck der vorliegenden kontrollierten klinischen Studie mit einem parallelen Design war die Überprüfung des Behandlungsergebnisses bei parodontalen Furkationsdefekten nach Wurzelreinigung und ,glättung bei Lappenoperationen (FDS) bei Zigarettenrauchern und Nichtrauchern. Material und Methoden: Nach der initialen Therapie wurden 31 systemisch gesunde Personen mit moderater bis schwerer Parodontitis, die mindestens einen Klasse I oder Klasse II Furkationsdefekt aufwiesen, ausgesucht. 19 Patienten (mittleres Alter 40,3 Jahre, 15 Männer) waren Raucher (,10 Zigaretten/Tag), 12 Patienten (mittleres Alter 44,8 Jahre, 3 Männer) waren Nichtraucher. Der Plaqueindex (FMPS) und die Provokationsblutung (FMBS) im gesamten Mund, die Sondierungstiefen (PPD), die vertikalen klinischen Befestigungsniveaus (v-CAL) und die horizontalen klinischen Befestigungsniveaus (h-CAL) wurden unmittelbar vor und 6 Monate nach der Operation erhoben. Ergebnisse: Insgesamt wurde ein statistisch signifikanter v-CAL Gewinn bei Rauchern (1,0±1,3 mm) und Nichtrauchern (1,3±1,1 mm) beobachtet, die Differenz wischen den Gruppen war statistisch signifikant (p=0,0003). Bei den approximalen Furkationsdefekten betrug der v-CAL Gewinn bei Nichtrauchern 2,3±0,7 mm verglichen zu den Rauchern mit 1,0±1,1 mm (p=0,0013). 6 Monate post operationem zeigten die Nichtraucher einen größeren h-CAL Gewinn (1,3±1,1 mm) verglichen mit den Rauchern (0,6±1,0 mm) mit einer statistischen Signifikanz zwischen den Gruppen (p=0,0089). Dieser Trend wurde sowohl bei den fazialen/lingualen Defekten (1,4±1,0 mm vs. 0,8±0,8 mm) und bei den approximalen Furkationsdefekten (1,2 v 1,3 mm vs. 0,5±1,2 mm) bestätigt. Das Verhältnis von Klasse II Furkationen, die post operationem eine Verbesserung zu Klasse I Furkationsdefekten zeigten, war bei Rauchern 27,6 % und 38,5 % bei Nichtrauchern. Nach 6 Monaten zeigten 3,4 % der Klasse I Furkationsdefekte bei Rauchern einen kompletten Verschluss verglichen mit 27,8 % bei Nichtrauchern. Zusammenfassung: Die Ergebnisse der vorliegenden Studie zeigten, dass 1) FDS eine klinische und statistisch signifikante PPD Reduktion, einen v-CAL Gewinn und h-CAL Gewinn bei Klasse I/II Molaren Furkationsdefekten erbringt; 2) Zigarettenraucher weniger gute Heilungsergebnisse nach Operationen sowohl bei v-CAL als auch bei h-CAL zeigten. Résumé Objectifs: cette étude clinique contrôlée en parallèle se proposait d'évaluer l'issue du trai-tement des lésions des furcations par un lam-beau de débridement (FDS) chez des fumeurs de cigarette par rapport à des non-fumeurs. Matériel et méthodes: Après un traitement initial, 31 sujets en bonne santé atteints de parodontite modérée à avancée et présentant au moins une lésion inter-radiculaire de classe I ou II sur une molaire, furent sélectionnés. 19 patients (d'âge moyen: 40.3 ans, 15 hommes) étaient fumeurs (,10 cigarettes/jour), 12 patients (d'âge moyen: 44.8 ans, 3 hommes) étaient non-fumeurs. Le score de plaque de toute la bouche (FMPS) et le score de saignement (FMBS), la profondeur de poche au sondage (PPD), le niveau clinique d'attache vertical (v-CAL), et horizontal (h-CAL) furent estimés immédiatement avant et 6 mois après la chirurgie. Résultats: D'une façon générale, un gain de v-CAL statistiquement significatif gain était observé chez les fumeurs (1.0±1.3 mm) et chez les non-fumeurs (1.3±1.1 mm), la différence entre les groupes étant statistiquement significative (p=0.0003). Pour les lésions des furcations proximales, le gain de v-CAL atteignait 2.3±0.7 mm chez les non-fumeurs et seulement 1.0±1.1 mm chez les fumeurs (p=0.0013). 6 mois après la chirurgie, les non-fumeurs présentaient un gain de h-CAL gain plus important (1.3±1.1 mm) que les fumeurs(0.6±1.0 mm), avec une différence statistiquement significative entre les groupes (p=0.0089). Cette tendance était confirmée à la fois sur les lésions des furcations vestibulo-linguales (1.4±1.0 mm vs 0.8±0.8 mm) et proximales (1.2±1.3 mm vs 0.5±1.2 mm). La proportion de furcations de Classe II s'améliorant après chirurgie en Classe I était de 27.6% chez les fumeurs et 38.5% chez les non-fumeurs. Après 6 mois, 3.4% des furcations initialement de Classe I étaient complètement fermées contre 27.8% chez les non-fumeurs. Conclusions: Les résultats de cette étude indiquent que: 1) FDS produit une réduction cliniquement et statistiquement significative de PPD, un gain de v-CAL et de h-CAL gain sur les lésions de furcations molaires de Classe I/II; 2) Les fumeurs de cigarette ont une cicatrisation moins favorable après chirurgie en terme de gain de v-CAL et de h-CAL. [source] Young, adult, and old rats have similar changes in mRNA expression of many skeletal genes after fracture despite delayed healing with ageJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 10 2006Ralph A. Meyer Jr. Abstract Genes active in fracture healing are not well understood. Because age slows skeletal repair, the change in gene expression between animals of differing ages may illuminate novel pathways important to this healing response. To explore this, 6-, 26-, and 52-week-old female Sprague-Dawley rats were subjected to mid-diaphyseal femoral fracture with intramedullary fixation. The fracture callus was collected at 0, 0.4 (3 days), 1, 2, 4, or 6 weeks after fracture. RNA was extracted and pooled between two animals for each sample. Three samples were done for