Oral manifestation of bleeding disorders and dental management of the same
also for more
https://youtu.be/aaJ6gpQohcs
https://youtu.be/REMKSUty0cE
https://youtu.be/fv3_tWZPJIU
https://youtu.be/GeZIbCwqKYU
if you want me to make ppt on some topic do let me know on the comment section of my youtube channel
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.
This document discusses diseases of the salivary glands. It begins by identifying the major salivary glands as the parotid, submandibular, and sublingual glands. It then discusses various diseases including developmental anomalies, sialadenitis (inflammatory disorders), obstructions, Sjögren's syndrome (an autoimmune disease causing dry mouth and eyes), sialadenosis (recurrent swelling), and HIV-associated salivary gland disease. For many of these diseases, it provides details on causes, clinical features, histopathology, and investigations. In summary, it provides an overview of the major diseases that can affect the salivary glands.
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.
Peripheral and central giant cell granulomaRijuwana77
This document discusses two types of non-epithelial tumours of the oral cavity: peripheral giant cell granuloma and central giant cell granuloma. Peripheral giant cell granuloma originates from the periodontal membrane or alveolar bone and presents as a soft tissue nodule composed of multinucleated giant cells. Central giant cell granuloma is a rare, benign, intraosseous lesion most commonly found in the mandible of young people that causes expansion of the bone and resorption of tooth roots. Both lesions contain proliferation of multinucleated giant cells and other cells and may require surgical excision, with central giant cell granuloma having a higher rate of recurrence.
This document discusses the causes, progression, and presentation of various periapical and periodontal infections and abscesses. It describes how untreated pulpitis can lead to periodontitis as bacteria spread through the root canal. Acute traumatic periodontitis is usually temporary and caused by occlusal trauma or dental procedures. Persistent irritation can lead to chronic periapical periodontitis characterized by bone resorption and granulation tissue formation. Abscesses may develop from these infections and spread in various directions depending on anatomical structures, presenting as facial swelling, palatal abscesses, or submandibular involvement in severe cases like Ludwig's angina.
This document discusses different types of gingival enlargement, including classifications based on etiology and location. Inflammatory enlargements can be acute or chronic, with chronic enlargement resulting from plaque accumulation. Systemic diseases like leukemia and granulomatous diseases can also cause enlargement. Neoplastic enlargements include benign tumors like fibromas and papillomas, as well as malignant tumors like squamous cell carcinoma. Drug-induced enlargement is a common side effect of medications like anticonvulsants, immunosuppressants, and calcium channel blockers. The document also covers indices used to grade the severity of enlargement.
Oral manifestation of bleeding disorders and dental management of the same
also for more
https://youtu.be/aaJ6gpQohcs
https://youtu.be/REMKSUty0cE
https://youtu.be/fv3_tWZPJIU
https://youtu.be/GeZIbCwqKYU
if you want me to make ppt on some topic do let me know on the comment section of my youtube channel
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.
This document discusses diseases of the salivary glands. It begins by identifying the major salivary glands as the parotid, submandibular, and sublingual glands. It then discusses various diseases including developmental anomalies, sialadenitis (inflammatory disorders), obstructions, Sjögren's syndrome (an autoimmune disease causing dry mouth and eyes), sialadenosis (recurrent swelling), and HIV-associated salivary gland disease. For many of these diseases, it provides details on causes, clinical features, histopathology, and investigations. In summary, it provides an overview of the major diseases that can affect the salivary glands.
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.
Peripheral and central giant cell granulomaRijuwana77
This document discusses two types of non-epithelial tumours of the oral cavity: peripheral giant cell granuloma and central giant cell granuloma. Peripheral giant cell granuloma originates from the periodontal membrane or alveolar bone and presents as a soft tissue nodule composed of multinucleated giant cells. Central giant cell granuloma is a rare, benign, intraosseous lesion most commonly found in the mandible of young people that causes expansion of the bone and resorption of tooth roots. Both lesions contain proliferation of multinucleated giant cells and other cells and may require surgical excision, with central giant cell granuloma having a higher rate of recurrence.
