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Oral Ulcerations Magdy K Hamam1*, Hamad N www.symbiosisonline.org Symbiosis www.symbiosisonlinepublishing.com Review Article Journal of Dentistry, Oral Disorders & Therapy Open Access Oral Ulcerations Magdy K Hamam1*, Hamad N. Albagieh2, AL dosari AM3 1Professor & Head Division of Oral Medicine, 2Assistant Professor, Chairman, Department of Oral Medicine & Diagnostic Sciences 3Professorof Oral Medicine , Former Dean , College of Dentistry, King Saud University, Saudi Arabia Received: January 08, 2021; Accepted: January 23, 2021; Published: February 02, 2021 *Corresponding author: Magdy K Hamam, Professor & Head Division of Oral Medicine, E-mail: [email protected] Introduction The Oral cavity is a mirror of systemic conditions. • Recurrent Herpes labialis. Many diseases have a similar clinical appearance, so a dentist • Herpes zoster. attempting to diagnose an ulcerative or vesiculobullous disease • Herpangina. of the mouth needs a good experience. The oral mucosa is thin, causing vesicles and bullae to break rapidly into ulcers, and ulcers • Hand, foot & mouth disease. are easily traumatized from teeth and food, and they become •B-Sub- Pemphigus Epithelial vulgaris. Vesiculobullous Lesions lesions that have a characteristic appearance on the skin to have secondarily infected by the oral flora. These factors may cause Bullous Pemphigoid locations.a nonspecific A complete appearance system on the review oral mucosa. should Oralbe obtained manifestations a brief Benign mucous membrane Pemphigoid may precede or follow the appearance of findings at other history and rapid clinical examination and full investigations for ErosiveErythema Lichen Multiforme Planus each patient, including questions regarding the presence of skin, EpidermolysisBullosa eye, genital, and rectal lesions. As well as symptoms such as joint pains, muscle weakness, dyspnea, diplopia, and chest pains [1,2]. DermatitisRecurrent HerpetiformisHerpes Simplex Virus infection A- Primary Herpetic Gingivostomatitis infection diagnosisSo , the ,present Treatment review & new article trends will . include , Definitions , Classifications ,Clinical features , Pathogenesis, Diferetional B- Recurrent Herpes Simplex infection.It contains DNA acid nucleus. Oral ulcers may be classified to Primary or Secondary ulcers It can remain latent in host neural cells there by evading the host lesion :- for example :- 1- Primary Ulcers which are not preceded by vesiculo-bullous immune response a-Traumatic b- Infective : Bacterial & fungal infection • A-HSV1 ( above the waist ) c- Neoplastic • Oral & pharyngeal infection d- Systemic : GIT & blood disorders • Meningoencephalitis e- Aphthous • Dermatitis above waist . f- Behcet ‘syndrome • B- HSV2 ( under the waist ) h- Reiter ‘s syndrome • Genital infections 2- Secondary ulcers: which are preceded by vesiculo-bullous lesion .Vesicles may be either:- • Infection in new born A- Intraepithelial or sub-epithelial • Dermatitis below waist rus infection • Recurrent Herpes Simplex Virus infection • a- Primary Herpetic gingivstomatitis • Primary Herpetic gingivostomatitis. Symbiosis Group *Corresponding author email: [email protected] Oral Ulcerations Copyright: © 2021 Magdy K Hamam, et al. ---------------------------------------------------------------------------------- Laboratory diagnosis • Prodromal symptoms. ( before oral lesions ) 1, 2days→Fever, headache, malaise, nausea, vomiting →2-3 days→Lesions → 7-10 days →self-limiting • 1- cytology the onset disease. HSV may continue to be present in the saliva for up to month after • Fresh vesicle & stained by Giemsa,Wright’s • Or Papanicolaou’s stain So , it can contaminate with injury of dentist finger to presented herpes simplex virus type 1 infection from rubbing the eye with • Searching for multinucleated giant cells as Primary herpetic Whitlow on the finger of a dentist. Ocular • Ballooning degeneration of nucleus stomatitis a saliva-contaminated finger in a patient with primary herpetic •Treatment Fluorescent staining of cytology smear (sensitive). b- Recurrent Herpes Simplex Virus infection 1- Acyclovir infected cells. • RHS is not a re-infection but re-activation of • No effect on normal cells but inhibits DNA replication in HSV- state. • Virus that remain latent in nerve tissue in a non-replicating • It is effective in first 72 hours • RHS may be activated by: • New antiherpes drugs are now available :- allowing for effective treatment with fewer dose.. • Trauma ,fever, sunburn, immunosuppression, menstruation • Val acyclovir&Famciclovir→→ it increased bioavailability • The virus travels down the nerve trunk to infect epithelial cells •----------------------------------------------------------------------------------- Spreading from cell to cell cause a lesion •2- Analgesic Antibiotics & Topicalare of anasethia.no help in ( mildtreatment case ) of primary herpes infection. Predisposing factors 3- Corticosteroid is contraindicated • Fever, menstruation, ultraviolet emotional stress 4----------------------------------------------------------------------------------- Vaccine (in future; geno-therapy). • Prodromal Varicella – Zoster Virus infection • Tingling or burning • Formation of a cluster of small vesicles, each • It is a herpes virus. • Vesicle 1-3 mm in diameter with the size of the neurons present in sensory ganglia. • It causes primary & recurrent infection & remains latent in • Cluster ranging from 1-2 cm. • Vesicles rupture → ulcer • VZV is responsible for 2 major clinical infection :- • Site :- (recurrent intra oral herpes-, gingiva, palate alveolar • Of humans Chic hen Pox ( varicella )( Primary infection) ---------------------------------------------------------------------------------- ridge (kerat.mucosa) dorsal root ganglia of spinal nerves or extramedully ganglia of Diagnosis cranial• After nervesthe primary disease is healed ,VZV become latent in the Case history, clinical examination & special investigations 1- Cytology • Shingles ( Herpes Zoster ) Varicella – Zoster Virus infection ( secondary infection ) of one trigeminal nerve branch. 2-Isolation HSV isolation & neutralization (most positive of a virus method) in tissue culture. • Vesicle are unilateral & accompanied by pain along the course Skin lesions 3- Antibody Titters. base , healing by scar . infection by demonstrating at • Painful , unilateral , shallow , small , round with erythematous A convalescent serum can confirm the diagnosis of primary HSV • N.B. Child without prior contact with VZV canDevelop chicken Least a fourfold rise in anti-HSV antibody pox after contact with an individual with HZ . Citation: Magdy K Hamam, Hamad N. Albagieh, AL dosari AM (2021) Oral Ulcerations. J Dent Oral Disord Ther 9(1): 1- 5 DOI: http:// 2 of 5 dx.doi.org/10.15226/jdodt.2021.001123 Page Oral Ulcerations Copyright: © 2021 Magdy K Hamam, et al. Complications reactions -→ tissue destruction) the mucocutaneous lesions have healed • Post herpetic neuralgia ; pain remaining for over a month after • 2-Poor oral hygiene, faulty dental restorations. • 3- Smoking. • Healing :- within 3-4 weeks by scar formation cell- mediated immunity. • 4- Emotional stress. The risk increases after the age of 60 years due to the decline in • 5- Leukemia & Aplastic anemia (defect of neutrophils)6- ------------------------------------------------- neuralgia . Malnutrition & HIV infection . • Immunosuppression does not increase the risk of post herpetic 3. Secondary Tuberculosis ( T. B .) Treatment Etiology :-Mycobacterium tuberculosisinfection. Chronic, indurate ulcer, irregular, undermined edge • To prevent post herpetic neuralgia in elder patient. Thick mucus material in the base • Dissemination in immunocompromisedpatient. • Acyclovir and reduce acute pain but they do not reduce the incidence of Painless,------------------------------------------------ without lymphadenitis post• Antiherpes herpetic drugs neuralgia ( valacyclovir – famciclovir ) accelerate healing 4-Cyclic Neutropenia • Capsaicin( sub extracted from hot chili peppers) recorded insome cases. • Etiology A hereditary autosomal dominant trait has been •----------------------------------------------------------------------------------- Chemical or surgical neurolysis done in refractory cases. Ramsay Hunt syndrome and • Clinical features The disease is usually manifested in childhood, infection of geniculate ganglion. • Definition:- It is special-form of HZ affecting the facial nerve via • The reduction of neutrophils occurs regularly in a 21-day cycle. malaise, anorexia, • Patients,typically may complain of low-grade fever, headache, • HerpaticOticus :- small crops of vesicles ( tragus of ear , extra auditory canal , tympanic membrane ) disorders,. • arthralgias, cervical lymphadenopathy, gastrointestinal • Oral manifestations • Unilateral localized oral pain affecting the anterior two thirds • Oral lesions present as a painful ulcer of the tongue , soft palate followed by vesicular lesions → ulcers • covered by a whitish membrane and surrounded by an • Bell ‘s Palsy erythematoushalo .Localized gingivitis is also a common finding. blood • Loss of taste sensation • Laboratory tests Determination of neutrophils in the peripheral •Deafness Complications - permanent :- course paralysisis rapid resolution within 7-10 days (usually----------------------------------------------------------------------- two or three times per week for eight weeks). 5. Agranulocytosis • Treatment: 2. Acute Necrotizing Ulcerative Gingivitis(ANUG ) • Prednisone 60 mg daily reduced to nil over 10 d characterizedby a severe reduction of the
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