Tissue expansion and serial excision in scar revision.

Scars in the head and neck caused by trauma or extirpative surgery can present a significant problem to the patient and may require revision. A variety of techniques, both surgical and nonsurgical, exists for treatment of unsightly scars. Surgical excision of scars relies upon recruitment of local tissue for closure of the ensuing defect. Tissue expansion and serial scar excision may be used to provide more tissue for advancement or local flap coverage of revised scars. Herein we review the history, technique, and complications of tissue expansion and serial excision as well as the basic scientific principles underlying these techniques.

Patterns of cell death in mouse anteroventral cochlear nucleus neurons after unilateral cochlea removal.

Developmental changes that influence the results of removal of afferent input on the survival of neurons of the anteroventral cochlear nucleus (AVCN) of mice were examined with the hope of providing a suitable model for understanding the cellular and molecular basis for these developmental changes in susceptibility. We performed unilateral cochlear ablation on wild-type mice at a variety of ages around the time of hearing onset to determine developmental changes in the sensitivity of AVCN neurons to afferent deprivation. In postnatal day 5 (P5) mice, cochlea removal resulted in 61% neuronal loss in the AVCN. By age P14, fewer than 1% of AVCN neurons were lost after this manipulation. This reveals a rather abrupt change in the sensitivity to disruption of afferent input, a critical period. We next investigated the temporal events associated with neuron loss after cochlea removal in susceptible animals. We demonstrate that significant cell loss occurs within 48 hours of cochlea removal in P7 animals. Furthermore, evidence of apoptosis was observed within 12 hours of cochlea removal, suggesting that the molecular events leading to cell loss after afferent deprivation begin to occur within hours of cochlea removal. Finally, we began to examine the role of the bcl-2 gene family in regulating afferent deprivation-induced cell death in the mouse AVCN. AVCN neurons in mature bcl-2 knockout mice demonstrate susceptibility to removal of afferent input comparable to neonatal sensitivity of wild-type controls. These data suggest that bcl-2 is one effector of cell survival as these cells switch from afferent-dependent to -independent survival mechanisms.

Tumors and tumorous masses presenting as temporomandibular joint syndrome.

OBJECTIVE: Neoplasms of the temporomandibular joint (TMJ) usually mimic common causes of TMJ syndrome, leading to delay in diagnosis. To increase awareness of TMJ neoplasms and establish guidelines for early intervention, we performed a retrospective analysis of a series of patients with neoplasms of the TMJ. STUDY DESIGN AND SETTING: A retrospective review of the records of patients with neoplasms of the TMJ from 1990 to 1997 was done. RESULTS: Six patients were identified. The neoplasms included benign and malignant neoplasms. The time from initial presentation to final diagnosis was in most cases prolonged, ranging from 3 months to 8 years. Patients typically showed advanced lesions radiographically. All patients required surgical extirpation. Postoperative radiation therapy was used for malignant lesions. Patient outcomes were delineated. CONCLUSIONS AND SIGNIFICANCE: Neoplasms, both benign and malignant, of the TMJ are rare but represent a challenging diagnostic problem. In patients with 1 month or more of recalcitrant TMJ swelling or pain, radiographic imaging may be considered to rule out these rare neoplasms. This may lead to earlier intervention and improved outcome.

Sialoblastoma of the submandibular gland: report of a case and review of the literature.

Sialoblastomas are rare perinatal epithelial salivary tumors, with only 22 reported cases in the literature. While they have been reported to occur predominantly in the parotid gland, we present one case of sialoblastoma of submandibular gland origin. The surgical management of this patient is discussed. Histopathologic examination, including immunochemical, ultrastructural and cytogenetic studies, was performed. Pertinent literature is reviewed.

Life and death in otolaryngology: mechanisms of apoptosis and its role in the pathology and treatment of disease.

OBJECTIVES: To review recent advances in our understanding of programmed cell death, or apoptosis, and discuss implications of these basic science advances in our understanding of causes and potential treatments of a variety of diseases of the head and neck. DATA SOURCES: Basic science literature relevant to the study of apoptosis and its clinical implications. CONCLUSIONS: Apoptosis is now understood to be important in the normal development and survival of all multicellular organisms. Deregulation of this normally tightly controlled process underlies a variety of disease states, including neoplasia, autoimmune disease, and disorders of the central nervous system. A better understanding of this process and its regulation may help otolaryngologists better understand diseases relevant to this specialty and will lead to improved therapeutic interventions.

Noise-induced hearing loss in young adults: the role of personal listening devices and other sources of leisure noise.

CONCEPT: No consensus exists regarding the magnitude of the risk of noise-induced hearing loss (NIHL) associated with leisure noise, in particular, personal listening devices in young adults. OBJECTIVE: Examine the magnitude of hearing loss associated with personal listening devices and other sources of leisure noise in causing NIHL in young adults. STUDY DESIGN: Prospective auditory testing of college student volunteers with retrospective history exposure to home stereos, personal listening devices, firearms, and other sources of recreational noise. METHODS: Subjects underwent audiologic examination consisting of estimation of pure-tone thresholds, speech reception thresholds, and word recognition at 45 dB HL. RESULTS: Fifty subjects aged 18 to 30 years were tested. All hearing thresholds of all subjects (save one-a unilateral 30 dB HL threshold at 6 kHz) were normal, (i.e., 25 dB HL or better). A 10 dB threshold elevation (notch) in either ear at 3 to 6 kHz as compared with neighboring frequencies was noted in 11 (22%) subjects and an unequivocal notch (15 dB or greater) in either ear was noted in 14 (28%) of subjects. The presence or absence of any notch (small or large) did not correlate with any single or cumulative source of noise exposure. No difference in pure-tone threshold, speech reception threshold, or speech discrimination was found among subjects when segregated by noise exposure level. CONCLUSION: The majority of young users of personal listening devices are at low risk for substantive NIHL. Interpretation of the significance of these findings in relation to noise exposure must be made with caution. NIHL is an additive process and even subtle deficits may contribute to unequivocal hearing loss with continued exposure. The low prevalence of measurable deficits in this study group may not exclude more substantive deficits in other populations with greater exposures. Continued education of young people about the risk to hearing from recreational noise exposure is warranted.