This document discusses the causes, progression, and presentation of various periapical and periodontal infections and abscesses. It describes how untreated pulpitis can lead to periodontitis as bacteria spread through the root canal. Acute traumatic periodontitis is usually temporary and caused by occlusal trauma or dental procedures. Persistent irritation can lead to chronic periapical periodontitis characterized by bone resorption and granulation tissue formation. Abscesses may develop from these infections and spread in various directions depending on anatomical structures, presenting as facial swelling, palatal abscesses, or submandibular involvement in severe cases like Ludwig's angina.
This document discusses different types of gingival enlargement, including classifications based on etiology and location. Inflammatory enlargements can be acute or chronic, with chronic enlargement resulting from plaque accumulation. Systemic diseases like leukemia and granulomatous diseases can also cause enlargement. Neoplastic enlargements include benign tumors like fibromas and papillomas, as well as malignant tumors like squamous cell carcinoma. Drug-induced enlargement is a common side effect of medications like anticonvulsants, immunosuppressants, and calcium channel blockers. The document also covers indices used to grade the severity of enlargement.
Tuberculosis is a disease characterized by granulomatous lesions caused by Mycobacterium Tuberculosis. A German scientist Robert Koch discovered the causative organism of TB in 1882.
Since time immemorial, it has been a global health problem. TB has shown a decline in its prevalence globally; however, it is still highly prevalent in Asian countries.
TB is usually overlooked in the differential diagnosis of oral lesions as it is supposed to be a rare entity.
Oral manifestations of TB occur either due to infected sputum or due to hematogenous spread.
TB is an age old disease and has been known to mankind for thousands of years.
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.
The document discusses various white oral lesions including leukoedema, leukoplakia, lichen planus, and candidiasis. Leukoedema is a common white lesion considered normal variation, while leukoplakia is a premalignant condition defined as a white patch that is not caused by other disease. Lichen planus is a chronic inflammatory disease presenting as bilateral white lesions, and candidiasis is an opportunistic fungal infection caused by Candida albicans.
This document discusses various types of odontogenic cysts. It begins with introducing cysts in general and then classifies odontogenic cysts based on etiology and tissue of origin. Several specific types of odontogenic cysts are then described in more detail, including their clinical features, radiographic features, and differential diagnosis. These include dentigerous cysts, eruption cysts, odontogenic keratocysts, gingival cysts of newborn and adult, lateral periodontal cysts, calcifying odontogenic cysts, periapical cysts, residual cysts, and paradental cysts.
Benign tumors of the jaw were discussed. Key points include:
- Benign tumors are slow-growing, do not metastasize or invade surrounding tissues, and have well-defined borders on radiographs.
- Common benign jaw tumors discussed include ameloblastoma, calcifying epithelial odontogenic tumor (Pindborg tumor), odontoma, and ameloblastic fibroma.
- Radiographic features help differentiate benign tumors and include location, well-defined or corticated borders, internal structure patterns like septa, and effects on surrounding structures like tooth displacement.
This document summarizes various blood disorders and their oral manifestations. It discusses disorders of red blood cells like iron-deficiency anemia, megaloblastic anemia, pernicious anemia, and sickle cell anemia. It also covers disorders of white blood cells such as leukemia and leukopenia. For each condition, it describes the causes, clinical features, diagnosis, and potential oral signs including gingival bleeding, ulcers, and infections. In general, these blood disorders can cause oral pallor, infections, and changes in taste or tooth development.
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
This document describes several different oral lesions including:
1) Squamous papilloma which presents as soft, painless nodules caused by HPV and treated with surgical excision.
2) Verrucous carcinoma which presents as dome shaped nodules on sun exposed areas, is painful, and treated with surgical excision.
3) Leukoplakia which presents as white patches or plaques of uncertain risk and can be treated with surgical excision or cryosurgery.
