Viral infections of oral cavity - Dr. Abhishek SolankiAbhishek Solanki
This document discusses various viral infections including herpes simplex virus, varicella, herpes zoster, infectious mononucleosis, cytomegalovirus, enteroviruses, rubeola, rubella, mumps, and human immunodeficiency virus. It provides details on the causative viruses, clinical manifestations, histopathological features, diagnosis and treatment of each infection. Complications are also mentioned for some viruses. Classification systems for HIV infected patients based on CD4 count and clinical categories are summarized.
This document discusses various vesiculobullous and ulcerative lesions that can occur in the oral cavity. It begins by defining vesicles, bullae, erosions, and ulcers. It then examines the causes of acute multiple oral lesions which can include viral infections like herpes simplex virus or coxsackievirus. It also discusses recurrent lesions like recurrent aphthous stomatitis. Chronic multiple lesions may be caused by conditions like pemphigus. Single ulcer lesions can result from fungal infections. The document then examines specific conditions in more detail like herpes infections, lichen planus, and pemphigus. It provides information on diagnosis and treatment of these oral conditions.
Bacterial infections can cause diseases that manifest in the oral cavity. Some diseases like scarlet fever are caused by specific bacteria, while others can be caused by a broad group of microorganisms. Common bacterial infections discussed in the document include scarlet fever caused by Streptococcus pyogenes, diphtheria caused by Corynebacterium diphtheriae, and tuberculosis caused by Mycobacterium tuberculosis. These bacteria can cause lesions, ulcers, and pseudomembranes in the oral cavity. Diagnosis involves identifying the bacteria through cultures or identifying their characteristics through microscopic examination after staining.
Not only the lesions in the body helps us to know about syphilis but also a minute nodule or lesion helps us to discover the syphilis. He who knows syphilis knows the medicine well. Earlier you found the disease the treatment and the prognosis will be good. Discover syphilis through your body's gateway.
This document provides information on class II cavity preparation. It begins by defining dental caries and tooth preparation. It then classifies cavities, including class II cavities which involve the proximal surfaces of bicuspids and molars. The principles of cavity preparation are outlined, including initial cavity preparation to establish form and depth, and final preparation involving removal of infected dentin and pulp protection. Modifications for cavity preparation in primary teeth are also discussed.
This document classifies and describes various oral white lesions. It discusses hereditary lesions such as leukoedema and white sponge nevus. Reactive lesions including frictional keratosis and nicotine stomatitis are covered. Preneoplastic lesions like actinic cheilitis and idiopathic leukoplakia are summarized. Other white lesions such as geographic tongue and lichen planus are also described. Non-epithelial lesions including candidiasis and Fordyce's granules are briefly outlined. Definitions of histopathological features and guidelines for differential diagnosis are provided.
Glass ionomer cement is a tooth-colored dental restorative material introduced in 1972. It bonds chemically to tooth structure and releases fluoride for a long period. It sets via an acid-base reaction between glass powder and polyacrylic acid liquid. Glass ionomer cement has properties like adhesion to tooth structure, anticariogenic activity due to fluoride release, and biocompatibility. However, its strength and esthetics are inferior to dental composites. Modifications to glass ionomer cement include resin-modified and metal-modified varieties to improve strength. The sandwich technique combines the benefits of glass ionomer cement with those of composite resin.
Viral infections of oral cavity - Dr. Abhishek SolankiAbhishek Solanki
This document discusses various viral infections including herpes simplex virus, varicella, herpes zoster, infectious mononucleosis, cytomegalovirus, enteroviruses, rubeola, rubella, mumps, and human immunodeficiency virus. It provides details on the causative viruses, clinical manifestations, histopathological features, diagnosis and treatment of each infection. Complications are also mentioned for some viruses. Classification systems for HIV infected patients based on CD4 count and clinical categories are summarized.
This document discusses various vesiculobullous and ulcerative lesions that can occur in the oral cavity. It begins by defining vesicles, bullae, erosions, and ulcers. It then examines the causes of acute multiple oral lesions which can include viral infections like herpes simplex virus or coxsackievirus. It also discusses recurrent lesions like recurrent aphthous stomatitis. Chronic multiple lesions may be caused by conditions like pemphigus. Single ulcer lesions can result from fungal infections. The document then examines specific conditions in more detail like herpes infections, lichen planus, and pemphigus. It provides information on diagnosis and treatment of these oral conditions.
Bacterial infections can cause diseases that manifest in the oral cavity. Some diseases like scarlet fever are caused by specific bacteria, while others can be caused by a broad group of microorganisms. Common bacterial infections discussed in the document include scarlet fever caused by Streptococcus pyogenes, diphtheria caused by Corynebacterium diphtheriae, and tuberculosis caused by Mycobacterium tuberculosis. These bacteria can cause lesions, ulcers, and pseudomembranes in the oral cavity. Diagnosis involves identifying the bacteria through cultures or identifying their characteristics through microscopic examination after staining.
Not only the lesions in the body helps us to know about syphilis but also a minute nodule or lesion helps us to discover the syphilis. He who knows syphilis knows the medicine well. Earlier you found the disease the treatment and the prognosis will be good. Discover syphilis through your body's gateway.
This document provides information on class II cavity preparation. It begins by defining dental caries and tooth preparation. It then classifies cavities, including class II cavities which involve the proximal surfaces of bicuspids and molars. The principles of cavity preparation are outlined, including initial cavity preparation to establish form and depth, and final preparation involving removal of infected dentin and pulp protection. Modifications for cavity preparation in primary teeth are also discussed.
This document classifies and describes various oral white lesions. It discusses hereditary lesions such as leukoedema and white sponge nevus. Reactive lesions including frictional keratosis and nicotine stomatitis are covered. Preneoplastic lesions like actinic cheilitis and idiopathic leukoplakia are summarized. Other white lesions such as geographic tongue and lichen planus are also described. Non-epithelial lesions including candidiasis and Fordyce's granules are briefly outlined. Definitions of histopathological features and guidelines for differential diagnosis are provided.
Glass ionomer cement is a tooth-colored dental restorative material introduced in 1972. It bonds chemically to tooth structure and releases fluoride for a long period. It sets via an acid-base reaction between glass powder and polyacrylic acid liquid. Glass ionomer cement has properties like adhesion to tooth structure, anticariogenic activity due to fluoride release, and biocompatibility. However, its strength and esthetics are inferior to dental composites. Modifications to glass ionomer cement include resin-modified and metal-modified varieties to improve strength. The sandwich technique combines the benefits of glass ionomer cement with those of composite resin.
White lesions of the oral mucosa can have many causes, including conditions like leukoplakia, lichen planus, lichenoid reactions, and hairy leukoplakia. These lesions are evaluated based on their medical history, clinical features, and potentially laboratory tests to determine the appropriate diagnosis and treatment. Common white lesions involve changes in the keratinization of the oral epithelium resulting in white patches or plaques in the mouth.
This document discusses red and white lesions of the oral cavity, focusing on oral candidiasis. It describes the various types of oral candidiasis including pseudomembranous, erythematous, chronic plaque-type, and median rhomboid glossitis. Predisposing factors, clinical findings, diagnosis, treatment with antifungal medications or surgery, and prognosis are summarized for each type. Chronic hyperplastic candidiasis may require long-term antifungal therapy or surgery due to risk of recurrence. Overall prognosis is generally good if predisposing factors can be addressed.
