Auricular Skin Research Articles

Mechanisms of quinolone phototoxicity

We examined the mechanisms of quinolone phototoxicity in vivo and in vitro. Simultaneous p.o. administration of a quinolone and ultraviolet-A (UVA) irradiation for 4 h induced auricular skin inflammation in BALB/c mice, including edema and neutrophil infiltration in the dermis. Antioxidants inhibited the inflammation in the early stage and cyclooxygenase inhibitors did in both the early and later stages, whereas 5-lipoxygenase inhibitors or histamine antagonists had no effect. The phototoxic inflammation was also induced in mast cell-deficient WBB6F1-W/Wv mice. Corresponding to the in vivo results, incubation with a quinolone under UVA irradiation stimulated BALB/c 3T3 mouse fibroblast cells to release prostaglandin E2 (PGE2) and 6-keto-PGF1α, but not leukotriene B4. In contrast, UVA-pre-irradiated quinolones did not affect PG release from fibroblasts. The PGE2 release was inhibited by cyclooxygenase inhibitors, antioxidants, protein kinase C (PKC) inhibitors and a tyrosine kinase (TK) inhibitor, but not by antibodies against tumor necrosis factor α (TNFα) and interleukin-1 (IL-1). These results lead to a hypothesis that reactive oxygen species generated from quinolones under UVA irradiation trigger PG release from dermal fibroblasts via PKC and TK activation, resulting in skin inflammation and that 5-lipoxygenase products, histamine, TNFα or IL-1 is ruled out from the mechanism.

Total ear reconstruction in post burn deformity

Severe thermal injuries to the external ear, in most cases, lead to a total destruction of the pinna. Total ear reconstruction in such cases of burns is one of the most difficult problems faced by a plastic surgeon. This is because of the paucity and poor quality of the skin available in the auricular region. Depending upon the quality and quantity of skin available in the auricular region, patients with total loss of ear following burns were divided into five groups. The surgical procedure for ear reconstruction differed in each group due to differences in skin available for coverage of the cartilage framework. Different covering methods which were used for the draping of the cartilage framework were, normal post auricular skin, local grafted or scarred but soft and supple skin, post auricular fascia, temporoparietal fascia (pedicled or free) and free radial forearm fascial flap. A temporoparietal fascial flap was the cover of choice if local skin was not healthy. During the past eight years, seventy six cases of total ear reconstruction were done for post burn ear deformities. The technique and results are presented here.

Rapid diagnosis of varicella zoster virus infection in acute facial palsy.

Patients with zoster sine herpete and Ramsay Hunt syndrome without pathognomonic vesicles at the initial visit are often misdiagnosed with Bell's palsy and treated without antiviral agents. With PCR, we found that varicella zoster virus genomes were frequently detectable in auricular skin exudate from patients with zoster sine herpete or Ramsay Hunt syndrome before the appearance of vesicles.

Neuronal connections between the auricular skin and the sympathetic pre- and postganglionic neurons of the dog as studied by using pseudorabies virus

Pseudorabies virus (PrV) as a neuronal tracer was microinjected into the concave surface of the puppy's left pinna to establish the morphological basis of somato-visceral linkage. The virus infected neurons were detected by FITC conjugated with polyclonal swine anti-PrV serum. Labelled neurons were localized in: (1) the trigeminal, geniculate and superior vagal ganglia; (2) the subnucleus caudalis of the spinal trigeminal nucleus; (3) the intermediolateral column (IML) of the thoracolumbar segments and (4) the sympathetic chain ganglia. Present results suggest that when injected into the peripheral nerves, PrV was retrogradely transported to the nerve cell bodies located in the respective sensory ganglia. From the first order sensory neurons, the virus would self-replicate and was transported trans-synaptically via the brainstem nuclei and IML to reach the neurons in the sympathetic ganglia.