Tuberculosis is an infectious disease caused by the Mycobacterium tuberculosis bacterium, which primarily affects the lungs but can infect any part of the body, including the oral cavity. It is transmitted through aerosolized droplets released when an infected person coughs, sneezes, speaks, or sings. Common symptoms include weight loss, cough, fever, and night sweats. Diagnosis involves chest x-rays and tuberculin skin tests. While oral TB lesions are rare, occurring in less than 1% of cases, they most commonly appear as painless ulcers on the tongue. Dentists are at low but present risk of exposure and should take precautions like wearing masks and gloves during treatment of
1. Dental pulp diseases include pulpitis, which can be acute or chronic. Acute pulpitis is reversible or irreversible, while chronic pulpitis can be closed or open.
2. Periapical diseases result from pulp necrosis and include acute or chronic apical periodontitis, periapical abscesses, cysts, and osteomyelitis. Chronic apical periodontitis often forms a periapical granuloma.
3. Symptoms, causes, histological features, radiographic features and treatments are described for each condition. Physical, chemical and microbial factors can all contribute to pulp and periapical diseases.
The document discusses various verrucal-papillary lesions of the oral cavity including reactive lesions such as papillary hyperplasia, condyloma latum, squamous papilloma, condyloma acuminatum, and focal epithelial hyperplasia. It also discusses neoplasms like keratoacanthoma and verrucous carcinoma. Rare lesions of unknown etiology discussed include pyostomatitis vegetans and verruciform xanthoma. Each lesion is described in terms of etiology, clinical features, histopathology, differential diagnosis, and treatment.
Fissural cysts arise along lines of fusion between embryonic processes. Nasopalatine duct cysts are the most common non-odontogenic cyst, arising from epithelial remnants of the nasopalatine duct. Median palatal cysts occur in the midline of the hard palate from entrapped epithelium. Dermoid and epidermoid cysts contain skin elements and arise from implantation of epithelium during embryonic development. These cysts are examined clinically and radiographically and often surgically removed.
This document defines and classifies different types of cysts that can occur in the oral cavity. It discusses epithelial cysts, which make up over 50% of oral cysts and includes radicular, dentigerous, and odontogenic keratocysts. Nonepithelial cysts are also mentioned. Specific cysts like paradental, nasopalatine, and solitary bone cysts are defined. Treatment options for jaw cysts include enucleation, marsupialization, a combination of both, and enucleation with curettage.
This document summarizes various diseases that can affect the jaw bone. It discusses inherited conditions like osteogenesis imperfecta and achondroplasia. It also covers infections like osteomyelitis, inflammatory conditions like fibrous dysplasia, and tumors originating from bone or other tissues that can develop in the jaw. For each condition, it provides details on characteristics, clinical presentation, radiographic appearance, and other relevant information.
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 provides an overview of non-neoplastic salivary gland disorders. It discusses various classifications of these disorders and then describes specific conditions in detail under categories such as developmental disorders, infections, traumatic/ischemic disorders, and autoimmune disorders. Key points include descriptions of common developmental disorders like ductal atresia and polycystic disease of the parotid. Infectious disorders covered include viral sialadenitis from mumps virus and bacterial sialadenitis. Conditions resulting from trauma or ischemia like cheilitis glandularis and necrotizing sialometaplasia are also summarized.
The document discusses age-related changes in the periodontium and their effects. It notes that with age, the gingival epithelium thins and becomes less keratinized. The gingival connective tissue becomes coarser and denser. The periodontal ligament has fewer fibroblasts and a more irregular structure. Cementum increases in width, especially apically and lingually. The alveolar bone surface becomes more irregular and collagen fiber insertion less regular. Aging may increase the inflammatory response to plaque and the progression of periodontal disease if plaque is not controlled. Response to periodontal treatment can be successful if patients maintain meticulous plaque control and thorough debridement is performed.
Tooth resorption is the progressive loss of dentine and cementum by the action of osteoclasts. This is a physiological process in the exfoliation of the primary dentition, caused by osteoclast differentiation due to pressure exerted by the erupting permanent tooth
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.
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.
Tuberculosis is a disease characterized by granulomatous lesions caused by Mycobacterium Tuberculosis. A German scientist Robert Koch discovered the causative organism of TB in 1882.
Since time immemorial, it has been a global health problem. TB has shown a decline in its prevalence globally; however, it is still highly prevalent in Asian countries.
