• Maxillofacial Plastic and Reconstructive Surgery
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• 제16권3호
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• pp.515-520
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• 1994

Herpes Zoster is an acute viral infection characterized by the appearance of vesicles that occur on the skin and mucous membrane along the pathway of an involved sensory nerve. Although Herpes zoster is usually as benign viral infection, complications may occur especially when cranial nerves are involved. There are few reports of bony and dental complications by Herpes Zoster infection, all of which were isolated in a single quadrant. These include devitalized teeth, abnormal development of permanent teeth, internal resoption and spontaneous exfoliation of teeth with osteonecrosis of the alveolar bone. No agreement has been reached concerning the pathogenesis of osteonecrosis and tooth exfoliation associated with herpes zoster infection. We recently experienced series of maxillary osteonecrosis and spontaneous teeth exfoliation in patients with Herpes Zoster infection and present two cases with review of literature.

• Maxillofacial Plastic and Reconstructive Surgery
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• 제33권1호
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• pp.89-92
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• 2011

Herpes simplex is caused by viruses of the herpesvirus hominus family. HSV have four categories: type 1, 2, 6, and 8. Generally HSV-1 affects the mouth. Once infected by HSV, the person's infection is permanent. Retrograde transport through adjacent neural tissue to sensory ganglia leads to a lifelong latent infection. Recently, we treated a patient with recurrent herpes-stomatitis mimicking acute necrotizing ulcerative gingivitis (ANUG). The results were satisfactorty so we report this case. 31 years old male patient showed sore throat, gingival ulceration, palpable both submandibular lymph node, and sulcular pus formation around posterior decayed teeth. This is the third time he has suffered from this symptom. Tentative diagnosis was acute necrotizing ulcerative gingivitis. Antibiotic therapy was started. But, intraoral symptom got worse in process of time. Especially ulcer of marginal gingiva got worse. Viral disease was suspected. We carried out viral cultivation. At the same time topical application of antiviral ointment (herpecid$^{(R)}$) was performed on oral ulcer unilaterally for the purpose of diagnosis and reducing pain experimentally. The next day pain was decreased dramatically on application area. Basing on the viral cultivation and clinical effect of antiviral ointment (herpecid$^{(R)}$), we have diagnosed it as a recurrent herpes-stomatitis and concluded that viral infection was major cause of disease and bacterial infection was secondary.

• Maxillofacial Plastic and Reconstructive Surgery
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• 제31권2호
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• pp.167-172
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• 2009

The maxilla rarely undergoes necrosis due to its rich vascularity. Maxillary necrosis can occur due to bacterial infections such as osteomyelitis. viral infections such as herpes zoster and fungal infections such as mucormycosis, aspergillosis etc. Herpes zoster is a common viral infection, the oral soft tissue manifestations of which are widely known and recognized. Extremely rare complications such as osteonecrosis, and secondary osteomyelitis in maxilla were observed. But, reports of spontaneous tooth exfoliation and jaw osteonecrosis following herpes zoster infection in the distribution of the trigeminal nerve are extremely rare in the literature. We report a case of maxillary necrosis by herpes zoster in an uncontrolled diabetic patient. There was extensive necrosis of the buccal and palatal mucoperiosteum and exposure of the alveolar bone. This patient was successfully treated using a removal of necrotic bone and nasolabial flap. We briefly discuss different diseases which can lead to maxillary necrosis and a review. Analysis of the pathogenesis of herpes zoster and bone necrosis are discussed.

• IMMUNE NETWORK
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• 제14권4호
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• pp.187-200
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• 2014

Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are the most common cause of genital ulceration in humans worldwide. Typically, HSV-1 and 2 infections via mucosal route result in a lifelong latent infection after peripheral replication in mucosal tissues, thereby providing potential transmission to neighbor hosts in response to reactivation. To break the transmission cycle, immunoprophylactics and therapeutic strategies must be focused on prevention of infection or reduction of infectivity at mucosal sites. Currently, our understanding of the immune responses against mucosal infection of HSV remains intricate and involves a balance between innate signaling pathways and the adaptive immune responses. Numerous studies have demonstrated that HSV mucosal infection induces type I interferons (IFN) via recognition of Toll-like receptors (TLRs) and activates multiple immune cell populations, including NK cells, conventional dendritic cells (DCs), and plasmacytoid DCs. This innate immune response is required not only for the early control of viral replication at mucosal sites, but also for establishing adaptive immune responses against HSV antigens. Although the contribution of humoral immune response is controversial, $CD4^+$ Th1 T cells producing IFN-${\gamma}$ are believed to play an important role in eradicating virus from the hosts. In addition, the recent experimental successes of immunoprophylactic and therapeutic compounds that enhance resistance and/or reduce viral burden at mucosal sites have accumulated. This review focuses on attempts to modulate innate and adaptive immunity against HSV mucosal infection for the development of prophylactic and therapeutic strategies. Notably, cells involved in innate immune regulations appear to shape adaptive immune responses. Thus, we summarized the current evidence of various immune mediators in response to mucosal HSV infection, focusing on the importance of innate immune responses.

