Beyond surgery: Pre- and post-operative care in children with ankyloglossia.

BACKGROUND: Surgical intervention for tongue-tie, or ankyloglossia performed by paediatric dentists can alleviate symptoms and improve functional abilities in infants and children. Despite widespread practice, there are currently no established clinical guidelines or consistent approaches for pre- and post-operative care of children. AIM: The aim of this study was to explore approaches to pre- and post-operative care for children with ankyloglossia having frenum surgery. DESIGN: A scoping review of peer-reviewed articles in four electronic databases was conducted. Intervention studies that reported on pre- or post-operative regimens for infants, children and adolescents (0 to 18 years) with a diagnosis of tongue-tie or ankyloglossia, who had surgical intervention such as frenotomy or frenectomy, were included and quality assessments performed. RESULTS: Twenty-three studies were identified, with seven studies incorporating both pre- and post-operative care, and 16 studies focussing solely on post-operative care. Tongue exercises were commonly prescribed, and only three studies examined the relationship between post-operative care and recovery outcomes. Considerable variability existed in study design, prescribed care and outcome measures. CONCLUSION: There was substantial variability in pre- and post-operative care protocols, including dosage, frequency and duration of exercises and other care regimens for infants and children having frenum surgery. Further research is needed to determine the most effective course of pre- and post-operative care for children undergoing frenum surgery.

Selective impairment in dendritic cell function and altered antigen-specific CD8+ T-cell responses in diet-induced obese mice infected with influenza virus.

There is a clear link between obesity and metabolic disorders; however, little is known about the effect of obesity on immune function, particularly during an infection. We have previously reported that diet-induced obese mice are more susceptible to morbidity and mortality during influenza infection than lean mice. Obese mice displayed aberrant innate immune responses characterized by minimal induction of interferon (IFN)-alpha/beta, delayed expression of pro-inflammatory cytokines and chemokines, and impaired natural killer cell cytotoxicity. To further examine the abnormal immune response of diet-induced obese mice, we analysed the cellularity of their lungs during influenza virus infection. We found delayed mononuclear cell entry with a marked decrease in dendritic cells (DCs) throughout the infection. Given the critical role of the DC in activating the cell-mediated immune response, we also analysed the functional capacity of DCs from obese mice. We found that, while obesity did not interfere with antigen uptake and migration, it did impair DC antigen presentation. This was probably attributable to an altered cytokine milieu, as interleukin (IL)-2, IL-12, and IL-6 were differentially regulated in the obese mice. Overall, this did not impact the total number of virus-specific CD8(+) T cells that were elicited, but did affect the number and frequency of CD3(+) and CD8(+) T cells in the lung. Thus, obesity interferes with cellular responses during influenza infection, leading to alterations in the T-cell population that ultimately may be detrimental to the host.

Stress-induced modulation of NK activity during influenza viral infection: role of glucocorticoids and opioids.

Activation of the hypothalamic-pituitary-adrenal axis (HPA) and sympathetic nervous system by stress has been shown to modulate both innate and adaptive immunity during an experimental influenza A/PR8 viral infection. HPA activation alters levels of glucocorticoids (GC) and opioids which are associated with suppression of lymphoid cellularity and NK activity. These experiments were designed to investigate the role that stress-induced GC and opioids have in modulating NK activity during an influenza viral infection. C57BL/6 mice were treated daily with mifepristone (RU486), a GC receptor antagonist or naltrexone (NTX), a non-specific opioid receptor antagonist. Mice were infected intranasally with A/PR8 virus and underwent daily restraint stress (RST). Phenotypic analysis of splenic cell populations and NK cytotoxicity were assessed at 3 days post-infection. RST of infected mice significantly suppressed splenic CD3(-)DX5+ cellularity and NK cytolytic activity. RU486 administration fully restored splenic NK cellularity but not cytolytic activity. NTX administration restored NK cytolytic activity but not splenic NK cell number. A similar restoration in NK cytolytic activity was observed after administration of beta-funaltrexamine (FNA), a mu-specific opioid receptor antagonist, but not the delta- or kappa-specific opioid receptor antagonists naltrindole or nor-binaltorphimine, respectively. Co-administration of RU486 and NTX restored both NK cellularity and cytolytic activity. The restoration of RST-induced suppression of NK activity by RU486 and NTX or FNA suggests that glucocorticoids modulate NK cellularity and opioids that bind to the mu-opioid receptor modulate NK cytotoxicity during periods of stress and viral infection.