TB is usually overlooked in the differential diagnosis of oral lesions as it is supposed to be a rare entity.
Oral manifestations of TB occur either due to infected sputum or due to hematogenous spread.
TB is an age old disease and has been known to mankind for thousands of years.
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.
The document discusses various white oral lesions including leukoedema, leukoplakia, lichen planus, and candidiasis. Leukoedema is a common white lesion considered normal variation, while leukoplakia is a premalignant condition defined as a white patch that is not caused by other disease. Lichen planus is a chronic inflammatory disease presenting as bilateral white lesions, and candidiasis is an opportunistic fungal infection caused by Candida albicans.
This document discusses various types of odontogenic cysts. It begins with introducing cysts in general and then classifies odontogenic cysts based on etiology and tissue of origin. Several specific types of odontogenic cysts are then described in more detail, including their clinical features, radiographic features, and differential diagnosis. These include dentigerous cysts, eruption cysts, odontogenic keratocysts, gingival cysts of newborn and adult, lateral periodontal cysts, calcifying odontogenic cysts, periapical cysts, residual cysts, and paradental cysts.
Benign tumors of the jaw were discussed. Key points include:
- Benign tumors are slow-growing, do not metastasize or invade surrounding tissues, and have well-defined borders on radiographs.
- Common benign jaw tumors discussed include ameloblastoma, calcifying epithelial odontogenic tumor (Pindborg tumor), odontoma, and ameloblastic fibroma.
- Radiographic features help differentiate benign tumors and include location, well-defined or corticated borders, internal structure patterns like septa, and effects on surrounding structures like tooth displacement.
This document summarizes various blood disorders and their oral manifestations. It discusses disorders of red blood cells like iron-deficiency anemia, megaloblastic anemia, pernicious anemia, and sickle cell anemia. It also covers disorders of white blood cells such as leukemia and leukopenia. For each condition, it describes the causes, clinical features, diagnosis, and potential oral signs including gingival bleeding, ulcers, and infections. In general, these blood disorders can cause oral pallor, infections, and changes in taste or tooth development.
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
This document describes several different oral lesions including:
1) Squamous papilloma which presents as soft, painless nodules caused by HPV and treated with surgical excision.
2) Verrucous carcinoma which presents as dome shaped nodules on sun exposed areas, is painful, and treated with surgical excision.
3) Leukoplakia which presents as white patches or plaques of uncertain risk and can be treated with surgical excision or cryosurgery.
Tuberculosis is an infectious disease caused by the Mycobacterium tuberculosis bacterium, which primarily affects the lungs but can infect any part of the body, including the oral cavity. It is transmitted through aerosolized droplets released when an infected person coughs, sneezes, speaks, or sings. Common symptoms include weight loss, cough, fever, and night sweats. Diagnosis involves chest x-rays and tuberculin skin tests. While oral TB lesions are rare, occurring in less than 1% of cases, they most commonly appear as painless ulcers on the tongue. Dentists are at low but present risk of exposure and should take precautions like wearing masks and gloves during treatment of
1. Dental pulp diseases include pulpitis, which can be acute or chronic. Acute pulpitis is reversible or irreversible, while chronic pulpitis can be closed or open.
2. Periapical diseases result from pulp necrosis and include acute or chronic apical periodontitis, periapical abscesses, cysts, and osteomyelitis. Chronic apical periodontitis often forms a periapical granuloma.
3. Symptoms, causes, histological features, radiographic features and treatments are described for each condition. Physical, chemical and microbial factors can all contribute to pulp and periapical diseases.
The document discusses various verrucal-papillary lesions of the oral cavity including reactive lesions such as papillary hyperplasia, condyloma latum, squamous papilloma, condyloma acuminatum, and focal epithelial hyperplasia. It also discusses neoplasms like keratoacanthoma and verrucous carcinoma. Rare lesions of unknown etiology discussed include pyostomatitis vegetans and verruciform xanthoma. Each lesion is described in terms of etiology, clinical features, histopathology, differential diagnosis, and treatment.