Effects of Mastoid Cavity Obliteration on the Growth of Experimentally Produced Residual Cholesteatoma

The effects of obliteration of the mastoid cavity on the growth of residual cholesteatoma were histologically studied in an animal model. A dermal cyst was produced by grafting a piece of autologous auricular skin in the otic bulla of 11 guinea-pigs. Three weeks after grafting, part of the cyst wall facing the cavity was removed and the debris accumulated inside was inserted into the surrounding granulation using a micropick. This procedure simulates the growth mechanism of cholesteatoma residue which sometimes occurs after middle ear surgery in human subjects. In six animals, the bulla was then obliterated with plaster of Paris. The remaining five animals were used as controls. Animals were killed for histological study at 2, 4 or 8 weeks postoperatively. Microscopic examinations revealed that in the obliteration group, severe inflammatory reactions were induced in the otic bulla, although the graft epithelium survived there; dermal cyst reformed in only one of six animals. In the controls, cyst reformation was recognized in all animals. This indicated that severe inflammation induced by plaster prevented growth of the graft epithelium in the otic bulla.

Perifollicular Transgenic Expression of Human Interleukin-1 Receptor Antagonist Protein following Topical Application of Novel Liposome-Plasmid DNA Formulations In Vivo

Expression plasmid DNA for the human interleukin-1 receptor antagonist (IL-1ra) protein was formulated with nonionic:cationic (NC) liposomes or phosphatidylcholine:cationic (PC) liposomes and applied to the auricular skin of hamsters in single- and multiple-dose protocols. Confocal microscopy identified delivery of plasmid DNA proximal to perifollicular cells, and successful transfection of perifollicular cells was identified by immunohistochemistry and ELISA. Skin treated for 3days with the NC liposomes had statistically significant levels of transgenic IL-1ra present for 5days post-treatment. Expression of transgenic IL-1ra was specific to areas of skin treated with NC liposomes but not PC liposomes. The results indicate that the NC liposomes can deliver expression plasmid DNA to perifollicular cells and mediate transient transfection in vivo.

術後喉頭機能を保存した甲状腺癌喉頭浸潤例

Papillary carcinoma of the thyroid gland rarely invades the larynx because of its low malignancy and slow progression. When it does invade the larynx, however, laryngeal function should be preserved if possible. We describe a case of a 74-year-old man with advanced papillary carcinoma of the thyroid gland. The papillary carcinoma of the thyroid gland severely invaded his larynx, trachea and esophagus. Accordingly, we performed a total thyroidectomy, left neck dissection, partial laryngectomy, and partial excision of the trachea. However, laryngeal function was successfully preserved by reconstruction of the larynx and trachea using a composite auricular cartilage and skin graft.

Effect of Antioxidants, Anti-inflammatory Drugs, and Histamine Antagonists on Sparfloxacin-Induced Phototoxicity in Mice

We examined the effects of antioxidants, anti-inflammatory drugs, and histamine antagonists on auricular inflammation and retinal degeneration induced by the phototoxicity of sparfloxacin (SPFX), a quinolone antibacterial agent. Catalase (CAT), dimethyl sulfoxide (DMSO), dexamethasone (DM), indomethacin (IM), phenidone (PD), AA-861 (AA), pyrilamine maleate (PY), or cimetidine (CM) was continuously administered to female Balb/c mice using microosmotic pumps for 72 hr and intraperitoneally once before SPFX administration. The mice were given a single oral administration of 50 or 100 mg/kg SPFX and irradiated with ultraviolet-A (UVA) light at 1.5 mW/cm2for 4 hr. SPFX administration plus UVA irradiation induced thickening and inflammation of the auricular skin and retinal degeneration in the eye. CAT and DMSO significantly inhibited the auricular thickening only 4 hr after SPFX administration. DM, IM, and PD also inhibited this toxicity from 4 to 48 or 72 hr. On the other hand, PY and CM showed no effect on this change. With regard to the eye, CAT and DMSO completely inhibited the occurrence of retinal degeneration and IM and PD tended to decrease its incidence, whereas DM, AA, PY, and CM showed no or an exacerbating effect. These results suggest that reactive oxygen species contribute to the initiation of auricular inflammation and retinal degeneration and that cyclooxygenase products are also involved in the initiation and later progression of auricular inflammation. They also show that histamine and 5-lipoxygenase products are not involved in either phototoxic lesion.

