Diabetes is a risk factor for periodontitis, an inflammatory bone disorder and the greatest cause of tooth loss in adults. Diabetes has a significant impact on the gut microbiota; however, studies in ...the oral cavity have been inconclusive. By 16S rRNA sequencing, we show here that diabetes causes a shift in oral bacterial composition and, by transfer to germ-free mice, that the oral microbiota of diabetic mice is more pathogenic. Furthermore, treatment with IL-17 antibody decreases the pathogenicity of the oral microbiota in diabetic mice; when transferred to recipient germ-free mice, oral microbiota from IL-17-treated donors induced reduced neutrophil recruitment, reduced IL-6 and RANKL, and less bone resorption. Thus, diabetes-enhanced IL-17 alters the oral microbiota and renders it more pathogenic. Our findings provide a mechanistic basis to better understand how diabetes can increase the risk and severity of tooth loss.
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•Diabetes increases periodontal bone resorption and tooth loss in mice•Diabetic mice have increased periodontal inflammation and IL-17 levels•Diabetic oral microbiota induces periodontitis in wild-type germ-free recipients•Blocking IL-17 reduces the pathogenic effect of diabetic oral microbiota
Diabetes increases periodontal disease, a major cause of tooth loss. Xiao et al. demonstrated, by transfer to germ-free mice, that oral microbiota from diabetic mice induced more periodontal inflammation and bone loss than microbiota from normal mice. Diabetes increased the pathogenicity of the oral microbiota through an IL-17-mediated mechanism.
Acquired sensorineural hearing loss is one of the most prevalent chronic diseases, and aging and acoustic overexposure are common contributors. Decades of study in animals and humans have clarified ...the cellular targets and perceptual consequences of these forms of hearing loss, and preclinical studies have led to the development of therapeutics designed to slow, prevent or reverse them. Here, we review the histopathological changes underlying age-related and noise-induced hearing loss and the functional consequences of these pathologies. Based on these relations, we consider the ambiguities that arise in diagnosing underlying pathology from minimally invasive tests of auditory function, and how those ambiguities present challenges in the design and interpretation of clinical trials.
•Noise exposure and aging are major causes of acquired sensorineural hearing loss.•Threshold shifts can be due to hair cell loss, stereocilia or strial damage.•IHC-ANF synapse loss contributes to hearing impairment without elevating thresholds.•Preclinical studies showing cochlear regeneration are spawning clinical trials.•Trial design is complicated by crude non-invasive diagnosis of underlying pathology.
Septic emboli are an unusual cause of sudden sensorineural hearing loss, for which few reports exist in the literature.
This paper presents two cases of sudden sensorineural hearing loss, initially ...considered as idiopathic, but which were caused by septic emboli. Hearing loss in these cases was bilateral, sequential and total. The first patient had mild fever one week prior to their presentation with sudden sensorineural hearing loss; the other patient had no additional symptoms at presentation. These patients were later diagnosed with infective endocarditis, at two and seven months following the sudden sensorineural hearing loss respectively, showing that septic emboli had been the cause of sudden sensorineural hearing loss.
Septic emboli should be considered as a possible cause of sudden sensorineural hearing loss in cases of total hearing loss. This form of hearing loss should prompt the otolaryngologist to further investigate for infective endocarditis.
Introduction
The BAHA (bone-anchored hearing aid) Attract is a magnetic transcutaneous bone conduction device anchored into the temporal bone. The standard surgical technique for BAHA Attract is a ...multi-tools time-consuming process, which requires a large cutaneous incision. The objective of this study is to describe and test the feasibility of a minimally invasive pocket (MIP) technique for Magnet Bone Implant Hearing Aid (MBIHA) with a modified magnet of BAHA Attract without fixation and without any tissue reduction. We use a 3-cm vertical skin incision and a subperiosteal pocket.
Method
A study of 10 patients with conductive or mixed hearing loss who benefited from a MBIHA using the MIP technique is presented. The pure tone average (PTA) (dB) for air-conduction thresholds and the speech recognition threshold (SRT) (dB) in speech audiometry in quiet are calculated. The Entific Medical Systems (EMS) questionnaire and the postoperative clinical outcomes are realized.