Fissural cysts arise along lines of fusion between embryonic processes. Nasopalatine duct cysts are the most common non-odontogenic cyst, arising from epithelial remnants of the nasopalatine duct. Median palatal cysts occur in the midline of the hard palate from entrapped epithelium. Dermoid and epidermoid cysts contain skin elements and arise from implantation of epithelium during embryonic development. These cysts are examined clinically and radiographically and often surgically removed.
This document defines and classifies different types of cysts that can occur in the oral cavity. It discusses epithelial cysts, which make up over 50% of oral cysts and includes radicular, dentigerous, and odontogenic keratocysts. Nonepithelial cysts are also mentioned. Specific cysts like paradental, nasopalatine, and solitary bone cysts are defined. Treatment options for jaw cysts include enucleation, marsupialization, a combination of both, and enucleation with curettage.
This document summarizes various diseases that can affect the jaw bone. It discusses inherited conditions like osteogenesis imperfecta and achondroplasia. It also covers infections like osteomyelitis, inflammatory conditions like fibrous dysplasia, and tumors originating from bone or other tissues that can develop in the jaw. For each condition, it provides details on characteristics, clinical presentation, radiographic appearance, and other relevant information.
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 provides an overview of non-neoplastic salivary gland disorders. It discusses various classifications of these disorders and then describes specific conditions in detail under categories such as developmental disorders, infections, traumatic/ischemic disorders, and autoimmune disorders. Key points include descriptions of common developmental disorders like ductal atresia and polycystic disease of the parotid. Infectious disorders covered include viral sialadenitis from mumps virus and bacterial sialadenitis. Conditions resulting from trauma or ischemia like cheilitis glandularis and necrotizing sialometaplasia are also summarized.
The document discusses age-related changes in the periodontium and their effects. It notes that with age, the gingival epithelium thins and becomes less keratinized. The gingival connective tissue becomes coarser and denser. The periodontal ligament has fewer fibroblasts and a more irregular structure. Cementum increases in width, especially apically and lingually. The alveolar bone surface becomes more irregular and collagen fiber insertion less regular. Aging may increase the inflammatory response to plaque and the progression of periodontal disease if plaque is not controlled. Response to periodontal treatment can be successful if patients maintain meticulous plaque control and thorough debridement is performed.
Tooth resorption is the progressive loss of dentine and cementum by the action of osteoclasts. This is a physiological process in the exfoliation of the primary dentition, caused by osteoclast differentiation due to pressure exerted by the erupting permanent tooth
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.
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 document classifies dental caries in several ways:
1. Based on anatomical site such as occlusal, root, and smooth surface caries. Occlusal caries are most prevalent.
2. Based on progression as acute, chronic, or arrested caries. Acute caries progresses rapidly while chronic caries is slow.
3. Based on the initial involvement of the tooth surface as primary or recurrent caries. Primary caries is the initial attack while recurrent caries occurs around restorations.
This document discusses root caries, including its definition, causes, classification, diagnosis and treatment. It describes the microbiology, clinical features and prognosis of root caries lesions. It also compares various restorative materials that can be used, including composites, glass ionomers and resin-modified glass ionomers. Emphasis is placed on the importance of preventive measures, proper isolation and adhesion to root surfaces for successful treatment of root caries.
INCLUDES DEFINITION, CAUSATIVE AGENT, CURRENT CONCEPT OF DENTAL CARIES, KEY'S TRIANGLE, CLASSIFICATION OF DENTAL CARIES BASED ON ANATOMICAL SITE, SEVERITY AND RATE OF PROGRESSION, CLINICAL VARIANTS AND SEQUELAE OF DENTAL CARIES, MANAGEMENT AND TREATMENT OF DENTAL CARIES
This document discusses the management of deep carious lesions. It begins by defining deep carious lesions as those that penetrate deeply into the dentin, potentially involving over half of the dentin thickness. It then covers the response of the pulpo-dentinal complex at different stages of carious lesion progression. This includes the cellular changes that occur as caries advances through enamel and into dentin. The document also discusses arrested caries, histopathology of carious dentin, effective depth of remaining dentin and its impact on pulpal response, prognosis of deep lesions, reparability of the pulpo-dentinal complex, and various treatment modalities including indirect pulp capping and stepwise excavation.