Transplante de cartilagem costal autóloga no reparo de desvio do pavilhão auricular de cães: estudo experimental

Neste experimento, 12 cães com idade entre 7 e 12 meses foram submetidos a técnica cirúrgica com objetivo de apresentar novo método para reparo de desvio lateral da orelha externa, mediante transplante autólogo de cartilagem costal. Verificou-se que as orelhas apresentaram postura ereta, movimentos aparentemente normais e ausência de desvio. Macroscopicamente o enxerto encontrava-se firmemente aderido a cartilagem auricular e a pele. Pela microscopia óptica observou-se em torno da cartilagem costal presença de tecido conjuntivo fibroso. A técnica cirúrgica avaliada poderá ser utilizada para correção de desvio lateral da orelha de cães.

Effect of Antioxidants, Anti-inflammatory Drugs, and Histamine Antagonists on Sparfloxacin-Induced Phototoxicity in Mice

We examined the effects of antioxidants, anti-inflammatory drugs, and histamine antagonists on auricular inflammation and retinal degeneration induced by the phototoxicity of sparfloxacin (SPFX), a quinolone antibacterial agent. Catalase (CAT), dimethyl sulfoxide (DMSO), dexamethasone (DM), indomethacin (IM), phenidone (PD), AA-861 (AA), pyrilamine maleate (PY), or cimetidine (CM) was continuously administered to female Balb/c mice using microosmotic pumps for 72 hr and intraperitoneally once before SPFX administration. The mice were given a single oral administration of 50 or 100 mg/kg SPFX and irradiated with ultraviolet-A (UVA) light at 1.5 mW/cm2 for 4 hr. SPFX administration plus UVA irradiation induced thickening and inflammation of the auricular skin and retinal degeneration in the eye. CAT and DMSO significantly inhibited the auricular thickening only 4 hr after SPFX administration. DM, IM, and PD also inhibited this toxicity from 4 to 48 or 72 hr. On the other hand, PY and CM showed no effect on this change. With regard to the eye, CAT and DMSO completely inhibited the occurrence of retinal degeneration and IM and PD tended to decrease its incidence, whereas DM, AA, PY, and CM showed no or an exacerbating effect. These results suggest that reactive oxygen species contribute to the initiation of auricular inflammation and retinal degeneration and that cyclooxygenase products are also involved in the initiation and later progression of auricular inflammation. They also show that histamine and 5-lipoxygenase products are not involved in either phototoxic lesion.

Evaluation of stellate ganglion block on auricular skin blood flow by laser-doppler flowmetry

Evaluation of stellate ganglion block on auricular skin blood flow by laser-doppler flowmetry

중이 진주종 및 만성중이염에서 랑게르한스 세포에 관한 면역조직화학적 연구

Middle ear cholesteatoma is biologically invasive keratinizing squamous epithelial cyst that contains the desquamated debris. And it is clinically important entity because it causes destruction of adjacent bones and serious complications. The pathogenesis and pathophysiology of cholesteatoma has been debated but there are basic theories of epithelial ingrowth and metaplasia of middle ear epithleium. Also there is concept that expanding process of desquamation causes bone destruction and that it may be due to proteolytic enzymes such as collagenase. Recent works suggest that Langerhans cells have an immunologic altering function and have a role of generating and maintaining the chronic inflammatory reacton which induces bone resorption. The morphologic feature of cholesteatoma was similar to that of the tympanic membrane but there was a increase of Langerhans cells in cholesteatoma. Langerhans cells are the bone marrow-derived immune cells of the epidermis. They express la antigens and receptors for the Fc portion of IgG and complement components. Langerhans cells appear to recognize antigen and present them to T-lymphocyte and possibly macrophage. The authors used immunohistochemical method to indentify and quantify distribution of Langerhans cells(S-100 protein), T-lymphocyte(HLA-DR, CD3) using monoclonal antibody techniques. We compared distribution of Langerhans cells in cholesteatoma matrix, infected tympanic membrane and adjacent canal skin of chrnic otitis media of which were taken from patients during operation. The obtained results were as follows : The Langerhans cells in cholesteatoma matrix increased significantly compared to those in chronic otitis media and post auricular skin. The Langerhans cells in chronic otitis media were more increased numbers than those in post auricular skin(p<0.05). The Langerhans cells and T lymphocytes with inflammatory reaction in subepithelial tissue of cholesteatoma were significantly higher than those chronic otitis media(p<0.05).