each time point for each age for a total of 54 Affymetrix U34A GeneChip microarrays. Of the 8700 genes on each array, 3300 were scored as present. Almost all of these genes were affected by femoral fracture with either upregulation or downregulation in the 6 weeks after fracture. Upregulated genes included markers for matrix genes for both cartilage and bone, osteoblasts, osteocytes, osteoclasts, fibroblasts, and mast cells. Downregulated genes included genes related to blood cell synthesis. Nearly all genes presently associated with bone metabolism showed the same response to fracture healing regardless of the age of the animal. In conclusion, skeletal fracture led to similar changes in RNA expression for most skeletal genes despite the delay in the formation of bone to bridge the fracture gap in old rats. Defects in the healing of skeletal trauma in older rats may lie in systems not normally studied by skeletal biologists. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:1933,1944, 2006 [source] Hyaluronan-based polymers in the treatment of osteochondral defectsJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 5 2000Luis A. Solchaga Articular cartilage in adults has limited ability for self-repair. Some methods devised to augment the natural healing response stimulate some regeneration, but the repair is often incomplete and lacks durability. Hyaluronan-based polymers were tested for their ability to enhance the natural healing response. It is hypothesized that hyaluronan-based polymers recreate an embryonic-like milieu where host progenitor cells can regenerate the damaged articular surface and underlying bone. Osteochondral defects were made on the femoral condyles of 4-month-old rabbits and were left empty or filled with hyaluronan-based polymers. The polymers tested were ACP sponge, made of crosslinked hyaluronan, and HYAFF-11 sponge, made of benzylated hyaluronan. The rabbits were killed 4 and 12 weeks after surgery, and the condyles were processed for histology. All 12-week defects were scored with a 29-point scale, and the scores were compared with a Kruskall-Wallis analysis of variance on ranks. Untreated defects filled with bone tissue up to or beyond the tidemark, and the noncalcified surface layer varied from fibrous to hyaline-like tissue. Four weeks after surgery, defects treated with ACP exhibited bone filling to the level of the tidemark and the surface layer was composed of hyaline-like cartilage well integrated with the adjacent cartilage. At 12 weeks, the specimens had bone beyond the tidemark that was covered with a thin layer of hyaline cartilage. Four weeks after surgery, defects treated with HYAFF-11 contained a rim of chondrogenic cells at the interface of the implant and the host tissue. In general, the 12-week defects exhibited good bone fill and the surface was mainly hyaline cartilage. Treated defects received significantly higher scores than untreated defects (p < 0.05), and ACP-treated defects scored significantly higher than HYAFF-11-treated defects (p < 0.05). The introduction of these hyaluronan-based polymers into defects provides an appropriate scaffolding and favorable microen-vironment for the reparative process. Further work is required to fully assess the long-term outcome of defects treated with these polymers. [source] Chronic antigen ingestion protects ovalbumin sensitized mice from severe manifestation of Leishmania major infectionPARASITE IMMUNOLOGY, Issue 11-12 2008J. C. S. SALDANHA SUMMARY In the present work, the development of experimental leishmaniasis was examined in sensitized BALB/c mice that were chronically fed with antigen. After an oral challenge with egg white solution, the ovalbumin (Ova)-sensitized mice showed an increase in serum anti-Ova IgE and IgG1 antibodies. Lesions induced by Leishmania major infection were reduced by the ingestion of Ova in sensitized mice, as assessed by reduced footpad growth, lower parasite loads and improved pathological outcome compared to sham sensitized mice. Moreover, such findings were connected to a shift to a Th1 response involving higher IFN-, production and serum levels of IgG2a anti- Leishmania antigens. The data appear to corroborate the suggestion that chronic ingestion of an antigen by sensitized mice modulates the immunological system through a shift in cytokine release, exhibiting a healing response and resistance to L. major infection. [source] Wound healing response is a major contributor to the severity of cutaneous leishmaniasis in the ear model of infectionPARASITE IMMUNOLOGY, Issue 10 2007T. BALDWIN SUMMARY In the conventional mouse model for cutaneous leishmaniasis involving infection with stationary phase Leishmania major promastigotes at the base of the tail, mice congenic for leishmaniasis resistance loci designated lmr1,2,3 cured their lesions more rapidly and laid down more ordered collagen fibres than the susceptible parental BALB/c mice, while the opposite was the case for the congenic mice carrying the susceptibility loci on the resistant C57BL/6 background. In that model, we showed that wound healing and not T cell responses played a major role in determining the resolution of skin infection. Here, we show a similar disease phenotype in the mouse model that mimics more closely the situation in humans, that is, strictly intradermal infection in the ear