Histopathology & microbiology of dental cariesAshish Karode
The document summarizes the histopathology of dental caries. It describes how dental caries is a microbial disease that causes demineralization of tooth enamel and dentin. It discusses the role of bacteria like Streptococcus mutans in producing acid that dissolves tooth structure. The summary describes the microscopic appearance of carious lesions in enamel and dentin, including the formation of zones of demineralization and bacterial invasion of dentin tubules over time. Advanced caries can ultimately lead to tooth cavitation and pulp involvement if left untreated.
Pediatric Endodontics - Indirect and Direct pulp capping,Pulpotomy, Pulpecto...Karishma Sirimulla
this seminar consists of basis differences in root canal pattern between primary and permanet teeth followed by various definitions techniques and medicaments used in indirect pulp capping, direct pulp capping, pulpotomy, pulpectomy, apexogenesis and apexification
This document provides an overview of methods for classifying and diagnosing dental caries. It discusses 8 ways caries can be classified based on anatomical site, progression, virginity, tissue involvement, number of tooth surfaces involved, chronology, surfaces to be restored, and Black's classification. It also outlines conventional diagnostic methods like visual examination with an explorer, bitewing radiography, fiberoptic transillumination, and electric measurements. Emerging technologies like intraoral cameras, direct/indirect digital radiography, and laser-based devices like Diagnodent are also summarized.
Dental caries is caused by acid-producing bacteria in dental plaque that metabolize sugars from the diet. As the bacteria lower the pH, minerals are dissolved from tooth enamel and dentin, leading to cavitation. The primary bacteria involved are mutans streptococci. Risk factors include frequency of sugar consumption. Early lesions appear as white spots on smooth surfaces or pits and fissures. Untreated, caries progresses through enamel and into dentin, forming zones of demineralization and bacterial invasion.
Dental caries is caused by acid-producing bacteria in dental plaque that metabolize sugars from the diet. As the bacteria lower the pH, minerals are dissolved from tooth enamel and dentin, leading to cavitation. The primary bacteria involved are mutans streptococci. Risk factors include frequent sugar consumption. Early lesions appear as white spots on smooth surfaces or pits and fissures. Untreated, caries progresses through enamel and into dentin, forming zones of demineralization and bacterial invasion.
Dental caries is caused by demineralization of tooth structure due to acid produced by oral bacteria. It is characterized by loss of both inorganic and organic components of the tooth. Dental caries has been defined and classified in various ways based on factors such as the anatomical site, severity, tissue involvement, number of surfaces affected, and chronology. The key etiological factors include the presence of cariogenic bacteria in dental plaque, a susceptible tooth substrate, and a cariogenic diet. Secondary factors like time, the dynamic process of demineralization and remineralization, and saliva also influence the development of dental caries.
Dental caries is a disease caused by an interaction between oral bacteria and fermentable carbohydrates that leads to demineralization of tooth structure over time. It progresses through enamel and into dentin, where multiple zones are formed - an outer infected dentin zone containing bacteria that must be removed, an affected dentin zone that can be left, and an inner normal dentin zone. Deep caries lesions near the pulp require assessment using symptoms, clinical tests of vitality, and radiographs to determine the extent of damage and appropriate treatment.
Dental caries is the most prevalent disease affecting humans, spreading to almost all populations worldwide regardless of socioeconomic status or age. It is caused by bacteria in the mouth that feed on sugars, producing acids that demineralize tooth enamel and dentin over time. If left untreated, it can progress from white spot lesions to cavities, and eventually to tooth pain, abscesses, and tooth loss. The document provides detailed information on the histopathological stages and presentation of dental caries in enamel, dentin, and cementum.
This document describes the stages of dental caries progression in dentin. It begins with early penetration of microorganisms into dentinal tubules, causing sclerosis and calcification. As it progresses, more tubules become involved and decalcification occurs, allowing microorganisms to spread deeper. Advanced stages see confluence of tubules, formation of liquefaction foci, and necrotic destruction of dentin in numerous focal areas. This leads to a leathery mass that can peel off in layers during excavation. The dentinal tubules act as pathways for microbes to spread from the enamel-dentin junction towards the pulp.