This document provides an overview of several common bacterial infections that can affect the oral cavity. It discusses tuberculosis, which is caused by Mycobacterium tuberculosis and can spread through airborne droplets to the lungs. If the oral cavity is involved, it typically presents as indurated chronic ulcers. Syphilis is caused by Treponema pallidum and has primary, secondary, and tertiary stages marked by chancres, rashes, and potential neurological/cardiovascular effects. Actinomycosis is caused by Actinomyces israelii and usually appears in the jaw after trauma or infection, causing hard swellings that may drain through the gums. Gonorrhea, caused by Ne
The document discusses direct gold restorations, including different types of direct filling golds such as gold foil, electrolytically precipitated gold, and powdered gold. It covers the properties, advantages, and disadvantages of direct gold, as well as indications and contraindications for its use. Guidelines are provided on cavity preparation and the general steps for placing direct gold restorations.
This document discusses the clinical features of gingivitis. It begins by defining gingivitis as inflammation of the gingiva and describes how plaque bacteria can damage gingival tissues. It then covers the different types of gingivitis based on duration and distribution. Key signs of gingivitis that are discussed include gingival bleeding, color changes, changes in consistency, size, surface texture, position and contour. Specific conditions like gingival recession are also explained in terms of definition, classification, etiology and clinical significance.
Clinical features and histopathology of dental cariesSAGAR HIWALE
This document provides an overview of the classification of dental caries based on various factors such as anatomical site, progression, extent of involvement, number of tooth surfaces affected, chronology, and whether caries was fully removed during treatment. It discusses 12 different classification systems for dental caries and provides details on types of caries such as pit and fissure, smooth surface, root surface, incipient, occult, and others based on these classification criteria. The document also covers the histopathology of caries in enamel and dentin.
The presentation explain white lesions in oral cavity and the classification the demonstrate the etiology, histopathology, diagnosis and treatment for each one.
Dental sequalae of pulpitis and management of apical lesionsVikram Perakath
The document discusses the dental sequelae of pulpitis, including defensive, bone, soft tissue, and blood reactions. It describes the acute and chronic pathways of pulpitis and various conditions that may arise such as periapical abscesses, osteomyelitis, cellulitis, periapical granulomas, and periapical cysts. Methods for managing apical lesions include nonsurgical approaches like root canal treatment and surgical treatment when nonsurgical methods are unsuccessful. Factors to consider in treatment planning include the diagnosis, proximity to other teeth, patient cooperation, and obstructions within the root canal.
This document discusses methods for plaque control and oral hygiene instruction. It describes techniques for mechanical plaque removal including toothbrushing and flossing, as well as chemical plaque control using mouthwashes. Toothbrushing techniques like the Bass and Stillman methods are outlined. The goals of polishing teeth are discussed along with contraindications. Recommendations are provided for motivating and educating patients on proper plaque control methods.
Gingival crevicular fluid (GCF) is a serum transudate that forms in the gingival sulcus. It contains cells, bacteria, serum components, and host mediators that make it useful for periodontal monitoring and diagnosis. GCF forms through increased permeability of blood vessels in the sulcus or through an osmotic gradient. Its composition varies in health and disease, making biomarkers of host enzymes, tissue breakdown products, and inflammatory mediators clinically significant. While non-invasive collection methods exist, contamination and variable recovery pose challenges. Further research on GCF components may aid in diagnosis and monitoring of periodontal disease progression and treatment outcomes.
The document discusses the classification and features of periodontal disease. It covers topics such as marginal periodontitis, juvenile periodontitis, trauma from occlusion, and periodontal atrophy. It also describes the periodontal pocket in detail, including its pathogenesis, morphology, contents, and relationship to bone loss. The extension of inflammation from the gingiva to the supporting periodontal tissues is discussed as well.
True generalized microdontia involves all teeth being smaller than normal and is seen in cases of pituitary dwarfism. Macrodontia refers to teeth being larger than normal. Geminated teeth arise from an attempt at division of a single tooth germ. Taurodontism is the enlargement of the tooth body and pulp chamber with displacement of the pulpal floor. Amelogenesis imperfecta represents hereditary defects of enamel formation. Dentinogenesis imperfecta affects dentin formation resulting in teeth that are gray to yellowish-brown.
Certain dyes called disclosing agents can be used to temporarily stain dental plaque and make it visible. The most common disclosing agents are erythrosin, which stains plaque red but can also stain soft tissues, and fluorescein dye, which stains plaque yellow without staining tissues but requires special lighting to see. Two-tone dyes stain mature plaque blue and new plaque red. Iodine-containing solutions were also used but are not preferred due to potential allergic reactions and unpleasant taste. Disclosing agents can be applied using a cotton swab or by rinsing the mouth.
This document provides information on oral submucous fibrosis (OSMF), including its definition, epidemiology, etiology, clinical features, histopathological classification, and management. OSMF is a precancerous condition characterized by fibrosis of the submucosa and juxta-epithelial inflammatory reaction. It predominantly affects people of Asian descent and is strongly associated with chewing areca nut and consumption of chili peppers. Clinically, it presents as blanching and stiffness of the oral mucosa leading to restricted mouth opening. Histopathological examination can classify the severity of fibrosis. Arecoline in areca nut is the main etiological agent that causes fibrosis through oxidative stress and increased collagen production.
The document discusses the classification of odontogenic cysts. It describes several classification systems proposed over time, including Robinson's classification from 1945, Thoma-Robinson-Bernier classification from 1960, Pindborg and Kramer's classification from 1971, and the WHO classification from 1971 and its update in 1992. The WHO classifications categorize cysts as developmental or inflammatory, and further divide developmental cysts into odontogenic and non-odontogenic types. Shafer's classification also categorizes cysts based on etiology as developmental or inflammatory, and further divides them based on the tissue of origin.
This document provides an overview of gingival enlargement (gingival overgrowth). It begins with definitions and classifications including by etiology, location/distribution, and degree. The main types discussed are inflammatory (chronic, acute), drug-induced, idiopathic, and those associated with systemic diseases. Neoplastic and false enlargements are also covered. Clinical features and treatments are described for various types. Treatment involves scaling, root planing, gingivoplasty and gingivectomy which can be performed conventionally, with electrosurgery, lasers, or chemosurgery.
The defense mechanism of gingiva includes GCF, Saliva, epithelial barrier and connective tissue cells. All these protect the periodontium from bacterial invasion.
This document provides an overview of oral pigmentation and pigmented lesions. It begins by defining pigment and describing normal oral mucosal color. Melanin is identified as the primary pigment producing brown coloration in the body. Factors that can affect melanogenesis are discussed such as sun exposure, drugs, hormones and genetic constitution. The document then classifies pigmentation into endogenous (originating from within the body such as melanin pigmentation) and exogenous (from external sources). Specific endogenous and exogenous pigmented lesions are described. The document concludes by discussing malignant melanoma, describing its clinical presentation and treatment which primarily involves wide local excision surgery.
This document discusses common white lesions of the oral cavity that can be seen during examination. It describes several conditions that present as white or pale lesions including leukoedema, white sponge nevus, frictional keratosis, morsicatio mucosae oris, smokeless tobacco keratosis, nicotine stomatitis, leukoplakia, hairy leukoplakia, candidiasis, oral submucous fibrosis, oral lichen planus, and chemical injuries of the oral mucosa. Differential diagnoses and clinical features of each condition are provided.
El banjo se desarrolló en Estados Unidos en el siglo XIX, donde los músicos negros explotaron su potencial rítmico. A finales del siglo XIX, el banjo se convirtió en parte integral de la música dixieland y pronto se estableció como el instrumento principal de la música tradicional estadounidense. Originalmente, el banjo tenía la parte posterior abierta, pero en el siglo XX se añadió un resonador de madera para cerrarlo.