pinna with small numbers of metacyclic promastigotes. The data show that at the site of infection the innate and adaptive immune responses act in concert to clear parasites, and induce tissue repair and wound healing. Importantly, the data show that the host responses controlled by the lmr loci, which act locally to control infection in the skin, are distinct from the host responses operating systemically in the draining lymph node. [source] Effects of Mitomycin-C on Normal Dermal Fibroblasts,THE LARYNGOSCOPE, Issue 4 2006Theodore Chen MD Abstract Objectives: To evaluate the effects of mitomycin-C on the growth and autocrine growth factor production of human dermal fibroblasts from the face. Study Design: In vitro study using normal adult dermal fibroblast cell lines in a serum-free model. Methods: Cell cultures were exposed to 4 mg/mL, 0.4 mg/mL, 0.04 mg/mL, 0.004 mg/mL, and 0.0004 mg/mL concentrations of mitomycin-C solution. Cell counts were performed, and the cell-free supernatants were collected at 0, 1, 3, and 5 days after the initial exposure. Population doubling times were calculated and supernatants were quantitatively assayed for basic fibroblast growth factor (bFGF) and transforming growth factor (TGF)-,1. Results: Continuous exposure to mitomycin-C caused fibroblast cell death by day 7 at all tested concentrations. A 4 minute exposure to mitomycin-C at 4 mg/mL caused rapid fibroblast cell death. A 4-minute exposure to mitomycin-C at either 0.4 mg/mL or 0.04 mg/mL resulted in decreased fibroblast proliferation. A 4 minute exposure to mitomycin-C at 0.4 mg/mL resulted in a marked increase in the production of both bFGF and TGF-,1. Conclusions: A clinically ideal concentration of mitomycin-C would slow fibroblast proliferation yet not cause cell death to allow for a wound healing response. Mitomycin-C 0.4 mg/mL for 4 minutes satisfies the above criteria in vitro. [source] Time and Dose Effects of Mitomycin C on Extracellular Matrix Fibroblasts and Proteins,THE LARYNGOSCOPE, Issue 1 2005Bryce Ferguson Abstract Objectives/Hypothesis: The objective was to determine treatment dose and time-dependent effects of injected mitomycin C on extracellular matrix fibroblasts, collagen, and fibronectin, important mediators in the wound healing response, in a rat cutaneous wound model. Study Design: A prospective, controlled animal study. Methods: Forty rats were injected with three different doses (0.4, 2.3, and 5.0 mg/mL) of mitomycin C at three different wound sites with a fourth wound site receiving saline as a control. The rats were grouped to have their tissue harvested at five different dates ranging from 1 week to 8 weeks. After death, samples from the wound site underwent Western blot analysis for collagen and fibronectin and histological analysis measuring fibroblast apoptosis. Results: Over an 8-week period, collagen and fibronectin significantly decreased and fibroblast apoptosis significantly increased. No correlation was found between the injected dose of mitomycin C and either the extracellular matrix protein concentration or the rate of fibroblast apoptosis. Conclusion: Mitomycin C demonstrated a long-term effect in a wound, inhibiting collagen and fibronectin production and inducing apoptosis. Use of mitomycin C in excess of 0.4 mg/mL did not alter protein concentrations or rate of apoptosis. [source] Functional and proteomic analysis of serum and cerebrospinal fluid derived from patients with traumatic brain injury: a pilot studyANZ JOURNAL OF SURGERY, Issue 7-8 2010Dieter Cadosch Abstract Background:, An enhanced fracture healing response has been reported in patients with traumatic brain injury (TBI). This has been attributed to circulating humoral factors that are thought to be proteins produced and released by the injured brain. However, these factors remain unknown. The aim of this study was to identify osteogenic factors in serum and cerebrospinal fluid (CSF) from TBI patients. This was carried out using in vitro proliferation assays with the human foetal osteoblastic 1.19 cell line (hFOB) combined with a novel proteomic approach. Methods:, Serum was collected from brain-injured (n = 12) and non-brain-injured (n = 9) patients with a comorbid femur shaft fracture. Similarly, CSF was obtained from TBI (n = 7) and non-TBI (n = 9) patients. The osteoinductive potential of these samples was determined by measuring the in vitro proliferation rate of hFOB cells. Highly osteogenic serum and CSF samples of TBI patients were chosen for protein analysis and were compared to those of non-brain-injured patients. A new hFOB cell-based method was used to enrich the proteins in these samples, which had a functional affinity for these osteoprogenitor cells. These enriched protein fractions were mapped using two-dimensional gel electrophoresis and protein imaging methods displaying serum and CSF proteins of brain-injured and control subjects that had an affinity for human osteoprogenitor cells. Results:, Serum and CSF derived from brain-injured patients demonstrated a greater osteoinductive potential (P < 0.05) than their non-brain-injured counterparts. Clear-cut differences in the pattern of proteins in two-dimensional gels were detected between TBI and control patients. Fourteen proteins were exclusively present in the serum of TBI patients, while other proteins were either up- or