Similar to Infections of teeth and bone - Oral Pathology (20)
Infections of the gingivae and oral mucosaSana Rasheed
This document discusses various infections that can affect the oral mucosa and gingivae. It describes acute necrotizing ulcerative gingivitis (ANUG), an infection of the gingiva caused by a complex of bacteria including fusobacteria and spirochetes. It presents syphilis and gonorrhea as examples of sexually transmitted infections that can manifest orally. It also discusses tuberculosis, non-specific urethritis, and various fungal infections including oral candidiasis. Treatment involves identifying the causative organism and using antibiotics or antifungals as appropriate.
Antiviral drugs are used to treat viral infections by inhibiting viral development rather than destroying the pathogen. The herpes virus is of particular interest to dentistry. Acyclovir is commonly used in dentistry to treat herpes simplex infections of the lips, gums, and mucous membranes as well as herpes zoster and chickenpox. It has minimal side effects but intravenous use can cause sweating, rashes, nausea and low blood pressure in some patients. Other topical antivirals used in dentistry include penciclovir and docosanol to treat herpes infections. Famciclovir and valaciclovir are also used orally to treat herpes zoster and genital
The document discusses neck and spine trauma, providing guidelines for patient assessment, physical examination, and classification and management of spinal and spinal cord injuries. It emphasizes approaching every trauma patient using ATLS principles, assuming a spinal injury until proven otherwise. A high index of suspicion of spinal injury is warranted if neurological deficit, multiple injuries, head or facial injury, or high-energy mechanisms are present. Physical examination includes identification of shock types and a full spinal examination and neurological assessment. Management principles involve spinal realignment, stabilization if the injury is unstable, and early decompression of neural elements.
This document discusses different types of head injuries, including primary and secondary brain injury. It classifies head injuries based on Glasgow Coma Scale and describes management of mild versus moderate to severe injuries. Surgical management is discussed for various intracranial hemorrhages like extradural hematoma, acute subdural hematoma, and cerebral contusions. Intracranial pressure monitoring and decompressive craniectomy are also mentioned for treatment.
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Thyroid Examination - General Surgery Sana Rasheed
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1. Infections of Teeth and Bone
Sana Rasheed
Akhtar Saeed Medical and Dental College, Lahore, Pakistan.
2. Dental Caries
Definition
Dental caries is a multifaceted disease involving interplay
among the teeth, the oral host factors of saliva and
microflora, and the external factor of diet.
Bacteria accumulate on the enamel surface, where they
elaborate acidic and proteolytic products that demineralize
the surface and digest its organic matrix.
Although dental
caries is restricted to the hard tissue of the
enamel, dentin, and cementum,
if left untreated, the process will
ultimately penetrate through the pulpal
canal beyond the tooth into the adjacent
soft tissue, where it will initiate
a painful and destructive inflammatory
reaction.
In this location it may spread into the
marrow spaces of the bone and possibly
the soft tissues and muscles of
the face and neck.
3. • Streptococci are essential
for development of caries,
particularly of smooth
(interstitial) surfaces.
• These are viridans
streptococci which are a
heterogeneous group
including
• Streptococcus mutans,
• S. sobrinus,
• S. salivarius,
• S. mitior
• S. sanguis
4.
5.
6.
7.
8. EPIDEMIOLOGY
• The caries activity in a particular society or
geographic area is closely correlated with the
amount of sugar consumed per capita.
• In the more industrialized countries, where
diets have traditionally had a high content of
refined carbohydrates, the caries rate has
been considerably higher than in less-
developed countries.
• In the very young, when diets are high in
sucrose and without adequate preventative
practices, the pits and fissures of the first
molars commonly become involved with
caries within the first 3 years after eruption.
• The second molars have the next highest
susceptibility, followed by the second
premolars.
• First the interproximal surfaces become
involved, followed by the buccal and lingual
surfaces.