• 대한바이러스학회지
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• 제29권3호
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• pp.165-174
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• 1999

To investigate viral pathogenesis and in vivo efficacy of acyclovir (ACV) in mouse HSV-1 encephalitis models, female BALB/c mice aged 5 weeks were inoculated with strain F either intranasally (IN) or intracerebrally (IC). ACV-treatment by intraperitomeal injection with 0, 5, 10 and 25 mg/kg b.i.d. for 6 days was commenced 1 h after infection. Body weight and signs of clinical disease were noted daily up to 2 weeks. $ED_{50}$ of ACV in IN infection was <5 mg/kg and 14.1 mg/kg in IC infection. Tissues of central nervous system were collected from 2 mice per group everyday up to 5 day p.i. and the virus titers were measured. In IN infection model, high titers in eyes and trigeminal nerves were observed. ACV-treatment showed significant reduction of the titers in all the isolated. In IC infection model, cerebrum, cerebellum and brain stem showed high virus titers. ACV-treatment showed less significant reduction of virus titers than that in IN infection model. Reactivation of explanted trigeminal nerves from mice 30 day p.i. was monitored. In all of ACV treated mice reactivation was observed, i.e. even the highest dose of ACV did not inhibit the establishment of viral latency.

• Annals of Clinical Neurophysiology
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• 제3권2호
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• pp.164-167
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• 2001

The etiology of neuralgia amyotrophy remains unclear. Herpes zoster induced neuralgia amyotrophy has been reported in extremely rare cases. In this case report, we describe the clinical features and electrophysiologic findings in a 68-year-old patient with neuralgia amyotrophy associated with herpes zoster infection. We suggest that brachial plexus inflammation due to viral infection may be a direct cause of reversible neuralgia amyotrophy.

• BMB Reports
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• 제38권1호
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• pp.34-40
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• 2005

GLPG (Ganoderma lucidum proteoglycan) was a bioactive fraction obtained by the liquid fermentation of the mycelia of Ganoderma lucidum, EtOH precipitation, and DEAE-cellulose column chromatography. GLPG was a proteoglycan with a carbohydrate: protein ratio of 10.4: 1. Its antiviral activities against herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) were investigated using a cytopathic inhibition assay. GLPG inhibited cell death in a dose-dependent manner in HSV-infected cells. In addition, it had no cytotoxic effect even at 2 mg/ml. In order to study the mode of action of the antiviral activity of GLPG, cells were treated with GLPG before, during, and after infection, and viral titer in the supernatant of cell culture 48 h post-infection was determined using a $TCID_{50}$ assay. The antiviral effects of GLPG were more remarkable before viral treatment than after treatment. Although the precise mechanism has yet to be defined, our work suggests that GLPG inhibits viral replication by interfering with the early events of viral adsorption and entry into target cells. Thus, this proteoglycan appears to be a candidate anti-HSV agent.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• 제11권1호
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• pp.70-74
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• 2008

저자들은 건강했던 12세 남아가 발열, 연하통, 삼킴 곤란 증세를 호소하여 시행한 내시경 상 식도의 궤양과 수포성 병변이 보이고 헤르페스 I형 항체 양성반응으로 진단된 헤르페스 식도염을 항바이러스제와 proton pump inhibitor 등 보존적 치료로 치유시킨 1예를 경험하였기에 문헌고찰과 함께 보고하는 바이다.

• Biomolecules & Therapeutics
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• 제1권1호
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• pp.98-102
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• 1993

The therapeutic effectiveness of adenine arabinoside(tora-A) and its conjugate of prednisone(BR-8702-AP) was compared in Herpes simplex Virus Type 1 (HSV-1) infected BALB/C mice. The BALB/C mouse was infected with HSV-1(700 PFU/mouse) intranasally. Among mice infected intranasally with virus, a mortality rate of 100% was observed. On the oral administration of non-toxic doses of ara-A or BR-8702-AP(125 mg /kg/day) for 5 consecutive days 2 hours after virus infection, the tora-A was highly effective in reducing mortality to 0% (P<0.001) and BR-8702-AP was also effective in reducing mortality to 15% (P<0.01). In this model infection, the virus was first replicated in the lung and transmitted to the brain. Both arts-A and BR-8702-AP did not inhibit the viral replication in the lung, but they inhibited the viral transmission to the brain. However, the BR-8702-AP was less effective than the aria-A to prevent transmission of virus to brain. Therefore, the reduced mortality due to tora-A or BR-8702-AP therapy was associated with inhibition of viral transmission to brain.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제38권3호
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• pp.177-183
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• 2012

Herpes zoster is a viral infection caused by the reactivation of the varicella zoster virus, an infection most commonly affecting the thoracolumbar trunk. Herpes Zoster Infection (HZI) may affect the cranial nerves, most frequently the trigeminal. HZI of the trigeminal nerve distribution network manifests as multiple, painful vesicular eruptions of the skin and mucosa which are innervated by the infected nerves. Oral vesicles usually appear after the skin manifestations. The vesicles rupture and coalesce, leaving mucosal erosions without subsequent scarring in most cases. The worst complication of HZI is post-herpetic neuralgia; other complications include facial scarring, motor nerve palsy and optic neuropathy. Osteonecrosis with spontaneous exfoliation of the teeth is an uncommon complication associated with HZI of the trigeminal nerve. We report several cases of osteomyelitis appearing on the mandible, caused by HZI, and triggering osteonecrosis or spontaneous tooth exfoliation.