The Effect of Exercise on Pulpal and Gingival Blood Flow in Physically Active and Inactive Subjects as Assessed by Laser Doppler

The effects of exercise on pulpal and gingival blood flow are undefined. The autonomic nervous system response suggests that they could increase or decrease with exercise, and they may be independent of each other. This study attempts to answer these questions

Histological evaluation of microfilled and conventional composite resins on monkey dental pulps

The pulpal responses to two micro-filled composite resins and a conventional composite resin were investigated in adult rhesus monkey teeth. All materials were randomly placed in unetched and unlined class V buccal cavity preparations. A total of 90 teeth were used in the study. Each material was evaluated at 3 days, 5 weeks and 8 weeks. Following perfusion, the teeth were prepared using routine histological procedures. The results indicated that the pulpal response to the microfilled and conventional composite resins were similar for all time periods, characterized by an initial slight to moderate response at 3 days, followed at 5 and 8 weeks by a zero to slight response with evidence of reparative dentine formation. Brown and Brenn staining for bacteria indicated positive staining reactions along the cavity wails of all teeth for all materials at each time period.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73366/1/j.1365-2591.1985.tb00453.x.pd

Neurotrophins and neurotrophin receptors in pulmonary sarcoidosis - granulomas as a source of expression

<p>Abstract</p> <p>Background</p> <p>Pulmonary sarcoidosis is an inflammatory disease, characterized by an accumulation of CD4⁺lymphocytes and the formation of non-caseating epithelioid cell granulomas in the lungs. The disease either resolves spontaneously or develops into a chronic disease with fibrosis. The neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) have been suggested to be important mediators of inflammation and mediate tissue remodelling. In support of this, we have recently reported enhanced NGF levels in the airways of patients with pulmonary sarcoidosis. However, less is known about levels of BDNF and NT-3, and moreover, knowledge in the cellular sources of neurotrophins and the distribution of the corresponding neurotrophin receptors in airway tissue in sarcoidosis is lacking.</p> <p>Methods</p> <p>The concentrations of NGF, BDNF and NT-3 in bronchoalveolar lavage fluid (BALF) of 41 patients with newly diagnosed pulmonary sarcoidosis and 27 healthy controls were determined with ELISA. The localization of neurotrophins and neurotrophin receptors were examined by immunohistochemistry on transbronchial lung biopsies from sarcoidosis patients.</p> <p>Results</p> <p>The sarcoidosis patients showed significantly enhanced NT-3 and NGF levels in BALF, whereas BDNF was undetectable in both patients and controls. NT-3 levels in BALF were found higher in patients with non-Löfgren sarcoidosis as compared to patients with Löfgren's syndrome, and in more advanced disease stage. Epithelioid cells and multinucleated giant cells within the sarcoid granulomas showed marked immunoreactivity for NGF, BDNF and NT-3. Also, immunoreactivity for the neurotrophin receptor TrkA, TrkB and TrkC, was found within the granulomas. In addition, alveolar macrophages showed positive immunoreactivity for NGF, BDNF and NT-3 as well as for TrkA, TrkB and TrkC.</p> <p>Conclusions</p> <p>This study provides evidence of enhanced neurotrophin levels locally within the airways of patients with sarcoidosis. Findings suggest that sarcoid granuloma cells and alveolar macrophages are possible cellular sources of, as well as targets for, neurotrophins in the airways of these patients.</p

Differential regulation of neurotrophin expression in human bronchial smooth muscle cells

BACKGROUND: Human bronchial smooth muscle cells (HBSMC) may regulate airway inflammation by secreting cytokines, chemokines and growth factors. The neurotrophins, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), have been shown to be elevated during airway inflammation and evoke airway hyperresponsiveness. We studied if HBSMC may be a source of NGF, BDNF and NT-3, and if so, how inflammatory cytokines may influence their production. METHODS: Basal and cytokine (IL-1β, IFN-γ, IL-4)-stimulated neurotrophin expression in HBSMC cultured in vitro was quantified. The mRNA expression was quantified by real-time RT-PCR and the protein secretion into the cell culture medium by ELISA. RESULTS: We observed a constitutive NGF, BDNF and NT-3 expression. IL-1β stimulated a transient increase of NGF, while the increase of BDNF had a later onset and was more sustained. COX-inhibitors (indomethacin and NS-398) markedly decreased IL-1β-stimulated secretion of BDNF, but not IL-1β-stimulated NGF secretion. IFN-γ increased NGF expression, down-regulated BDNF expression and synergistically enhanced IL-1β-stimulated NGF expression. In contrast, IL-4 had no effect on basal NGF and BDNF expression, but decreased IL-1β-stimulated NGF expression. NT-3 was not altered by the tested cytokines. CONCLUSION: Taken together, our data indicate that, in addition to the contractile capacity, HBSMC can express NGF, BDNF and NT-3. The expression of these neurotrophins may be differently regulated by inflammatory cytokines, suggesting a dynamic interplay that might have a potential role in airway inflammation