DIFFERENTIATION OF HISTOLOGICAL CHANGES INDUCED BY ULTRAVIOLET-A AND -B LIGHT IRRADIATION IN THE AURICULAR SKIN AND EYE OF ALBINO BALB/C MICE

We differentiated the histological changes induced by irradiation with ultraviolet-A (UVA) and -B (UVB) light in the auricular skin and eye in female Balb/c mice. The animals were irradiated (1.30mW/cm2) with UVA for 1, 3, or 7 days, or with UVB for 2, 4, or 8 hr or 1, 3, or 7 days. Irradiation with UVA and UVB induced inflammation in the auricular skin, but the early changes were different. UVA-irradiation caused neutrophil infiltration without apparent edema, while UVB-irradiation induced marked edema with degranulation of mast cells and enlargement of endothelial cells of blood vessels in the dermis. These lesions became more severe with time progression, with the auricle showing partial necrosis at the later stage. UVA-irradiation caused retinal degeneration with vesiculation of the photoreceptor outer segment as an early change. In contrast, UVB-irradiation initially induced degeneration of corneal cells, followed by degeneration of lens epithelial cells. Although the incidence of retinal changes induced by UVB-irradiation was much lower than that by UVA, the number of migrating cells in the photoreceptor segments with UVB significantly increased at the later stage.

Involvement of arachidonic acid-metabolites in auricular skin inflammation induced by quinolone phototoxicity in albino mice

Involvement of arachidonic acid-metabolites in auricular skin inflammation induced by quinolone phototoxicity in albino mice

The efficacy of orally applied terbinafine, itraconazole and fluconazole in models of experimental trichophytoses

The antimycotic efficacy of terbinafine, itraconazole and fluconazole was evaluated in guinea-pig trichophytoses (Trichophyton mentagrophytes, Trichophyton rubrum) by use of the hair root invasion test (HIT) and the auricular skin temperature test (STT). In the prophylactic HIT model using T. mentagrophytes as the infective agent, statistical evaluation of the ratios of protected/inoculated animals revealed ED50 values of 2.8 mg kg-1 for terbinafine, 10.7 mg kg-1 for itraconazole and 11.6 mg kg-1 for fluconazole. When T. rubrum was used in the same model the ED50 value of terbinafine was 7.3 mg kg-1 whereas only two of eight animals became protected by itraconazole and fluconazole at the highest dose of 16 mg kg-1. In the therapeutic HIT model carried out with T. mentagrophytes, the curative doses were increased for all test compounds, revealing an ED50 of 12.3 mg kg-1 for terbinafine and > 40 mg kg-1 for itraconazole and fluconazole. In the STT model, decline of temperature was quicker and more pronounced during therapy with terbinafine than during treatment with the triazole derivatives. Skin temperature was back to normal on day 8 (after seven treatments) with 20 mg kg-1 terbinafine, whereas a decline to, or almost to, physiological skin temperature was not observed until day 24 (5 days after the last treatment) in animals treated with 40 mg kg-1 itraconazole or fluconazole.

Phototoxic lesions induced by quinolone antibacterial agents in auricular skin and retina of albino mice.

The phototoxic effects of quinolone antimicrobial agents on mouse auricular skin and retina were examined histologically. Sparfloxacin at 50 or 100 mg/kg, which alone causes no histologic change, was orally administered to albino Balb/c mice, which were irradiated with ultraviolet A for 4 hr immediately after administration. In the auricle, degeneration of basal epidermal cells was sporadically observed at 2 hr (during the irradiation). Foci of slight edema with degenerated fibroblasts were seen in the dermis at 4 hr. Edema and neutrophil infiltration in the dermis became severe up to 96 hr. Initial changes in the retina were observed at 2 hr. Vacuolation of the photoreceptor segments (particularly the inner segment) was occasionally associated with swelling of retinal pigment epithelial cells. The segments became disorganized with time, and the outer nuclear layer showed reduced cellularity. The segments and layer were partially thinned and lost 96 hr later. Enoxacin at 400 and 800 mg/kg induced similar lesions to those of sparfloxacin. Levofloxacin caused similar lesions in the auricle but no change in the retina. The combination of oral administration of quinolone and ultraviolet A irradiation, which never caused apparent morphological changes alone, was shown to be able to induce phototoxic lesions in albino mice. Therefore, this method is thought to be useful to examine morphological changes caused by quinolone phototoxicity.