White lesions of the oral mucosa can have many causes, including conditions like leukoplakia, lichen planus, lichenoid reactions, and hairy leukoplakia. These lesions are evaluated based on their medical history, clinical features, and potentially laboratory tests to determine the appropriate diagnosis and treatment. Common white lesions involve changes in the keratinization of the oral epithelium resulting in white patches or plaques in the mouth.
This document discusses red and white lesions of the oral cavity, focusing on oral candidiasis. It describes the various types of oral candidiasis including pseudomembranous, erythematous, chronic plaque-type, and median rhomboid glossitis. Predisposing factors, clinical findings, diagnosis, treatment with antifungal medications or surgery, and prognosis are summarized for each type. Chronic hyperplastic candidiasis may require long-term antifungal therapy or surgery due to risk of recurrence. Overall prognosis is generally good if predisposing factors can be addressed.
This document provides an overview of several common bacterial infections that can affect the oral cavity. It discusses tuberculosis, which is caused by Mycobacterium tuberculosis and can spread through airborne droplets to the lungs. If the oral cavity is involved, it typically presents as indurated chronic ulcers. Syphilis is caused by Treponema pallidum and has primary, secondary, and tertiary stages marked by chancres, rashes, and potential neurological/cardiovascular effects. Actinomycosis is caused by Actinomyces israelii and usually appears in the jaw after trauma or infection, causing hard swellings that may drain through the gums. Gonorrhea, caused by Ne
The document discusses direct gold restorations, including different types of direct filling golds such as gold foil, electrolytically precipitated gold, and powdered gold. It covers the properties, advantages, and disadvantages of direct gold, as well as indications and contraindications for its use. Guidelines are provided on cavity preparation and the general steps for placing direct gold restorations.
This document discusses the clinical features of gingivitis. It begins by defining gingivitis as inflammation of the gingiva and describes how plaque bacteria can damage gingival tissues. It then covers the different types of gingivitis based on duration and distribution. Key signs of gingivitis that are discussed include gingival bleeding, color changes, changes in consistency, size, surface texture, position and contour. Specific conditions like gingival recession are also explained in terms of definition, classification, etiology and clinical significance.
Clinical features and histopathology of dental cariesSAGAR HIWALE
This document provides an overview of the classification of dental caries based on various factors such as anatomical site, progression, extent of involvement, number of tooth surfaces affected, chronology, and whether caries was fully removed during treatment. It discusses 12 different classification systems for dental caries and provides details on types of caries such as pit and fissure, smooth surface, root surface, incipient, occult, and others based on these classification criteria. The document also covers the histopathology of caries in enamel and dentin.
The presentation explain white lesions in oral cavity and the classification the demonstrate the etiology, histopathology, diagnosis and treatment for each one.
Dental sequalae of pulpitis and management of apical lesionsVikram Perakath
The document discusses the dental sequelae of pulpitis, including defensive, bone, soft tissue, and blood reactions. It describes the acute and chronic pathways of pulpitis and various conditions that may arise such as periapical abscesses, osteomyelitis, cellulitis, periapical granulomas, and periapical cysts. Methods for managing apical lesions include nonsurgical approaches like root canal treatment and surgical treatment when nonsurgical methods are unsuccessful. Factors to consider in treatment planning include the diagnosis, proximity to other teeth, patient cooperation, and obstructions within the root canal.
This document discusses methods for plaque control and oral hygiene instruction. It describes techniques for mechanical plaque removal including toothbrushing and flossing, as well as chemical plaque control using mouthwashes. Toothbrushing techniques like the Bass and Stillman methods are outlined. The goals of polishing teeth are discussed along with contraindications. Recommendations are provided for motivating and educating patients on proper plaque control methods.
Gingival crevicular fluid (GCF) is a serum transudate that forms in the gingival sulcus. It contains cells, bacteria, serum components, and host mediators that make it useful for periodontal monitoring and diagnosis. GCF forms through increased permeability of blood vessels in the sulcus or through an osmotic gradient. Its composition varies in health and disease, making biomarkers of host enzymes, tissue breakdown products, and inflammatory mediators clinically significant. While non-invasive collection methods exist, contamination and variable recovery pose challenges. Further research on GCF components may aid in diagnosis and monitoring of periodontal disease progression and treatment outcomes.
The document discusses the classification and features of periodontal disease. It covers topics such as marginal periodontitis, juvenile periodontitis, trauma from occlusion, and periodontal atrophy. It also describes the periodontal pocket in detail, including its pathogenesis, morphology, contents, and relationship to bone loss. The extension of inflammation from the gingiva to the supporting periodontal tissues is discussed as well.
True generalized microdontia involves all teeth being smaller than normal and is seen in cases of pituitary dwarfism. Macrodontia refers to teeth being larger than normal. Geminated teeth arise from an attempt at division of a single tooth germ. Taurodontism is the enlargement of the tooth body and pulp chamber with displacement of the pulpal floor. Amelogenesis imperfecta represents hereditary defects of enamel formation. Dentinogenesis imperfecta affects dentin formation resulting in teeth that are gray to yellowish-brown.
Certain dyes called disclosing agents can be used to temporarily stain dental plaque and make it visible. The most common disclosing agents are erythrosin, which stains plaque red but can also stain soft tissues, and fluorescein dye, which stains plaque yellow without staining tissues but requires special lighting to see. Two-tone dyes stain mature plaque blue and new plaque red. Iodine-containing solutions were also used but are not preferred due to potential allergic reactions and unpleasant taste. Disclosing agents can be applied using a cotton swab or by rinsing the mouth.
This document provides information on oral submucous fibrosis (OSMF), including its definition, epidemiology, etiology, clinical features, histopathological classification, and management. OSMF is a precancerous condition characterized by fibrosis of the submucosa and juxta-epithelial inflammatory reaction. It predominantly affects people of Asian descent and is strongly associated with chewing areca nut and consumption of chili peppers. Clinically, it presents as blanching and stiffness of the oral mucosa leading to restricted mouth opening. Histopathological examination can classify the severity of fibrosis. Arecoline in areca nut is the main etiological agent that causes fibrosis through oxidative stress and increased collagen production.
The document discusses the classification of odontogenic cysts. It describes several classification systems proposed over time, including Robinson's classification from 1945, Thoma-Robinson-Bernier classification from 1960, Pindborg and Kramer's classification from 1971, and the WHO classification from 1971 and its update in 1992. The WHO classifications categorize cysts as developmental or inflammatory, and further divide developmental cysts into odontogenic and non-odontogenic types. Shafer's classification also categorizes cysts based on etiology as developmental or inflammatory, and further divides them based on the tissue of origin.
This document provides an overview of gingival enlargement (gingival overgrowth). It begins with definitions and classifications including by etiology, location/distribution, and degree. The main types discussed are inflammatory (chronic, acute), drug-induced, idiopathic, and those associated with systemic diseases. Neoplastic and false enlargements are also covered. Clinical features and treatments are described for various types. Treatment involves scaling, root planing, gingivoplasty and gingivectomy which can be performed conventionally, with electrosurgery, lasers, or chemosurgery.
The defense mechanism of gingiva includes GCF, Saliva, epithelial barrier and connective tissue cells. All these protect the periodontium from bacterial invasion.
This document provides an overview of oral pigmentation and pigmented lesions. It begins by defining pigment and describing normal oral mucosal color. Melanin is identified as the primary pigment producing brown coloration in the body. Factors that can affect melanogenesis are discussed such as sun exposure, drugs, hormones and genetic constitution. The document then classifies pigmentation into endogenous (originating from within the body such as melanin pigmentation) and exogenous (from external sources). Specific endogenous and exogenous pigmented lesions are described. The document concludes by discussing malignant melanoma, describing its clinical presentation and treatment which primarily involves wide local excision surgery.