Results
We found a significant improvement of 33.8 dB on average for the PTA and 44.8 dB for the SRT with MBIHA at 3 months, compared with unaided situation. No implant was removed or displaced after 2 years of follow-up. The skin condition remains intact in all the cases.
Conclusion
The minimally subperiosteal pocket surgical technique MIP without fixation and with tissue preservation for the MBIHA is safe, rapid and effective for patients with conductive or mixed hearing loss. It opens new perspectives of development and modify conventional concept in magnetic coupling of bone-conducted device.
Significant hyperbilirubinemia (SHB) may cause chronic auditory toxicity (auditory neuropathy spectrum disorder and/or sensorineural hearing loss); however, total serum bilirubin (TSB) does not ...discriminate neonates at risk for auditory toxicity. Our objective was to compare TSB, bilirubin albumin molar ratio (BAMR), and unbound bilirubin (UB) for their association with chronic auditory toxicity in neonates with SHB (TSB ≥20 mg/dL or TSB that met criteria for exchange transfusion).
Infants ≥34 weeks' gestational age (GA) with SHB during the first 2 postnatal weeks were eligible for a prospective longitudinal study in India. Comprehensive auditory evaluations were performed at 2 to 3 months of age by using auditory brainstem response, tympanometry, and an otoacoustic emission test and at 9 to 12 months of age by using audiometry. The evaluations were performed by an audiologist unaware of the degree of jaundice.
A total of 93 out of 100 infants (mean GA of 37.4 weeks; 55 boys, 38 girls) who were enrolled with SHB were evaluated for auditory toxicity. Of those, 12 infants (13%) had auditory toxicity. On regression analysis controlling for covariates, peak UB (but not peak TSB or peak BAMR), was associated with auditory toxicity (odds ratio 2.41; 95% confidence interval: 1.43-4.07;
.001). There was significant difference in the area under the receiver operating characteristic curves between UB (0.866), TSB (0.775), and BAMR (0.724) for auditory toxicity (
= .03) after controlling for covariates.
Unconjugated hyperbilirubinemia indexed by UB (but not TSB or BAMR) is associated with chronic auditory toxicity in infants ≥34 weeks' GA with SHB.
Cisplatin is widely used but highly ototoxic. Effects of cumulative cisplatin dose on hearing loss have not been comprehensively evaluated in survivors of adult-onset cancer.
Comprehensive ...audiological measures were conducted on 488 North American male germ cell tumor (GCT) survivors in relation to cumulative cisplatin dose, including audiograms (0.25 to 12 kHz), tests of middle ear function, and tinnitus. American Speech-Language-Hearing Association criteria defined hearing loss severity. The geometric mean of hearing thresholds (0.25 to 12 kHz) summarized overall hearing status consistent with audiometric guidelines. Patients were sorted into quartiles of hearing thresholds of age- and sex-matched controls.
Increasing cumulative cisplatin dose (median, 400 mg/m(2); range, 200 to 800 mg/m(2)) was significantly related to hearing loss at 4, 6, 8, 10, and 12 kHz (P trends, .021 to < .001): every 100 mg/m(2) increase resulted in a 3.2-dB impairment in age-adjusted overall hearing threshold (4 to 12 kHz; P < .001). Cumulative cisplatin doses > 300 mg/m(2) were associated with greater American Speech-Language-Hearing Association-defined hearing loss severity (odds ratio, 1.59; P = .0066) and worse normative-matched quartiles (odds ratio, 1.33; P = .093) compared with smaller doses. Almost one in five (18%) patients had severe to profound hearing loss. Tinnitus (40% patients) was significantly correlated with reduced hearing at each frequency (P < .001). Noise-induced damage (10% patients) was unaffected by cisplatin dose (P = .59). Hypertension was significantly related (P = .0066) to overall hearing threshold (4 to 12 kHz) in age- and cisplatin dose-adjusted analyses. Middle ear deficits occurred in 22.3% of patients but, as expected, were not related to cytotoxic drug dosage.