downregulated in samples collected from TBI patients (P < 0.05). Conclusion:, Osteoinductive factors are present in the serum and CSF of brain-injured patients. These may include one or more of those proteins identified as having an affinity for osteoprogenitor cells that are either exclusively present or up- or downregulated in the serum and CSF of brain-injured patients. [source] Expression, purification, and characterization of pro-phenoloxidase-activating serine protease from Spodoptera lituraARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY (ELECTRONIC), Issue 2 2009Naresh Arora Abstract One of the important trigger molecules for innate immunity is a serine protease that activates zymogen phenol oxidase (PPO). Central to wound healing response is the activation of phenol oxidase zymogen. Molecular characterization of phenol oxidase has been recently reported by us. Here, we report isolation, cloning, expression, and purification of prophenol oxidase activating enzyme 1 (slppae1) from polyphagous pest, Spodoptera litura. SLPPAE1 is induced within 6,h of physical injury. The structural features of the mature polypeptide are reminiscent of other lepidopteran PPAE in having a signal peptide, propeptide, and catalytically active polypeptide. The cDNA has been expressed in Sf21 cells using baculovirus expression vector. Fractionation of expressing Sf21 cells revealed its expression in the membranes. The recombinant protein was solubilized from membranes and purified by Ni-NTA affinity chromatography. The purified enzyme is catalytically active on chromogenic substrate, activates recombinantly expressed prophenol oxidase (PPO) of S. litura, and is sensitive to inhibition by aprotenin. N-terminal sequencing of processed phenol oxidase revealed 11,kDa propeptide instead of in-silico predicted 6,kDa polypeptide. © 2009 Wiley Periodicals, Inc. [source] Use of biodegradable urethane-based adhesives to appose meniscal defect edges in an ovine model: a preliminary studyAUSTRALIAN VETERINARY JOURNAL, Issue 6 2008JR FIELD Objective To evaluate the biological response to two urethane-based adhesives used to repair full thickness meniscal wounds created in the partially vascularised (red-white) zone. Design An ovine bilateral meniscal defect model was used to evaluate the initial biological response of the meniscal cartilage and synovium over a 1-month period. A 10-mm full-thickness defect was created in the medial meniscus of each femorotibial joint. The defects were either left untreated or repaired using the urethane-based adhesives. Synovial fluid, synovial membrane and the meniscal cartilages were retrieved at necropsy for cytological and histological assessment. Results The ovine model proved to be a suitable system for examining meniscal repair. Untreated defects showed no tissue apposition or cellular healing response, whereas all eight defects repaired with the two urethane-based adhesive formulations showed signs of repair and tissue regeneration with indications of cell infiltration and new collagen deposition in and around the polymer. No adverse cellular response to the adhesives was observed in the meniscal defect or in the synovial membrane and fluid. Conclusion Trauma to the knee commonly results in tears to the meniscal cartilage, with the majority of these occurring in the partially vascularised (red-white) or non-vascularised (white) zones of the meniscus. Repair, and subsequent healing, of these tears is poor because of the reduced vascularity and limited surgical access. The present data indicate that an ovine model is a suitable system for examining meniscal repair, and that development of urethane-based adhesives offers a strategy that may be clinically effective for the treatment of these injuries. [source] Effects of weak static magnetic fields on endothelial cellsBIOELECTROMAGNETICS, Issue 4 2010Carlos F. Martino Abstract Pulsed electromagnetic fields (PEMFs) have been used extensively in bone fracture repairs and wound healing. It is accepted that the induced electric field is the dose metric. The mechanisms of interaction between weak magnetic fields and biological systems present more ambiguity than that of PEMFs since weak electric currents induced by PEMFs are believed to mediate the healing process, which are absent in magnetic fields. The present study examines the response of human umbilical vein endothelial cells to weak static magnetic fields. We investigated proliferation, viability, and the expression of functional parameters such as eNOS, NO, and also gene expression of VEGF under the influence of different doses of weak magnetic fields. Applications of weak magnetic fields in tissue engineering are also discussed. Static magnetic fields may open new venues of research in the field of vascular therapies by promoting endothelial cell growth and by enhancing the healing response of the endothelium. Bioelectromagnetics 31:296,301, 2010. © 2010 Wiley-Liss, Inc. [source] 4255: Integrating the interplay between innate and adaptive immunity in the development of non infectious uveitisACTA OPHTHALMOLOGICA, Issue 2010AD DICK Purpose Whilst uveitis is a CD4 T cell mediated disease, there remains both the interplay with innate immunity at both the affector (initiation) of disease and moreso the phenotype and severity of the effector stages of disease. Methods