This document discusses common white lesions of the oral cavity that can be seen during examination. It describes several conditions that present as white or pale lesions including leukoedema, white sponge nevus, frictional keratosis, morsicatio mucosae oris, smokeless tobacco keratosis, nicotine stomatitis, leukoplakia, hairy leukoplakia, candidiasis, oral submucous fibrosis, oral lichen planus, and chemical injuries of the oral mucosa. Differential diagnoses and clinical features of each condition are provided.
El banjo se desarrolló en Estados Unidos en el siglo XIX, donde los músicos negros explotaron su potencial rítmico. A finales del siglo XIX, el banjo se convirtió en parte integral de la música dixieland y pronto se estableció como el instrumento principal de la música tradicional estadounidense. Originalmente, el banjo tenía la parte posterior abierta, pero en el siglo XX se añadió un resonador de madera para cerrarlo.
Este documento describe las características y amenidades de un fraccionamiento residencial llamado Lomas de la Rioja. Ofrece lotes urbanizados con rápidas vías de acceso, áreas comerciales con vigilancia las 24 horas, áreas verdes y una asociación de vecinos. Además, menciona servicios subterráneos, una plaza cercana, supermercado, universidad, colegios, playas y campos de golf a solo 5 minutos. También ofrece pagos diferidos de hasta 7 años para comprar un lote en el fraccionamiento.
Prezentare susținută în cadrul cursului de API-FITO-TERAPIE realizat de către Societatea Română de Apiterapie - 18 iunie 2016.
Drepturile aparțin autorului: Andreea - Liana Buzea
Informațiile și studiile de caz din prezenteare nu reprezintă diagnostic medical, respectiv recomandări de tratament. Orice tratament natural se realizează doar sub îndrumare de specialitate, pe baza unor analize personale și particularitățile fiecărui caz, fiecărei afecțiuni și fiecărei persoane în parte.
Andrew Goodwin analyzed the key features of music videos in his book "Dancing in the Distraction Factory". He identified 6 common features of music videos, including demonstrating genre characteristics, relating visuals to lyrics and music, and including references to looking and the female body. Goodwin also described 5 ways to analyze a music video, such as examining the structure and voice of the song, the narrative and star performance, and how the visuals relate to and illustrate, amplify, or create disjuncture with the song.
Askozia Desktop Telephony Server - flyer 2015, EnglishAskozia
Askozia's Desktop Telephony Server for small and medium-sized businesses, with low energy consumption, passively cooled, and without proprietary lock-in, per-user nor per-channel fees.
This document discusses special methods for teaching individuals with visual impairments. It begins by defining visual impairment and classifying types, including totally blind, low vision, and classifications based on age of onset such as congenitally blind. Various eye conditions that cause visual impairments are described, along with characteristics of visually impaired children. Common tests used to measure visual acuity are explained. Different program models for educating visually impaired students are outlined, and special equipment and materials like Braille writers and tactile aids are covered. The roles of professionals who provide support services are defined. Finally, key special teaching methods are emphasized, such as individualization, use of concrete objects, multisensory instruction, additional stimulation, and self-activity
Las 3 oraciones son:
1) Una variable estadística es cada una de las características o cualidades que poseen los individuos de una población. 2) Existen variables cualitativas y cuantitativas, donde las cualitativas no se pueden medir numéricamente y las cuantitativas sí. 3) Una muestra es una parte representativa de una población total seleccionada científicamente para realizar un estudio estadístico.
PCOS is a common hormonal disorder characterized by oligomenorrhea and hyperandrogenism. It can cause long term health risks like diabetes, cardiovascular disease, and endometrial cancer. Management involves lifestyle changes like weight loss through diet and exercise to improve symptoms. Medications may be used to treat irregular periods, hirsutism, and help with ovulation induction and fertility. Screening for metabolic complications is recommended due to increased risk.
BACTERIAL INFECTCTIONS OF ORAL CAVITY i /certified fixed orthodontic courses ...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
This document discusses bacterial infections of the oral cavity, summarizing the etiology, clinical features, and histopathological features of tetanus, syphilis, gonorrhea, and rhinoscleroma in 3 sentences or less for each. It provides an overview of how tetanus is caused by Clostridium tetani and presents as muscle spasms. It describes how syphilis is caused by Treponema pallidum and presents in three stages: primary, secondary, and tertiary lesions. It notes gonorrhea affects the genitourinary tract and can cause oral ulcerations. Finally, it states rhinoscleroma is caused by Klebsiella rhinoscleromatis and
Este documento describe las propiedades de Bacillus anthracis, el microorganismo que causa el ántrax. B. anthracis es un bacilo gram positivo que a menudo se encuentra en cadenas. Su capsula antifagocítica contiene D-glutamato. No es móvil. Las esporas persisten en el suelo y la infección humana ocurre por contacto con animales infectados o sus productos. La bacteria produce una toxina compuesta de tres componentes que causan la enfermedad.
Bacteria can spread through airborne droplets from coughing or sneezing, contact with contaminated surfaces or fluids, or interaction with other living beings. They are classified based on microscopic appearance and staining properties. Risk factors for bacterial infections include medical history, treatments, lifestyle, occupation, and travel history.
This document provides information on desquamative gingivitis, including its historical background, classification, clinical features, etiology, histopathology, treatment, and differential diagnosis. Desquamative gingivitis is characterized by chronic redness and desquamation of the gingiva and can be associated with various underlying conditions. It is classified based on etiology and may involve areas beyond the gingiva. Treatment focuses on managing the underlying cause, improving oral hygiene, and using topical or systemic corticosteroids. Differential diagnosis includes lichen planus, pemphigoid, and pemphigus, which can be distinguished through histological examination.
This document discusses acute gingival infections, including primary herpetic gingivostomatitis, necrotizing ulcerative gingivitis (NUG), and pericoronitis. NUG is characterized by necrosis and sloughing of gingival tissues due to an impaired host response allowing pathogenic bacteria to invade. Clinically, it presents with crater-like gingival ulcers, pseudomembranes, pain, and systemic symptoms. The etiology involves both specific bacteria like fusospirochetal complexes and an underlying host immunosuppression. Treatment focuses on improving nutrition, antibiotics, and palliative care. Differential diagnosis includes herpes, desquamative gingivitis,
Allergic and Immunologic Diseases of the Oral Cavity.pptxDr.Shubham Patel
The document outlines several allergic and immunologic diseases that can affect the oral cavity. It discusses recurrent aphthous stomatitis, its classification and clinical features. It also covers Behcet's disease, Reiter's syndrome, sarcoidosis, Wegener's granulomatosis and other conditions like contact stomatitis, perioral dermatitis, latex allergy and lichenoid reactions that can impact the oral mucosa. For each condition, it provides details on etiology, clinical presentation and histopathological findings.
Necrotizing ulcerative gingivitis (NUG) is an acute, painful infection of the gums caused by an interaction between plaque bacteria like fusiform bacillus and spirochetes and the host immune response. It is characterized by necrosis and sloughing of gum tissue, presenting as punched-out ulcerations covered by a pseudomembrane. Diagnosis is based on clinical findings of painful ulcers with pseudomembrane, fetid odor, and potentially fever and lymphadenopathy. Treatment focuses on mechanical plaque removal and antibiotics to eliminate pathogenic bacteria.