Applications of sensory and physiological measurement in oral‐facial dental pain

Dentists regularly employ a variety of self‐report and sensory techniques to aid in the diagnosis and treatment of tooth‐related disease. Many of these techniques leverage principles borrowed from psychophysics, the quantitative measurement of the relationship between stimuli and evoked sensations, which falls under the larger umbrella of quantitative sensory testing (QST). However, most clinicians fail to meet the bar for what could be considered quantitative sensory testing, and instead focus on qualitative and dichotomous “yes/no” aspects of sensory experience. With our current subjective measurements for pain assessments, diagnosis and treatment of dental pain in young children and individuals (any age) with severe cognitive impairment rely extensively on third‐party observations. Consequently, the limitation of inadequate pain diagnosis can lead to poor pain management. In this review, it discusses mechanisms that underlie acute and chronic dental pain. It details the measurement of somatosensory responses and pulpal blood flow as objective measures of tooth health and pain. It proposes that bridging these varied methodologies will significantly improve diagnosis and treatment of orofacial pain and pathology. It concludes that improving the precision of sensory measurements could yield important improvements in diagnostic challenges in pulpal pathology for noncommunicative and cognitively impaired individuals.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146659/1/scd12323.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146659/2/scd12323_am.pd

Management of Crown-related Fractures in Children: An Update Review

Traumatic dental injuries (TDIs) are a serious public health problem. Epidemiology of dental trauma indicates that these injuries are more prevalent in child population of the world. Children are the sufferers in two-thirds of all TDIs observed. Although being a major fraction, crown-related fractures are a less severe form of TDIs with respect to their complications and sequelae. However, as with other types of traumatic injuries, the delay in seeking for immediate care following a traumatic injury and the lack of appropriate treatment may compromise long-term outcomes. This article reviews the occurrence, management, and prognosis of crown-related fractures in primary and permanent teeth in light of the recent literature

Studies on nitric oxide in autonomic neurotransmission

The aim of the present thesis was to study nitric oxide (NO) as a mediator in autonomic neurotransmission in the enteric nervous system, including studies on the mechanism for neuronal release of NO, as well as the effects of NO on intestinal smooth muscle and enteric neurones. Furthermore, the signal transduction pathway for the evoked effects of NO and nitrergic neurotransmission were investigated. Nerve-induced NO/NO2- release in isolated guinea-pig colon was quantified by chemiluminescence technique in order to identify mechanisms involved in neuronal NO release. A considerable part of the nerve-mediated NO release likely results from muscarinic M1 receptor activation. Hence, M1 receptor activation was shown to evoke a smooth muscle relaxation in rat small intestine, which was demonstrated to be mediated via a nerve-dependent nitrergic mechanism. The dependence on vesicular exocytosis for nerve-induced NO release was investigated by use of botulinum toxin B (BTX B), which is known to cleave the synaptic vesicle protein synaptobrevin/VAMP and inhibit calcium-mediated exocytotic release of neurotransmitters. Pre-treatment with BTX B blocked the exatatory cholinergic and tachykininergic neurotransmission as well as the acetylcholine release in the guinea-pig colon, whereas the inhibitory nitrergic neurotransmission and nerve-induced NO/NO2 release were unaffected. This indicates that neuronal release of NO is non-vesicular. The nitrergic neurotransmission was shown to constitute a substantial portion of the inhibitory neurotransmission, evoking smooth muscle relaxation in guinea-pig colon. The NO-dependent relaxation was shown to be mediated exclusively through the soluble guanylyl cyclase transduction pathway. NO may also modulate excitatory cholinergic and tachykininergic neuroeffector responses in guinea-pig ileum. The inhibitory modulation by NO was to a large extent a postjunctional effector-modulation on the smooth muscle, but a prejunctional neuromodulation may also exist. In addition to the inhihtory effect of NO in intestine, NO was shown to evoke an excitatory response resulting in smooth muscle contraction in the guinea-pig small intestine. The contractile response to NO was likely mediated via activation of excitatory cholinergic and tachykininergic neurones, via a pathway utilising the soluble guanylyl cyclase. An additional inhibitory transmission, operating in parallel with NO, was also shown to evoke smooth muscle relaxation in guinea-pig colon. This transmission had a more rapid onset in comparison with the nitrergic transmission, but was independent of the soluble guanylyl cyclase transduction pathway. Similar to NO, this principle seemed independent of synaptic vesicular exocytosis. In conclusion, the present study lends support to the hypothesis that NO is released from enteric neurones upon nerve-activation as a consequence of direct nerve depolarisation as well as via M1 muscarinic receptor activation. Nerve-mediated NO release in itself appears to be independent of synaptic vesicular exocytosis, but may be influenced by other vesicularly stored transmitters. Evoked effects by NO in intestine include smooth muscle relaxation, modulation of excitatory neurotransmission as well as excitatory effects on intestinal smooth muscle through neuronal activation. Thus, NO is proposed as a neurotransmitter with possible dual effects on gastrointestinal motility. Keywords: acetylcholine, autonomic neurotransmission, botulinum toxin, colon, guinea pig, ileum, intestine, nitric oxide, rat, tachykinin