The talk will describe the experimental evidence to describe the interplay of T cells and myeloid cells within the retina during intraocular inflammation. Results TNF, whilst a pleitropic cytokine, has significant influence of the disease phenotype and disease course we observe experimentally. TNF is requred for activation of myeloid cells (macrophages)when in presence of Th1 CD4 T cells, which results in contribution to tissue damage but also controlling T cell proliferation in situ via generation of myeloid suppressor cells. Moreover, the role of resident myeloid cells (microglia) is to down-regulate the immune response. The role of myeloid cells in the healing response and angiogenesis will also be discussed with respect to T cell responses. Conclusion Myeloid cells are actively conditioned by their envirnoment (cognate and soluble factors) to respond accordingly. As such the regulation of immune response and healing that follows is dictated by the innate system in response to changes in local and systemic conditions. [source] Dystrophia Smolandiensis: a novel morphological picture of recurrent corneal erosionsACTA OPHTHALMOLOGICA, Issue 4 2010Björn Hammar Abstract. Purpose:, The aim of this study was to describe morphological changes in Dystrophia Smolandiensis, a corneal disease that is characterized by recurrent corneal erosive episodes and the formation of central corneal keloid-like opacities in approximately half of those affected. Methods:, The corneas of seven affected individuals were examined using in-vivo confocal microscopy. Specimens of one primary corneal graft, one regraft and one biopsied keloid-like region , all obtained from members of a large family with the disease , were re-examined with a light microscope. Sections were stained with Congo red and analysed immunohistochemically for fibronectin and S100A4. Results:, Light microscopic examination revealed epithelial hyperplasia, absence of Bowman's layer and subepithelial fibrosis. Fibronectin was expressed in the area of subepithelial fibrosis, and the keratocytes in this area generally expressed S100A4. The biopsy specimen stained positive for Congo red, suggesting an amyloid deposit. In-vivo confocal microscopy confirmed epithelial abnormalities, loss of Bowman's layer and significant alterations of the subbasal nerve plexus in affected individuals. Conclusion:, The morphological picture in Dystrophia Smolandiensis is novel for a condition dominated by recurrent corneal erosions at the clinical level. Although no single morphological feature unique to the disease could be found, the general morphological pattern of pathology (true keloid formation, absence of Bowman's layer, subepithelial fibrosis and abnormal subbasal nerves) probably reflects a novel phenotypic expression of the healing response to recurrent erosion of the corneal epithelium. However, the pathogenesis of Dystrophia Smolandiensis remains to be elucidated fully. [source] Dystrophia Helsinglandica , corneal morphology, topography and sensitivity in a hereditary corneal disease with recurrent erosive episodesACTA OPHTHALMOLOGICA, Issue 4 2010Waldir Neira Abstract. Purpose:, The aim of this study was to describe the morphology, corneal topography and sensitivity in individuals with Dystrophia Helsinglandica. This autosomal dominant corneal disease is characterized by recurrent corneal erosive episodes and progressive subepithelial fibrosis not significantly affecting visual acuity. Methods:, The corneas of nine affected and nine unaffected individuals were examined using slit-lamp biomicroscopy, in vivo confocal microscopy (IVCM) and videokeratography. Corneal mechanical sensitivity was also measured using a non-contact esthesiometer. Results:, Slit-lamp biomicroscopy revealed that the affected individuals represented different stages of corneal changes, from a nearly normal cornea to subepithelial fibrosis of the central cornea. Corneal changes in affected individuals did not significantly decrease the best spectacle-corrected visual acuity. In vivo confocal microscopy detected morphological changes in the epithelium and stroma. Subepithelial opacity formation including altered keratocytes could be found in the anterior stroma in all affected eyes. With the exception of two eyes (one affected and one unaffected), all videokeratographies showed irregular astigmatism. Corneal sensitivity was significantly lower in affected individuals (p = 0.01). Age and corneal sensitivity showed no correlation. Conclusion:, The main morphological findings in affected individuals were discrete and progressive subepithelial fibrosis, in the in vivo confocal microscope corresponding to optically dense extracellular matrix and activated keratocytes. Subbasal nerve morphology was changed in the affected family members who also showed a decreased corneal sensitivity. The findings are per se not specific to the disease. The changes probably reflect a healing response to erosive events on the corneal surface influenced by the genotype. [source] Wound healing response in the presence of stromal irregularities after excimer laser treatmentACTA OPHTHALMOLOGICA, Issue 4 2001Beat A. Weber ABSTRACT. Purpose: To trace the fate of stromal irregularities after excimer laser treatment and to increase our knowledge of the reasons why surface irregularities in the ablation