This document outlines diseases of the oral cavity and upper airways. It begins with an outline of topics including diseases of the teeth/supporting structures, inflammatory/reactive lesions of the oral cavity, infections, oral manifestations of systemic diseases, precancerous and cancerous lesions, and odontogenic cysts and tumors. It then provides more detailed descriptions of several common conditions including dental caries, gingivitis, periodontitis, aphthous ulcers, irritation fibroma, pyogenic granuloma, peripheral ossifying fibroma, herpes simplex virus, oral candidiasis, hairy leukoplakia, leukoplakia/erythroplakia, squamous cell carcinoma
This document summarizes common lesions of the oral cavity, including ulcers caused by infections (viral like herpes, bacterial like Vincent's infection, fungal like candidiasis), immune disorders (aphthous ulcers, Behcet's syndrome), trauma, skin disorders (lichen planus, pemphigus vulgaris), and submucous fibrosis caused by chewing areca nut. It describes the etiology, clinical features, and management of each condition. Major types of oral ulcers and lesions are infections, immune disorders, trauma, neoplasms, and skin disorders that may manifest in the oral cavity.
Rhinosinusitis is inflammation of the nose and paranasal sinuses that is classified as acute or chronic based on duration of symptoms. Acute rhinosinusitis lasts less than 12 weeks and is usually viral in origin, while chronic rhinosinusitis lasts over 12 weeks with ongoing symptoms. Chronic rhinosinusitis can be further classified based on the presence of nasal polyps and type of inflammation present. Type 2 inflammation involving cytokines IL-4, IL-5 and IL-13 is associated with treatment failure, asthma, and higher rates of polyp formation. The sinus mucosa acts as an immune barrier, and type 2 inflammation can cause barrier weakness and failure, predisposing to recurrence of rhinosinusitis
This document summarizes and provides details on three acute gingival infections: necrotizing ulcerative gingivitis (NUG), primary herpetic gingivostomatitis, and pericoronitis. NUG is characterized by ulcerations of the gums that can progress to bone loss if left untreated. It is caused by bacterial infection and often occurs during times of stress or illness that weaken the immune system. Primary herpetic gingivostomatitis is a viral infection of the mouth caused by the herpes simplex virus, appearing as sores and blisters on the gums and mouth in children. Pericoronitis refers to inflammation under an impacted wisdom tooth, which can
The document summarizes various oral mucosal diseases and lesions. It discusses lichen planus, describing its prevalence, clinical presentations, associations with systemic diseases, and potential malignant transformation. It also briefly outlines the management of lichen planus, noting debates around treating asymptomatic lesions to potentially prevent malignant conversion.
The document summarizes various oral mucosal diseases and lesions. It discusses lichen planus, describing its prevalence, clinical presentations, associations with systemic diseases, and potential malignant transformation. It also briefly outlines the management of lichen planus, noting debates around treating asymptomatic lesions to potentially prevent malignant conversion.
Acute gingival infections and desquamative gingivitisRebekah James
This document provides an overview of various acute gingival infections and desquamative gingivitis conditions. It discusses necrotizing ulcerative gingivitis in depth, covering its historical background, clinical features, histopathology, relation to bacteria, diagnosis, differential diagnosis, etiology, and management. It also summarizes primary herpetic gingivostomatitis, pericoronitis, and desquamative gingivitis, outlining their key clinical features, diagnoses, and treatment approaches for each condition. The document serves as a reference for dental students to understand these oral infections and inflammatory conditions.
This PowerPoint presentation demonstrate a useful review of Oral candidiosis, including its different types, clinical presentations, differential diagnosis, and treatment options.
Necrotizing ulcerative gingivitis and necrotizing ulcerative periodontitisyeahlifehai
This document provides an overview of necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP). It discusses the history and epidemiology of these conditions, describing outbreaks among military troops. Clinically, NUG presents as ulcerated and necrotic gingival tissue with characteristic punched out lesions. Untreated, it can progress to involve the underlying bone as NUP. Predisposing factors include poor oral hygiene, preexisting gingivitis, smoking, nutritional deficiencies, systemic illnesses, fatigue, stress and immunodeficiencies. Microorganisms play a role in conjunction with an impaired host response.
The document discusses the layers of the mucosal lining from basal to horny layers. It then covers various diseases of the oral mucosa caused by microorganisms like viruses, fungi and bacteria. It also discusses histological terms used to describe changes in the layers. Specific conditions covered include viral infections like herpes, fungal infections like oral candidiasis, and bacterial infections like Vincent's infection.
Desquamative Gingivitis Diagnosis and Managementvinoth kumar
Desquamative gingivitis is characterized by erythema, desquamation and ulceration of the gingiva. It is often caused by mucocutaneous diseases like lichen planus, mucous membrane pemphigoid, and pemphigus vulgaris. A definitive diagnosis requires histopathological examination and direct immunofluorescence testing. Treatment depends on the underlying condition but generally includes topical or systemic steroids and immunosuppressants. Patients require long-term follow up due to the risk of recurrence.
Acute necrotizing ulcerative gingivitis (ANUG) is a painful bacterial infection of the gums that causes ulceration and necrosis. It is characterized by bleeding gums, pseudomembrane formation, and halitosis. Predisposing factors include poor oral hygiene, stress, smoking, and nutritional deficiencies. Treatment involves removing necrotic tissue, antibiotics, and improving oral hygiene through rinses and scaling. Proper treatment can resolve symptoms within a week.
Most deep fungal infections have their primary foci in the lungs, therefore those presenting with distant organs or skin involvement should be managed aggressively as untreated or severe disease can lead to severe scarring, disfigurement and even death.
Similar to bacterial infections and their oral manifestations (20)
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
29. treatment
o Draining the abscess
o Excising sinus tract with
high doses of antibiotics
to accelerate healing
o Penicillin
o Tetracycline
o Erythromycin
30.
31. Acute infection of nervous
system
Intense activity of motor
neurons
Severe muscle spasms
Gram positive bacillus
Clostridium tetani
Acts at synapse of
interneurons of inhibitary
pathways & motor neurons
to produce blockade of
spinal inhibition
35. *General measures:
*Remove spores at site of wound
*Cardiopulmovary monitoring
*Sedation,airway & nutrition to be maintained
*Penicillin 10-12million units IV for 10days
*Metronidazole 1gm every 12hrs
*Antitoxin injected to neutralise circulating toxin & unbound toxin with
wound.
*Prophylaxis : wound debridement & TT booster doses
*Unimmunized individuals : anti tetanus serum(ATS)
1500units or TIG 250units.
treatment
37. o Veneral disease
o Male & female genitourinary
Tract
o Neisseria gonorrhoeae
o Gram negative
o Nonmotile, nonspore forming
o Grows in pairsage : 15-29yrs
oIncubation pd : 1-5 days
o Oropharyngeal gonorrhoea in
20% women
Clinical features
41. Treponema pallidium
Episodes of active
disease interrupted by
Period of latency
Gram positive, motile
Microaerophillic
Darkfield microscope
Route of transmission:
Sexual contact
Mother to child in utero
42. ACQUIRED SYPHILLIS
PRIMARY STAGE
Chancre : at site of innoculation
3-90 days after infection
Solitary
m/c site males: penis
females: cervix or
vulva
95% occur in genitalia
Extragenital syphillis : increase in
altered sexual activity & contact
among
Infected homosexuals.
44. SECONDARY STAGE
Skin: macules or papules,
painless
Oral lesions: MUCOUS
PATCHES, multiple, painless
Gray white plaques overlying
ulcerated surface.
Tongue, gingiva, buccal
mucosa
HIGHLY INFECTIOUS
,contain vast number of
micro-organisms
Serologic reaction is always
+ve
Explosive, widespread form :
LUES MAILGNA
MUCOUS PATCHES
Leão JC, Gueiros LA, Porter SR. Oral manifestations of syphilis. Clinics
(Sao Paulo). 2006 Apr;61(2):161-6. Epub 2006 Apr 25.