Follow-up of adult-onset cancer survivors given cisplatin should include routine inquiry for hearing status and tinnitus, referral to audiologists as clinically indicated, and hypertension control. Patients should be urged to avoid noise exposure, ototoxic drugs, and other factors that further damage hearing.
Objective:
To characterize the prevalence, imaging characteristics, and cochlear implant candidacy of pediatric patients with single-sided deafness (SSD).
Methods:
An audiometric database of patients ...evaluated at a large tertiary academic medical center was retrospectively queried to identify pediatric patients (<18 years old) with SSD, defined as severe to profound sensorineural hearing loss in one ear and normal hearing in the other. Medical records of identified patients were reviewed to characterize the prevalence, etiology, and cochlear implant candidacy of pediatric patients with SSD.
Results:
We reviewed audiometric data obtained from 1993 to 2018 for 52,878 children at our institution. 191 (0.36%) had the diagnosis of SSD. Cochlear nerve deficiency (either hypoplasia or aplasia) diagnosed on MRI and/or CT was the most common etiology of SSD and was present in 22 of 88 (25%) pediatric SSD patients with available imaging data. 70 of 106 (66%) pediatric SSD patients with available imaging had anatomy amenable to cochlear implantation.
Conclusions:
Pediatric SSD is a rare condition and the most common etiology based on radiology is cochlear nerve deficiency. High resolution imaging of the temporal bone is essential to determine cochlear nerve morphology prior to consideration of cochlear implantation.
Objective: Establish up-to-date evidence-based guidelines for recommending cochlear implantation for young children. Design: Speech perception results for early-implanted children were compared to ...children using traditional amplification. Equivalent pure-tone average (PTA) hearing loss for cochlear implant (CI) users was established. Language of early-implanted children was assessed over six years and compared to hearing peers. Study sample: Seventy-eight children using CIs and 62 children using traditional amplification with hearing losses ranging 25-120 dB HL PTA (speech perception study). Thirty-two children who received a CI before 2.5 years of age (language study). Results: Speech perception outcomes suggested that children with a PTA greater than 60 dB HL have a 75% chance of benefit over traditional amplification. More conservative criteria applied to the data suggested that children with PTA greater than 82 dB HL have a 95% chance of benefit. Children implanted under 2.5 years with no significant cognitive deficits made normal language progress but retained a delay approximately equal to their age at implantation. Conclusions: Hearing-impaired children under three years of age may benefit from cochlear implantation if their PTA exceeds 60 dB HL bilaterally. Implantation as young as possible should minimize any language delay resulting from an initial period of auditory deprivation.
The hallmark of mechanosensory hair cells is the stereocilia, where mechanical stimuli are converted into electrical signals. These delicate stereocilia are susceptible to acoustic trauma and ...ototoxic drugs. While hair cells in lower vertebrates and the mammalian vestibular system can spontaneously regenerate lost stereocilia, mammalian cochlear hair cells no longer retain this capability. We explored the possibility of regenerating stereocilia in the noise-deafened guinea pig cochlea by cochlear inoculation of a viral vector carrying Atoh1, a gene critical for hair cell differentiation. Exposure to simulated gunfire resulted in a 60-70 dB hearing loss and extensive damage and loss of stereocilia bundles of both inner and outer hair cells along the entire cochlear length. However, most injured hair cells remained in the organ of Corti for up to 10 days after the trauma. A viral vector carrying an EGFP-labeled Atoh1 gene was inoculated into the cochlea through the round window on the seventh day after noise exposure. Auditory brainstem response measured one month after inoculation showed that hearing thresholds were substantially improved. Scanning electron microscopy revealed that the damaged/lost stereocilia bundles were repaired or regenerated after Atoh1 treatment, suggesting that Atoh1 was able to induce repair/regeneration of the damaged or lost stereocilia. Therefore, our studies revealed a new role of Atoh1 as a gene critical for promoting repair/regeneration of stereocilia and maintaining injured hair cells in the adult mammal cochlea. Atoh1-based gene therapy, therefore, has the potential to treat noise-induced hearing loss if the treatment is carried out before hair cells die.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Sudden hearing loss is a frightening symptom that often prompts an urgent or emergent visit to a health care provider. It is frequently but not universally accompanied by tinnitus and/or vertigo. ...Sudden sensorineural hearing loss affects 5 to 27 per 100,000 people annually, with about 66,000 new cases per year in the United States. This guideline update provides evidence-based recommendations for the diagnosis, management, and follow-up of patients who present with sudden hearing loss. It focuses on sudden sensorineural hearing loss in adult patients aged ≥18 years and primarily on those with idiopathic sudden sensorineural hearing loss. Prompt recognition and management of sudden sensorineural hearing loss may improve hearing recovery and patient quality of life. The guideline update is intended for all clinicians who diagnose or manage adult patients who present with sudden hearing loss.