bed cause inferior postoperative results. Methods: Twelve New Zealand White rabbits received a transepithelial photoablation to a preset depth of 60 ,m. An electron microscopy specimen grid was then placed on the denuded stroma and another 20 ,m ablation was applied in order to produce surface irregularities. Another six rabbits received a plano transepithelial photoablation to a preset depth of 80 ,m. The treated corneas were harvested at various timepoints and differentially further processed for microradiography, hematoxylin-eosin -, hyaluronan (HA)- and leukocyte protein L1 staining. Results: In the grid treated corneas the subepithelial mesh pattern is clearly discernible after 1 week, and after 4 weeks it is replaced by a subepithelial layer containing HA and water. The thinning of this layer between 1 and 12 weeks is statistically significant (p<0.05). After 4 and 8 week the plano treated corneas only exhibit some subepithelial HA- and water accumulation. After 1 day the grid treated corneas show an extensive stromal infiltration of leukocytes. In the plano treated corneas the leukocytes mainly remain on the surface. Conclusions: During the healing process stromal irregularities are flattened, leaving a homogeneous zone with increased water content. This subepithelial layer is rarefying as new subepithelial tissue is forming. Postablational irregularities induce a more pronounced healing reaction when compared to a smooth ablation surface. Leukocyte infiltration seems to play a role in this process. [source] The alpha-3 polypeptide chain of laminin 5: insight into wound healing responses from the study of genodermatosesCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 4 2005K. J. Hamill Summary Laminin 5 (kalinin/epiligrin/nicein) is an essential structural component of the dermal,epidermal junction, composed of three polypeptide subunits: laminin ,3, ,3 and ,2. Studies of the inherited skin fragility disorder junctional epidermolysis bullosa (JEB) have suggested that the major role of this heterotrimeric protein is to act as an adhesive ligand essential for binding the epidermis to the underlying dermis and thus maintaining the integrity of the skin. Protein interaction studies have shown that the C terminus of the ,3 subunit binds to a range of integrin complexes depending on the motility status of keratinocytes. This allows laminin 5 to interact with either hemidesmosomes or the actin cytoskeleton. Recently we have reported that the absence of the N-terminal region of laminin ,3a in laryngo-onchyo-cutaneous syndrome causes excessive granulation tissue production at wound sites. As granulation tissue production is also a problem in JEB, this implicates laminin 5 in control of this wound healing response. [source] Transmucosal healing around peri-implant defects: crestal and subcrestal implant placement in dogsCLINICAL ORAL IMPLANTS RESEARCH, Issue 8 2010Binh L. T. Tran Abstract Objective: This study was designed to evaluate the transmucosal healing response of implants placed with the junction of the smooth surfaces, either crestal or subcrestal, into simulated extraction defects after healing periods of 1 and 3 months. Materials and methods: A total of 23 Straumann SP ,3.3 mm NN, SLA® 10 mm implants were placed in the mandibular premolar regions of three greyhound dogs 3 months after the teeth were removed. Five control implants were placed at the crestal bone level, and test implants with surgically created peri-implant defects of 1.25 mm wide × 5 mm depth were placed either at the crestal (nine implants) or at the 2 mm subcrestal (nine implants) bone level. Implants on the right side were placed 1 month before the dogs were sacrificed, and implants on the left side were placed 3 months before sacrifice. All dogs had daily plaque control following surgery and were sacrificed 3 months after implant placement for histological and histometric analyses. Results: Mesial,distal ground sections of the control and test implant specimens showed a greater %BIC in the coronal defect region after 3 months of healing. This healing response was incomplete for the test implants compared with the control implants after a 1-month healing period. The histometric measurements for test implants placed at the crestal bone level or 2 mm subcrestal with surgically created peri-implant defects were more coronal or closer to the implant margin compared with the control implants. Additionally, the degree of osseointegration between the newly formed bone and the implant surface was similar between the test implants. Conclusion: Peri-implant defects of 1.25 mm width healed with spontaneous bone regeneration around implants placed transmucosally at crestal or 2 mm subcrestal with a high degree of osseointegration after a 3-month healing period. To cite this article: Tran BLT, Chen ST, Caiafa A, Davies HMS, Darby IB. Transmucosal healing around peri-implant defects: crestal and subcrestal implant placement in dogs. Clin. Oral Impl. Res. 21, 2010; 794,803. doi: 10.1111/j.1600-0501.2010.01911.x [source] Orthodontic loading of titanium miniplates in dogs: microradiographic and histological evaluationCLINICAL ORAL IMPLANTS RESEARCH, Issue 10 2008M. A. Cornelis Abstract Objectives: The objectives of this animal study were to evaluate if orthodontic loading has an impact on osseointegration of