45. *Late syphilis
*Do not appear for years
*CVS & CNS
*Noninfectious
*Gumma: result of hypersensitivity
*Focal, granulomatous inflammatory
*Process with central necrosis
*i/o gumma : tongue & palate
*Firm nodular mass in tissue
*May ulcerate to deep painless ulcer
*Palate: perforation by sloughing
*Herxheimer reaction
TERTIARY SYPHILIS
46. Atrophic or interstitial glossitis is most characteristic &
important lesion of syphilis & is due to endarteritis obliterans
SYPHILITIC GLOSSITIS
Tongue surface gets broken up by fissures.
Atrophy & fibrosis of tongue musculature.
Hyperkeratosis
May undergo carcinomatous transformation
47. Transmitted to offspring by
Mother
Frontal bossae
Short maxilla
High palatal arch
Saddle nose
Mulberry molars
Higoumenakis sign
Relative protuberance of mandible
Rhagades
Saber shin
CONGENITAL
SYPHILIS
RHAGADES
FRONTAL
BOSSAE
INTERSTITIAL
KERATITIS
HIGOUMENAKIS SIGNSADDLE NOSE
SABER SHIN
48. Diagnosis & treatment
Penicillin: DOC
Surgical correction
of facial defects
gives good esthetic
51. Clinical features
Hypopigmented
patches
Total loss of
cutaneous sensation
light touch to be
affected first
Thickening of nerves
Presence of acid fast
bacilli in skin or nasal
smear
GENERAL
FEATURES
Single/ multiple
macular
erythematous
eruptions
Dermal &
peripheral nerve
trunk involvement
Loss of sensation
Loss of sweating
of affected skin
Tuberculoid Leprosy
Early erythematous
macules or papules
Thickening of skin
Characteristic
nodules
Severe disfigurement
Lepromatous Leprosy
60. PAIN
INTERDEN
TAL
ULCERATI
ON
ANUG
GINGIVAL
BLEEDING
Involves free gingival margin,
crest of gingiva, interdental
papillae
May spread to soft palate &
tonsillar areas : vincents angina
Necrotizing ulcerative
periodontitis
Associated with HIV
Common in young & adults
etiology
• Fusiform bacillus & borrelia
vincentii
• Vibrio & coccal forms
• Acc to mc donald , Bacteroides
melaninogenicus : main causative
agent
• Stress , immunosupression
,smoking
• Upper resp tract infection , local
trauma
• Poor nutritional status , poor oral
Predisposingfactors
61. *Loesche WJ, Syed SA, Laughon BE, Stoll J. The bacteriology of acute
necrotizing ulcerative gingivitis. J Periodontol. 1982 Apr;53(4):223-
30.
*Treponema and Selenomonas sp., 32 and 6%, respectively, of the
microscopic count;
*B. melaninogenicus ssp. intermedius and Fusobacterium sp., which
averaged 24 and 3%, respectively, of the viable count.
*Plaque samples from 22 ulcerated sites in 8 patients with ANUG.
*
62. Clinical features
Painful, hyperemic gingiva, sharply
punched out crater like erosions
of interdental paillae
Grayish green necrotic
pseudomembrane
Fetid odour
Inability to eat
Gingival bleeding
Incubation zone
63. Diagnosis based on clinical finding :
gingival pain, ulceration & bleeding
Bacterial smear from gingiva
Fusiform bacillus: elongated rod with
Tapered ends 5-14microns in length
0.5-1.0microns diameter.
Weakly gram+ve
Borrellia vincentii: gram-ve
10-15microns length
Diagnosis
A- spirochete; B- bacillus fusiformis; C-
filamentous organism; D- streptococcus;
E- vibrio; F- treponema microdentinum
64. treatmentFIRST VISIT:
Medical history,
diet
background,smoking,
rest , risk factors
for HIV, stress
Examination of
general appearance,
halitosis, fever
Topical anesthetic6,
area swabbed with
moist cotton
Pseudomembrane &
non attached debris
removed
Superficial calculus
removed by
ultrasonic scaling
Antibiotics:
Amox 500mg 6hrs for
10days
Metronidazole 500mg
twice daily for 7days
Tooth xtraction or pdl
surgery
Postponed until 4weeks
Rinse with equal
amount of 3% h2o2 &
warm water every
2hrs or twice daily
with CHX
Adequate rest
Ultrasoft brush
NSAID for pain relief
SECOND VISIT
1,2 days after 1st
visit
Diminished pain
Gingival margins
erythematous but
without
Pseudomembrane
Scaling if needed
THIRD VISIT
5 DAYS after
Resolution of
symptoms
Plaque control
procedures
Counselling on
nutrition, smoking
cessation
CHX rinses for 2-4
weeks
Reevaluation after 1
month
Gingival contouring :
gingivoplasty
Nutritional
supplements
65.
66. small ulcer of gingiva spreads
involve surrounding tissues of jaw,lip
& cheeks by gangrenous necrosis.
rapidly spreading
Gangrenous stomatitis
m/c in children
seen in persons who are
undernourished or debilated
from infection
diptheria,dysentry,tb,syphilli
s,anemia…
Secondary complication of
systemic disease rather than
a primary disease.
Specific infection by
vincents organisms,
ANUG…soon complicated by
secondary invasion of
streptococci, staphylococci &
Clinical features
67. Area of
stagnation
Around fixed
bridge or crown
Overlying skin
inflammed,edem
atous & necrotic
Large mass of
tissue slough out.
Blackening of
skin.
Subcutaneous fat
undergoes
necrosis.
Foul odour
High
temperature,sec
ondary infection,
death from
toxemia
73. * : inflammatory lesion occuring around the
impacted or partially erupted tooth.
Mixed infection(anaerobes)
*Mand 3rd molar
*Pain & swelling
*Difficulty in opening & chewing
Mildly ill, fever & regional lymphadenopathy
Sixou JL, Magaud C, Jolivet-Gougeon A, Cormier M, Bonnaure-Mallet M. Microbiology of
mandibular third molar pericoronitis: incidence of beta-lactamase-producing bacteria. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod. 2003 Jun;95(6):655-9
PERICORONITIS
Clinicalfeatures
alpha-hemolytic streptococci (26/26)
Prevotella (15/26), Veillonella (15/26),
Bacteroides (9/26), and
Capnocytophaga (9/26)
74. *Gently flushing area with warm water
*Entrapped food debris must be removed
*Swabbing with antiseptic after elevating flap
Gently from tooth with a scaler
*Upper tooth when involved should be
ground or extracted
*Radiograph help in assessing position of tooth
*Surgical removal after acute symptoms subside
*Antibiotics to relieve symptoms & to prevent spread of
infection.
treatment
76. *Originate as a response of tissue
*To a nonspecific infection.
*Tumor like growth : exaggerated
*Conditioned response to minor
* trauma
Infection staphylococci or streptococci
Arise as a result of minor trauma to
tissues
Pathway for invasion of nonspecific
type of micro-organism.
Surface of pyogenic granuloma in cases
of ulceration abounds with typical
colonies of saprophytic organisms.
Sulfhydryl radical
etiology
80. *Multifactorial disease affecting commissure of lips
*m/c in denture wearers
*Associated with infection
*Reduced vertical dimension of mouth
*60% : candida albicans & staphylococcus
*20%: staphylococcus
*20%: candida albicans
*Nutritional deficiencies: fe, vit B, folic acid
*Ariboflavinosis: circumoral lesions
*Seen in diabetes, neutropenia, AIDS
81. *Occur in both young children & adults
*Dryness, burning sensation at corners
*Wrinkled skin at commissure
*Deep fissures & cracks
*Fissures stop at mucocutaneous
junction
Clinical features
82. Depending on the specific cause, the following treatments may
be useful:
*Lip balm or thick emollient ointment, applied frequently.