The purpose of this guideline update is to provide clinicians with evidence-based recommendations in evaluating patients with sudden hearing loss and sudden sensorineural hearing loss, with particular emphasis on managing idiopathic sudden sensorineural hearing loss. The guideline update group recognized that patients enter the health care system with sudden hearing loss as a nonspecific primary complaint. Therefore, the initial recommendations of this guideline update address distinguishing sensorineural hearing loss from conductive hearing loss at the time of presentation with hearing loss. They also clarify the need to identify rare, nonidiopathic sudden sensorineural hearing loss to help separate those patients from those with idiopathic sudden sensorineural hearing loss, who are the target population for the therapeutic interventions that make up the bulk of the guideline update. By focusing on opportunities for quality improvement, this guideline should improve diagnostic accuracy, facilitate prompt intervention, decrease variations in management, reduce unnecessary tests and imaging procedures, and improve hearing and rehabilitative outcomes for affected patients.
Consistent with the American Academy of Otolaryngology-Head and Neck Surgery Foundation's "Clinical Practice Guideline Development Manual, Third Edition" (Rosenfeld et al.
. 2013;1481:S1-S55), the guideline update group was convened with representation from the disciplines of otolaryngology-head and neck surgery, otology, neurotology, family medicine, audiology, emergency medicine, neurology, radiology, advanced practice nursing, and consumer advocacy. A systematic review of the literature was performed, and the prior clinical practice guideline on sudden hearing loss was reviewed in detail. Key Action Statements (KASs) were updated with new literature, and evidence profiles were brought up to the current standard. Research needs identified in the original clinical practice guideline and data addressing them were reviewed. Current research needs were identified and delineated.
The guideline update group made
the following: (KAS 1) Clinicians should distinguish sensorineural hearing loss from conductive hearing loss when a patient first presents with sudden hearing loss. (KAS 7) Clinicians should educate patients with sudden sensorineural hearing loss about the natural history of the condition, the benefits and risks of medical interventions, and the limitations of existing evidence regarding efficacy. (KAS 13) Clinicians should counsel patients with sudden sensorineural hearing loss who have residual hearing loss and/or tinnitus about the possible benefits of audiologic rehabilitation and other supportive measures. These strong recommendations were modified from the initial clinical practice guideline for clarity and timing of intervention. The guideline update group made
following: (KAS 3) Clinicians should
order routine computed tomography of the head in the initial evaluation of a patient with presumptive sudden sensorineural hearing loss. (KAS 5) Clinicians should
obtain routine laboratory tests in patients with sudden sensorineural hearing loss. (KAS 11) Clinicians should
routinely prescribe antivirals, thrombolytics, vasodilators, or vasoactive substances to patients with sudden sensorineural hearing loss. The guideline update group made
the following: (KAS 2) Clinicians should assess patients with presumptive sudden sensorineural hearing loss through history and physical examination for bilateral sudden hearing loss, recurrent episodes of sudden hearing loss, and/or focal neurologic findings. (KAS 4) In patients with sudden hearing loss, clinicians should obtain, or refer to a clinician who can obtain, audiometry as soon as possible (within 14 days of symptom onset) to confirm the diagnosis of sudden sensorineural hearing loss. (KAS 6) Clinicians should evaluate patients with sudden sensorineural hearing loss for retrocochlear pathology by obtaining magnetic resonance imaging or auditory brainstem response. (KAS 10) Clinicians should offer, or refer to a clinician who can offer, intratympanic steroid therapy when patients have incomplete recovery from sudden sensorineural hearing loss 2 to 6 weeks after onset of symptoms. (KAS 12) Clinicians should obtain follow-up audiometric evaluation for patients with sudden sensorineural hearing loss at the conclusion of treatment and within 6 months of completion of treatment. These recommendations were clarified in terms of timing of intervention and audiometry and method of retrocochlear workup. The guideline update group offered the following KASs as
: (KAS 8) Clinicians may offer corticosteroids as initial therapy to patients with sudden sensorineural hearing loss within 2 weeks of symptom onset. (KAS 9a) Clinicians may offer, or refer to a clinician who can offer, hyperbaric oxygen therapy combined with steroid therapy within 2 weeks of onset of sudden sensorineural hearing loss. (KAS 9b) Clinicians may offer, or refer to a clinician who can offer, hyperbaric oxygen therapy combined with steroid therapy as salvage therapy within 1 month of onset of sudden sensorineural hearing loss.