screws supporting miniplates, and to describe the histological components of the bone,screw interface. Materials and methods: Eighty orthodontic miniplates were placed in the jaws of 10 dogs. After 2 weeks, a 125 g force was applied between the miniplates of one upper quadrant of each dog and between those of the controlateral lower quadrant. The others, nonloaded miniplates, were considered as controls. Five dogs were sacrificed 7 weeks after implantation and the remaining five dogs after 29 weeks [Short Term (ST) and Long Term (LT) groups, respectively]. Fluorochromes were injected at implantation and at sacrifice. Jaw quadrants were dissected, embedded, cut into undecalcified transverse sections through the screws and finally submitted to microradiographic analysis to allow assessment of bone,implant contact (BIC) and bone volume/total volume (BV/TV). The sections were observed under UV light and stained in order to examine them under ordinary light. Results: Osseointegration occurred around 90/160 screws and consisted mainly in limited repair and remodelling processes of lamellar bone, without inflammation. Wide variations were observed in BIC and BV/TV, but without any significant difference, neither between the loaded and the nonloaded screws, nor according to the direction of load, whereas they were significantly higher in the LT than in the ST group. Nonosseointegrated screws were surrounded by fibrous tissue. Osteoblastic activity, when present in front of these screws, was not sufficient to achieve stability. Conclusions: Osseointegration underlying orthodontic anchorage was not affected by loading. BIC increased with time and varied according to implantation site. Particularly the tight-fitting screw insertion appeared crucial in determining the appropriate bone healing response. [source] Long-term prognosis of crown-fractured permanent incisors.INTERNATIONAL JOURNAL OF PAEDIATRIC DENTISTRY, Issue 3 2000The effect of stage of root development, associated luxation injury Objectives. The aim of the present study was to investigate pulp healing responses following crown fracture with and without pulp exposure as well as with and without associated luxation injury and in relation to stage of root development. Patient material and methods. The long-term prognosis was examined for 455 permanent teeth with crown fractures, 352 (246 with associated luxation injury) without pulpal involvement and 103 (69 with associated luxation injury) with pulp exposures. Initial treatment for all patients was provided by on-call oral surgeons at the emergency service, University Hospital (Rigshospitalet), Copenhagen. In fractures without pulpal involvement, dentin was covered by a hard-setting calcium hydroxide cement (Dycal®), marginal enamel acid-etched (phosphoric acid gel), then covered with a temporary crown and bridge material. In the case of pulp exposure, pulp capping or partial pulpotomy was performed. Thereafter treatment was identical to the first group. Patients were then referred to their own dentist for resin composite restoration. Results. Patients were monitored for normal pulp healing or healing complications for up to 17 years after injury (x = 2·3 years, range 0·2,17·0 years, SD + 2·7). Pulp healing was registered and classified into pulp survival with no radiographic change (PS), pulp canal obliteration (PCO) and pulp necrosis (PN). Healing was related to the following clinical factors: stage of root development at the time of injury, associated damage to the periodontium at time of injury (luxation) and time interval from injury until initial treatment. Crown fractures with or without pulp exposure and no concomitant luxation injury showed PS in 99%, PCO in 1% and PN in 0%. Crown fractures with concomitant luxation showed PS in 70%, PCO in 5% and PN in 25%. An associated damage to the periodontal ligament significantly increased the likelihood of pulp necrosis from 0% to 28% (P < 0·001) in teeth with only enamel and dentin exposure and from 0% to 14% (P < 0·001) in teeth with pulp exposure. Conclusions. In the case of concomitant luxation injuries, the stage of root development played an important role in the risk of pulp necrosis after crown fracture. However, the primary factor related to pulp healing events after crown fracture appears to be compromised pulp circulation due to concomitant luxation injuries. [source] Inflammatory inert poly(ethylene glycol)-protein wound dressing improves healing responses in partial- and full-thickness woundsINTERNATIONAL WOUND JOURNAL, Issue 4 2006Article first published online: 12 DEC 200 No abstract is available for this article. [source] Progranulin: normal function and role in neurodegenerationJOURNAL OF NEUROCHEMISTRY, Issue 2 2008Jason L. Eriksen Abstract Progranulin (PGRN) is a multifunctional protein that has attracted significant attention in the neuroscience community following the recent discovery of PGRN mutations in some cases of frontotemporal dementia. Most of the pathogenic mutations result in null alleles, and it is thought that frontotemporal dementia in these families results from PGRN haploinsufficiency. The neuropathology associated with PGRN mutations is characterized by the presence of tau-negative, ubiquitin-immunoreactive neuronal inclusions (frontotemporal lobar degeneration with ubiquitinated inclusions) that