*Topical antiseptics.
*Topical or oral antistaphylococcal antibiotic.
*Topical antifungal cream.
*Oral antifungal medication
*.ketoconazole tab 200-400mg twice daily with food for 2weeks
* Fluconazole cap 50-100mg once daily for 2-3weeks
*Nutritional supplements.
treatment
84. *:
*Cellulitis is a diffuse inflammation of soft tissues which is
not circumscribed or confined to one area, but which, in
contrary to the abscess, tends to spread through tissue
spaces and along fascial planes.
*Common causative agent : streptococci viridans
*Produce : streptokinase, hyaluronidase, fibrinolysins
*Prevotella & porphyromonas : destroy collagen
*As result of apical abscess, osteomyelitis, following pdl
infection
*Pericoronitis
*Injection with infected needle
CELLULITIS
85.
86. *Moderately ill
*Elevated temperature
*Leukocytosis
*Firm & brawny, painful swelling of soft tissues
*Inflammatory edema
*Inflammed , orange peel appearance
*Regional lymphadenitis
*Infections in maxilla perforate outer cortical layer
Of bone above buccinator attachment : swelling of upper half
of face
*Eye: cavernous sinus thrombosis
*Infection in mandible perforate outer
cortical plate below buccinator :
*diffuse swelling of lower half of face
*Spread to cervical tissue : respiratory discomfort
Clinical features
87. histology
Diffusion exudation
of
Polymorphonuclear
Leukocytes,
lymphocytes
Separation of
connective tissue or
muscle fibers
treatment
Treatment for cellulitis depends on what
caused the infection, the severity of
symptoms and the general state of health.
Hospital treatment may be necessary if
symptoms such as fever, nausea and
vomiting suggesting infection has spread
from skin to bloodstream or other parts of
the body.
Antibiotics:
flucloxacillin, 25mg/kg(max 500mg) 6hr for
7days
Flucloxacillin 50mg/kg iv 6hr
Ceftriaxone 50mg/kg/dose iv 12 hr
Drink plenty of fluids to avoid dehydration.
NSAIDS : pain control
89. *
*Ludwig's angina, otherwise known as angina ludovici, is a
serious, potentially life-threatening cellulitis, or
connective tissue infection, of the floor of the mouth,
usually occurring in adults with concomitant dental
infections and if left untreated, may obstruct the
airways, necessitating tracheotomy.
Acute, toxic begin in
submandibular space
* secondarily involve sublingual &
submental spaces spaces.
* dental origin
* mandibular molar : chief
source of infection
* other causes :
LUDWIG’S
ANGINA
90. 2nd & 3rd molars: m/c
Unusual speech(hot potato in mouth)
Bilateral sublingual space infection
Bilateral submandibular space infection
Brawny edema
Elevated tongue
Airway obstruction
Paucity of pus
CLINICALFEATURES
HALLMARK SIGNS
3’F’ :
FEARED
FATAL(often)
FLUCTUANT(rarely)
94. * ETIOLOGY:
*microbial overgrowth in association with a reduction in salivary flow
*subsequent to dehydration and debilitation
*trauma to the duct system and hematogenous spread of infection from other
areas.
*The most commonly isolated organisms in parotitis : penicillin-resistant
Staphylococcus aureus, Streptococcus viridans, and Streptococcus pneumoniae
* presence of a painful swelling,
*low-grade fever
*malaise headache
*gland is extremely tender Trismus
*purulence at the duct orifice may be produced by gentle pressure on the
involved gland or duct.
* If infection is not eliminated early, suppuration may extend beyond the
limiting capsule of the parotid gland.
*Extension into surrounding tissues along fascial planes in the neck or
extension posteriorly into the external auditory canal may follow.
CLINICAL FEATURES
95.
96. *Laboratory studies :
*elevated erythrocyte sedimentation rale(ESR)
*leukocytosis, often with a characteristic shift to the left,
indicating acute infection.
* elimination of the causative organism
*rehydration of the patient
*drainage of purulence, if present.
*Culture and sensitivity testing of the exudate at the orifice of
the duct is the first step in antibiotic management.
*After a culture is obtained, patients empirically be placed on
regimen of a penicillinase-resistant antibiotic such as
semisynthetic penicillin. Along with rehydration and attempts
at establishing and encouraging salivary flow, moist
compresses, analgesics, and rest are in order.
*Medications containing parasympathomimetic agents, which
reduce salivary flow, should be reduced or eliminated.
Treatment & prognosis
97. *A biopsy and retrograde sialography should be avoided.
* may cause sinus tract formation, may allow infection to proceed beyond the
boundaries of the gland into surrounding" soft tissues.
* With prompt and effective treatment, recurrence is generally avoided.
* recurrent parotitis, considerable destructive glandular changes can be seen.
* juvenile, variant, of parotitis, intermittent unilateral or bilateral painful
swelling is accompanied by fever and malaise.
*initial attack : ages 2 and 6 years,
* neonatal form of suppurative parotitis may develop, with S. aureus being
the most common causative pathogen.
* Gross destruction of the parenchymal and ductal elements may be noted on
sialographic examination.
*Absence of secretory acinar components and a damaged ductal system with
numerous punctate globular spaces.
*Spontaneous regeneration of parotid salivary tissue.
99. *Sarcoidosis a multisystem granulomatous disease of unknown origin
characterized by the formation of uniform ,discrete, compact, non-caseating
epithelioid granulomas. I
*blacks >>whites.
* infectious etiology : Mycobacterium and Propionibacterium
* young adults
*lesions most common in the lungs, skin, lymph nodes, salivary glands,
spleen, bones,& the mouth.
*characterized by depression of delayed-type hypersensitivity
suggesting an impaired cell-mediated immunity, and raised or
abnormal serum immunoglobulins suggesting lymphoproliferation
*interferon gamma (IFN-J) and cytokines such as TNF-D, IL-12 and
IL-18 play an important role in the formation of granulomatous
lesions
103. Oral manifestations
Small papular nodular
plaques, resemble
herpetic lesions or fever
blisters
Bleblike, containing
clear yellowish
fluid, or as solid
nodules
LIPS
HARD PALATE
BUCCAL MUCOSA
104. Intracutaneous test: kveim siltzbach test
A lip biopsy may occasionally provide evidence of sarcoid involvement of minor
salivary glands in support of a clinical impression of pulmonary disease.
* Lab assay for angiotensin I—converting enzyme
* Elevation of this enzyme in conjunction with a positive chest radiograph has a
high diagnostic reliability
* Spontaneous resolution
* Corticosteroids: doc for symptomating pulmonary sarcoidosis
* Chloroquine anti TNF agents
* Immunosuppresive drugs to those not responding to steroids
* Levamisole for arthritic symptoms
* Good prognosis
diagnosis
TREATMENT
105. HISTOLOGY
Nests of epitheloid cells with
multinucleated giant cells
Non caesating
Solid, amorphous,eosinophillic,
hyaline mass
106. *a form of sarcoidosis in which characteristically there is
firm, painless, usually bilateral enlargement of the parotid
glands, accompanied by inflammation of the uveal tracts of
the eye and cranial nerve involvement.
*The submandibular and sublingual glands may be involved
* chronic, low-grade fever lassitude, malaise and vague
gastrointestinal disturbances nausea, and vomiting.
*Xerostomia is common.
* patchy erythema of the skin
*Enlargement of the cervical lymph nodes
earliest symptom : uveitis
*
*most common nerve involvement is unilateral or bilateral
seventh nerve paralysis,in one-third to one-half of all cases
UVEOPAROTID FEVER (HEERFORDT SYNDROME)
108. *Tuberculosis (TB) is a specific infectious granulomatous disease
caused by Mycobacterium tuberculosis
*M. tuberculosis is a rod-shaped, nonspore forming, and thin
aerobic bacteria called acid-fast bacilli,
*once stained, it cannot be decolorized by acid alcohol.