Mitochondrial regulation of calcium in the avian cochlear nucleus.

The role of mitochondria and the endoplasmic reticulum in buffering [Ca2+]i in response to imposed calcium loads in neurons of the chick cochlear nucleus, nucleus magnocellularis (NM), was examined. Intracellular calcium concentrations were measured using fluorometric videomicroscopy. After depolarization with 125 mM KCl, NM neurons demonstrate an increase in [Ca2+]i that returns to near-basal levels within 6 min. Addition of the protonophore carbonylcyanide m-chlorophenylhydrazone (CCCP) dissipated the mitochondrial membrane potential, as evidenced by increased fluorescence when cells were loaded with rhodamine-123. Two micromolar CCCP had minimal effect on baseline [Ca2+]i. However, 2 or 10 microM CCCP interfered with the ability of NM cells to buffer [Ca2+]i in response to KCl depolarization without significantly affecting peak [Ca2+]i. Oligomycin also interfered with postdepolarization regulation of [Ca2+]i, but blocked late (7-8 min postdepolarization) increases in [Ca2+]i caused by CCCP. Thapsigargin had no effect on baseline, peak, or postdepolarization [Ca2+]i in NM cells. These results suggest that normal mitochondrial membrane potential and ATP synthesis play an important role in buffering [Ca2+]i in response to imposed calcium loads in NM neurons. Furthermore, the endoplasmic reticulum does not appear to play a significant role in either of these processes. Thus increases in mitochondrial number and function noted in NM cells after deafferentation may represent an adaptive response to an increased cytosolic calcium load.

Brainstem multiple sclerosis in an 11-year-old child presenting as acute disseminated encephalomyelitis.

Multiple sclerosis and acute disseminated encephalomyelitis are demyelinating disorders of the central nervous system that can present initially as an acute focal demyelinating syndrome. We report an 11-year-old girl who initially presented with intractable vomiting and hypertension and later developed a subacute onset of focal neurologic (brainstem) signs. Magnetic resonance imaging (MRI) demonstrated a large solitary demyelinating lesion of the brain stem consistent with acute disseminated encephalomyelitis. Because of the morbidity associated with biopsy and its questionable value in the course of management of this patient, she was treated empirically with aggressive supportive measures and high-dose corticosteriod therapy. She had near full recovery, with only minimal neurologic sequelae. Six months later, she presented with similar focal neurologic signs, and a new lesion was found on MRI. Because of the separation of her two episodes in time and central nervous system location, a diagnosis of multiple sclerosis was made. Herein, we used this patient to illustrate the difficulty in distinguishing acute disseminated encephalomyelitis from multiple sclerosis in patients who present initially with an acute focal demyelinating syndrome.

The aminosteroid U-73122 inhibits muscarinic receptor sequestration and phosphoinositide hydrolysis in SK-N-SH neuroblastoma cells. A role for Gp in receptor compartmentation.

The relationship between muscarinic receptor activation of phosphoinositide hydrolysis and the sequestration of cell surface muscarinic receptors has been examined for both intact and digitonin-permeabilized human SK-N-SH neuroblastoma cells. Addition of the aminosteroid 1-[6-[[17 beta-3-methoxyestra-1,3,5(10)-trien-17-yl]amino] hexyl]-1H-pyrrole-2,5-dione (U-73122) to intact cells resulted in the inhibition of oxotremorine-M-stimulated inositol phosphate release and of Ca2+ signaling by greater than 75%. In contrast, when phospholipase C was directly activated by the addition of the calcium ionophore ionomycin, inclusion of U-73122 had little inhibitory effect. Addition of U-73122 to intact cells also inhibited the agonist-induced sequestration of cell surface muscarinic receptors and their subsequent down-regulation with an IC50 value (4.1 microM) similar to that observed for inhibition of inositol phosphate release (3.7 microM). In contrast, when oxotremorine-M-stimulated phosphoinositide hydrolysis was inhibited by depletion of extracellular Ca2+, no reduction in the extent of receptor sequestration was observed. When introduced into digitonin-permeabilized cells, U-73122 more markedly inhibited inositol phosphate release elicited by either oxotremorine-M or guanosine-5'-O-(3-thiotriphosphate) than that induced by added Ca2+. Addition of oxotremorine-M to permeabilized cells resulted in muscarinic receptor sequestration and down-regulation. Both the loss of muscarinic acetylcholine receptors and activation of phosphoinositide hydrolysis in permeabilized cells were inhibited by the inclusion of guanosine-5'-O-(2-thiodiphosphate). The results indicate that the agonist-induced sequestration of muscarinic acetylcholine receptor in SK-N-SH cells requires the involvement of a GTP-binding protein but not the production of phosphoinositide-derived second messenger molecules.