外耳皮膚移植による実験的中耳真珠腫に関する研究

The pathogenesis of middle ear cholesteatoma has been thought to be invasion of squamous epithelium originated from the external ear skin including the tympanic membrane. There is no evidence, however, that the external ear skin has more potential to form cholesteatoma than that of other sites. In this report experimental middle ear cholesteatoma of guinea pigs originated from the external ear skin was histologically compared with that originated from the auricular skin. Cholesteatoma as dermal cyst was seen in the middle ear of almost all animals (25/28 = 89.3%), using a free skin graft (3 x 3 mm), regardless of the skin taken from superior (group A) or inferior (group B) part of the external ear, or the auricle (group C) eight weeks after skin implantation. The activity of epithelium such as keratinization was evident in group C. There is, however, no obvious difference in surrounding granulation tissues among group A, B, and C. In a half of this series, cyst wall was broken and its contents (debris) mainly consisted of keratin were put on surrounding granulation tissues three weeks after skin implantation. Striking keratinized epithelium and subepithelial inflammations in relation to the amount of debris were observed at the eighth week. These findings suggest that the external ear skin does not have specific potential to form cholesteatoma and keratin plays some roles in growth of cholesteatoma.

Development of the Low Impedance Points in the Auricular Skin of Experimental Peritonitis Rats

Electrical impedance of the auricular skin was measured in experimental peritonitis rats. Constant voltage pulses (10ms, 4V) were applied to the skin, then the impedance was estimated. Low impedance points were gradually increased after the operation for 7-14 days then they returned to the control level. The pseudo-sweating responses accompanied by the development of peritonitis were also observed. Histological study could not find any sweat glands in the auricular skin. These results suggest that the activation of the sweat glands is not the major cause of the formation of the low impedance points. Other possibilities of these phenomena were discussed.

Facial nerve paresis as the presenting symptom of leukemia

Leukemic involvement of the temporal bone is not uncommon and may present in a variety of ways including auricular or external canal skin lesions, red or thick tympanic membrane, middle ear effusions, otitis media, hearing loss or mastoiditis. Symptomatic facial nerve involvement, on the other hand, is extremely unusual. We discuss a pediatric patient whose sudden onset facial nerve paresis was the presenting symptom that led to her diagnosis of leukemia. At the time of mastoidectomy, a granulocytic sarcoma or chloroma was noted to be overlying the VIIth nerve.

Surgical correction of temporomandibular joint ankylosis

The correction of temporomandibular joint ankylosis is frequently followed by re-ankylosis, occlusal disturbance and alteration of functional masticatory movements. A multitude of surgical procedures have been devised in an attempt to overcome the complication of re-ankylosis in particular, and to create a functioning pseudoarthrosis where distance between resected bone surfaces and/or interpositional autogenous, homologous or alloplastic material is relied upon to prevent re-ankylosis and facilitate functional joint activity. Success in preventing re-ankylosis is said also to depend on long-term patient compliance in undertaking frequent and usually painful mandibular movement exercises. Achieving a functioning joint often precludes the maintenance of the occlusion and depends on resection of large amounts of bone and the use of alloplastic implants. A surgical technique is presented whereby a minimal gap arthroplasty in the region of the obliterated temporomandibular joint is completed. This minimizes deviation of the mandible to the operated side with the formation of an anterior open bite. Separation of the resected bone surfaces is accomplished using a composite free auricular skin and cartilage graft in order to prevent re-ankylosis as efficaciously as possible, while allowing for the promotion of immediate postoperative mandibular function, continued growth and the construction of a joint similar in broad terms to the pre-existing joint. A two-stage correction of temporomandibular joint ankylosis and concomitant secondary maxillofacial deformity is recommended. The results in 13 patients (17 joints) with a follow-up range of 1.5 to 5.5 years show that in all but one instance (of fibrous re-ankylosis following postoperative joint infection), satisfactory postoperative mandibular function and mouth opening was achieved.