*Its acid-fastness is due to the high content of mycolic acids,
long chain cross-linked fatty acids and other cell wall lipids.
*Males are more affected than females in India though it
affects all ages, from an average of 1% in the under-five age
group.
M. tuberculosis is a facultative intracellular
atypical or opportunistic mycobacteria: pulmonary or
generalized infection in immunocompromised individuals
etiology
109. *M. tuberculosis is most commonly transmitted from a
person with infectious pulmonary TB by droplet nuclei,
which are aerosolized by coughing, sneezing, or speaking.
The tiny droplets dry rapidly; the smallest (<5–10 μm in
diameter) may remain suspended in the air for several
hours and may reach the terminal air passages when
inhaled. There may be as many as 3000 infectious nuclei
per cough
110.
111.
112. Exposure to TB
No infection(70-90%) Infection (10-30%)
Latent TB (90%) well
Never develop TB
Not infectious
Active TB (10%) ill
5% develop TB within 2
yr
5% develop TB many yrs
later
untreated treated
50% die
within 5
years
25% remain
sick
25% recover
cured
121. *Demonstration of organism by microbial stains
*Culture of sputum or infected tissue : lj medium middle brook media
*Presence of acid fast bacilli in sputum : gold standard
*Radiograph
*Tuberculin test
*CT scan: mediastinal or hilar lymphadenopathy
*MRI : extrapulmonary TB
*Ziehl Nielsen stain, Kinyouns stain , rhodamine staining for fluorescent
microsopy
*Minimum of 5 acidfast bacilli on fluorescent microscopy positive
*3 on ZN staining
*Rapid slide culture technique
*Radiometric culture method
*Radioimmunoassay
*ELISA
*PCR
DIAGNOSIS
126. *Global TB statistics
*In 2014 1.5 million people died of TB. Of these people 0.4 million people
were HIV positive.
*TB now annually causes more deaths worldwide than HIV.
*In 2014 1.2 million people died of HIV and this includes the 0.4 million TB
deaths among HIV positive people. People who have both TB and
HIV when they die, are internationally classified as having died from HIV.
*There were an estimated 9.6 million new cases of TB in 2014.There were
an estimated 3.2 million cases and 480,000 TB deaths among women.
*There were also an estimated 1.0 million cases of TB in children and
140,000 deaths.
127.
128.
129.
130. * The World Health Organisation (WHO) current estimates in 2015 are that 1 million children
currently suffer from TB worldwide (<15 years), and that more than 136,000 die each year.
* 70-80% of children with TB have the disease in their lungs (pulmonary TB). The rest are
affected by TB disease in other parts of their body (extra pulmonary TB) –
* Some children are at greater risk of getting TB than others and these include: A child that
lives in the same household as a person who has been recently diagnosed with smear
positive TB
* A child less than 5 years old
* A child with HIV infection
* A child with severe malnutrition
* in children with pulmonary TB the commonest chronic symptoms are a chronic cough that
has been present for more than 21 days, a fever, and weight loss or failure to thrive.
TB & CHILDREN
131. *The 2010 WHO TB drug dosage guidance for children
*The major recommendations of the WHO drug dosage guidance
for children were that:
*1) The dosages of the following four TB drugs should be:
• Isoniazid(H) 10mg/kg (range 10-15 mg/kg); maximum dose 300
mg/day
• Rifampicin(R) 15mg/kg (range 10-20 mg/kg); maximum dose 600
mg/day
• Pyrazinamide(Z) 35mg/kg (30-40) mg/kg)
• Ethambutol(E) 20mg/kg (15-25 mg/kg)
*As children approach a body weight of 25kg, adult dosages can
be used.
134. *Osteomyelitis is defined as the inflammation of bone and its
marrow contents.
* trauma and road traffic accidents;
*gunshot wounds, radiation damage, Paget’s disease, and osteopetrosis.
*Systemic conditions like malnutrition, acute leukemia, uncontrolled diabetes
mellitus, sickle cell anemia, and chronic alcoholism.
CLASSIFICATION
SUPPURATIVE NONSUPPURATIVE
ACUTE CHRONIC CHRONIC
SCLEROSI
NG
FOCAL DIFFUSEGARRE
PREDISPOSING FACTORS:
136. *
*serious sequela of periapical infection that often results in a diffuse spread
of infection throughout the medullary spaces, with subsequent necrosis of a
variable amount of bone.
*MAXILLA : well localised MANDIBLE : diffuse & widespread
* neonatal maxillitis in infants and young children
*severe pain, trismus, and paresthesia of the lips : mandibular involvement
*elevation of temperature regional lymphadenopathy.
*WBC elevated.
teeth loose and sore eating is difficult,
Pus may exude from the gingival margin.
Until periostitis develops, there is no swelling or reddening of the skin or
mucosa.
ACUTE SUPPURATIVEOSTEOMYELITIS
CLINICAL FEATURES
138. Chronic
osteomyelitis
Most infectious
(bacterial)
Varaiable pain,
swelling,
drainage
Radiolucent or
mottled
pattern
Appropriate
antibiotic,
sequestromy
Chronic
osteomyelitis
with
proliferative
periostitis
Sequelae of
tooth abscess,
extraction
Usually
associated
with lower
molar,perioste
um involved
children
Radiolucent or
mottled with
concentric
periosteal
opacities
Tooth removal,
antibiotics
Diffuse
sclerosing
osteomyelitis
Probably low
grade
infection,
pulpitis,period
ontal disease
Ocassional
pain, swelling,
drainage
mandible
Opacification
throughout jaw
Antibiotics,
find cause &
treat if
possible
Focal
sclerosing
osteitis
Low grade
focal bone
irritation
Asymptomatic,
Found on
routine
examination
Opaque mass
usually at root
apex
Treat offending
tooth
Etiology Clinical
features
Radiographs Treatment
139. * a reaction to mild bacterial infection entering the bone through a carious
tooth in persons who have a high degree of tissue resistance and tissue
reactivity.
the tissues react to the infection by proliferation rather than destruction,
since infection acts as a stimulus rather than an irritant. .
MOST COMMON : CHILDREN
mandibular first molar with a large carious lesion. Endodontic treatment
or extraction
mild pain associated with an infected pulp.
CONDENSINGOSTEITIS
treatment
140. Medical management:
1.Systemic antibiotics- penicillin(empirical) 2-4 months
Metronidazle
Clindamycin
Cephalosporins
Vancomycin
2.Local application of antibiotics
PMMA beads- antibiotic impregnated beads
Surgical management:
Removal of necrotic foci
a) sequestrectomy- dead necrotic bone(avascular, antibiotics donot penetrate)
b) Saucerisation
c) Decortication- lateral & inferior cortical bone is removed
d) Ressection & reconstruction
MANAGEMENT
HBO THERAPY
141.
142. *1) Harrison’s principles of internal medicine.19th edition
*2)Scott C Kachlany. Deadly diseases and epidemics. Infectious diseases of the
mouth.2007
*3) Shafer.Hine.Levy. Textbook of OralPathology.7th edition
*4)Greenberg. Glick. Ship. Burket’s OralMedicine.11th edition
*5) Regezi.Sciubba.Jordan. OralPathologyClinical pathological correlations.4th
edition
6)Philip D Marsh. Michael V Martin. Oral Microbiology.5th edition
*7)Michael Miloro. Peterson’s Principles of Oral And Maxillofacial Surgery.2nd
edition
references