Incorporation of new evidence profiles to include quality improvement opportunities, confidence in the evidence, and differences of opinion Included 10 clinical practice guidelines, 29 new systematic reviews, and 36 new randomized controlled trials Highlights the urgency of evaluation and initiation of treatment, if treatment is offered, by emphasizing the time from symptom occurrence Clarification of terminology by changing potentially unclear statements; use of the term
to mean idiopathic sudden sensorineural hearing loss to emphasize that >90% of sudden sensorineural hearing loss is idiopathic sudden sensorineural hearing loss and to avoid confusion in nomenclature for the reader Changes to the KASs from the original guideline: KAS 1-When a patient first presents with sudden hearing loss, conductive hearing loss should be distinguished from sensorineural. KAS 2-The utility of history and physical examination when assessing for modifying factors is emphasized. KAS 3-The word "routine" is added to clarify that this statement addresses nontargeted head computerized tomography scan that is often ordered in the emergency room setting for patients presenting with sudden hearing loss. It does not refer to targeted scans, such as temporal bone computerized tomography scan, to assess for temporal bone pathology. KAS 4-The importance of audiometric confirmation of hearing status as soon as possible and within 14 days of symptom onset is emphasized. KAS 5-New studies were added to confirm the lack of benefit of nontargeted laboratory testing in sudden sensorineural hearing loss. KAS 6-Audiometric follow-up is excluded as a reasonable workup for retrocochlear pathology. Magnetic resonance imaging, computerized tomography scan if magnetic resonance imaging cannot be done, and, secondarily, auditory brainstem response evaluation are the modalities recommended. A time frame for such testing is not specified, nor is it specified which clinician should be ordering this workup; however, it is implied that it would be the general or subspecialty otolaryngologist. KAS 7-The importance of shared decision making is highlighted, and salient points are emphasized. KAS 8-The option for corticosteroid intervention within 2 weeks of symptom onset is emphasized. KAS 9-Changed to KAS 9A and 9B. Hyperbaric oxygen therapy remains an option but only when combined with steroid therapy for either initial treatment (9A) or salvage therapy (9B). The timing of initial therapy is within 2 weeks of onset, and that of salvage therapy is within 1 month of onset of sudden sensorineural hearing loss. KAS 10-Intratympanic steroid therapy for salvage is recommended within 2 to 6 weeks following onset of sudden sensorineural hearing loss. The time to treatment is defined and emphasized. KAS 11-Antioxidants were removed from the list of interventions that the clinical practice guideline recommends against using. KAS 12-Follow-up audiometry at conclusion of treatment and also within 6 months posttreatment is added. KAS 13-This statement on audiologic rehabilitation includes patients who have residual hearing loss and/or tinnitus who may benefit from treatment. Addition of an algorithm outlining KASs Enhanced emphasis on patient education and shared decision making with tools provided to assist in same.
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