are also positive for the transactivation response DNA binding protein with Mr 43 kD. The clinical phenotype includes behavioral abnormalities, language disorders and parkinsonism but not motor neuron disease. There is significant clinical variation between families with different PGRN mutations and among members of individual families. The normal function of PGRN is complex, with the full-length form of the protein having trophic and anti-inflammatory activity, whereas proteolytic cleavage generates granulin peptides that promote inflammatory activity. In the periphery, PGRN functions in wound healing responses and modulates inflammatory events. In the CNS, PGRN is expressed by neurons and microglia; consequently, reduced levels of PGRN could affect both neuronal survival and CNS inflammatory processes. In this review, we discuss current knowledge of the molecular genetics, neuropathology, clinical phenotype and functional aspects of PGRN in the context of neurodegenerative disease. [source] A novel model of wound healing in the SCID mouse using a cultured human skin substituteAUSTRALASIAN JOURNAL OF DERMATOLOGY, Issue 1 2009Martin L Windsor SUMMARY Studies of skin graft behaviour in rodent excisional wound models are limited by the dominance of wound contracture and graft sloughing as primary healing responses. To slow skin contraction, polytetrafluoroethylene (Teflon) rings were inserted into dorso-lateral full-thickness wounds in SCID mice. Cultured skin substitutes (OrCel), composed of cultured human keratinocytes and fibroblasts in a bovine collagen sponge, were implanted within the rings. Examination and histology of grafts 14 days later showed graft take in four of six recipients, with 90% epithelialization and wound contraction of 31,47%. Immunohistochemical studies, using human-specific antisera to distinguish graft from host tissues, showed that regenerated tissue was predominantly human. Staining with anticytokeratin, revealed a multilayered, stratified neoepidermis. HBG were identified in keratinocytes in all epidermal layers. Langerhans cells were absent. Antihuman vimentin, used as a fibroblast marker, confirmed that cells of the neodermis were primarily of human origin. Neoepidermal keratinocytes, primarily in the basal and suprabasal layers, were also stained. Results suggest that the poly(tetrafluoroethylene) ring inhibited graft sloughing and provided a more favourable environment for the skin substitute to regenerate a substantially normal human skin. [source] Heat-shock protein 70 gene polymorphism is associated with the severity of diabetic foot ulcer and the outcome of surgical treatmentBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 10 2009K. A. Mir Background: Foot ulcer is a significant cause of morbidity in diabetics. Genetic make-up can determine inflammatory and healing responses. This study examined the hypothesis that specific polymorphisms of the heat-shock protein 70 gene could predispose to the severity of diabetic foot ulceration. Methods: Some 106 consecutive diabetic patients (101 evaluable) with foot ulceration admitted to a tertiary care hospital were managed according to a standard protocol. DNA was extracted from venous blood and examined by polymerase chain reaction,restriction fragment length analysis for two specific polymorphisms: G1538A in the HSPA1B and C2437T in the HSPA1L gene. Results: HSPA1B genotyping showed that 70 patients were AG and 30 GG (one not amplified). The AG genotype was significantly associated with the severity of foot ulceration (Wagner grade) (P = 0·008, ,2 test), need for amputation (relative risk 2·02, 95 per cent confidence interval 1·02 to 4·01; P = 0·025) and median length of hospital stay (8 versus 5 days for GG; P = 0·043). HSPA1L genotypes (78 TT, 22 CT, one CC) did not show any significant association with these parameters. Conclusion: The HSPA1B genotype, was associated with the severity of diabetic foot ulceration, need for amputation and duration of hospitalization in these patients. Copyright © 2009 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] The alpha-3 polypeptide chain of laminin 5: insight into wound healing responses from the study of genodermatosesCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 4 2005K. J. Hamill Summary Laminin 5 (kalinin/epiligrin/nicein) is an essential structural component of the dermal,epidermal junction, composed of three polypeptide subunits: laminin ,3, ,3 and ,2. Studies of the inherited skin fragility disorder junctional epidermolysis bullosa (JEB) have suggested that the major role of this heterotrimeric protein is to act as an adhesive ligand essential for binding the epidermis to the underlying dermis and thus maintaining the integrity of the skin. Protein interaction studies have shown that the C terminus of the ,3 subunit binds to a range of integrin complexes depending on the motility status of keratinocytes. This allows laminin 5 to interact with either hemidesmosomes or the actin cytoskeleton. Recently we have reported that the absence of the N-terminal region of laminin ,3a in laryngo-onchyo-cutaneous syndrome causes excessive granulation tissue production at wound sites. As granulation tissue production is also a problem in JEB, this implicates laminin 5 in control of this wound healing response. [source] | |||||||||||||||||||||||||