1st molars 2nd molars
2nd
premolars
Interproximal
surfaces
Buccal and
lingual
surfaces
Smooth
surfaces of
Anterior teeth
11. Pit and fissure caries
• most common type
• appear at an early age
• occlusal and buccal
surfaces of the molars of
the primary and
secondary dentition
This form of caries is the most destructive, because it
quickly goes deeply into the dentin, remains hidden
as it undermines the enamel, and becomes clinically
evident as
pain caused by pulpal involvement or as a large cavity
when a substantial portion of the tooth crumbles.
13. • less common
• occurs on the interproximal
(contact) areas of the teeth,
cervical regions of the buccal
and lingual surfaces of the
teeth
• In adults, smooth-surface
cervical caries is usually the
result of a major alteration in
the quantity or quality of the
saliva.
• Reasons: radiation therapy,
medications, autoimmune
diseases
Baby bottle caries : When caries is present on the labial surfaces of the
primary teeth of infants, it is nearly always caused by a habit of leaving the
feeding bottle containing milk or juice in the infant’s mouth when sleeping
15. • Recurrent caries
• caries that arises around an
existing restoration
• results in marginal “ditching” or
or leakage
• Progress at variable rates,
depending on the extent of
sclerosis of the adjacent dentin
and the patient’s diet and oral
hygiene habits
Acute (rampant) caries and chronic caries
• Young patients are most susceptible to acute or
rampant caries, because they have teeth with large
pulpal chambers and wide and short dentinal tubules
containing little or no sclerosis.
• this is often combined with a diet high in refined
carbohydrates and less-than-adequate oral hygiene
They are capable of simultaneously developing multiple
rapidly advancing carious lesions that quickly destroy
tooth structure, penetrate into the pulp, and elicit severe
pain.
Chronic caries is most common in older
patients whose teeth have smaller pulpal chambers,
usually with additional deposits of a denser and less tubular dentin on the pulpal walls, referred to as tertiary
or secondary dentin. Additionally they have dentinal
tubules that have undergone significant degrees of sclerosis,
which offers some degree of resistance to the progression
of the carious process
17. • This process of enamel caries is a
dynamic one and, initially at least,
consists of alternating phases of
demineralisation and remineralisation,
rather than a continuous process of
dissolution.
• Alteration occurs in the loss and
redeposition of mineralizing salts that is
caused by fluctuations in the pH in that
particular location.
In some situations
if the pH can be stabilized in its normal
range, the whole process may stop or
even reverse, which is referred
to as arrested caries.
Arrested caries may also occur
when
• an adjacent tooth is extracted or
• when an undermined cusp fractures
off, making the carious area self-
cleansing
• Improved oral hygiene
18. • Four zones can be identified
• (1) translucent zone, the
advancing front of initial
demineralization;
• (2) dark zone, where the
previously liberated salts are
redeposited;
• (3) body of lesion, containing
the region of maximal
demineralization; and
• (4) surface zone, remaining
relatively unaffected until it is
sufficiently undermined to
collapse, resulting in
cavitation.
19. The early lesion
• The earliest visible changes are seen as a white opaque spot that
forms just adjacent to a contact point.
• The enamel is hard and smooth to the probe.
• The initial lesion is conical in shape with its apex towards the dentine,
and a series of four zones of differing translucency can be seen.
20.
21.
22. There is no more than a pinhole lesion in an occlusal pit, but cutting away
the surrounding enamel shows it to be widely undermined?
• Once bacteria have penetrated the enamel they reach the amelodentinal junction
and spread laterally to undermine the enamel.
• This has three major effects.
• 1. The enamel loses the support of the dentine and is therefore greatly
weakened.
• 2. It is attacked from beneath.
• 3. Spread of bacteria along the amelodentinal junction allows them to attack the
dentine over a wide area.
24. • The lesion is therefore conical with its apex towards the pulp.
• Dentin caries progresses at a much faster rate than enamel caries.
• It is more porous, because it contains dentinal tubules and is less
densely mineralized.
• For caries to progress in dentin, bacterial strains capable of producing
large amounts of proteolytic and hydrolytic enzymes are needed,
rather than the acid-producing types of enamel caries. Lactobacilli
may be important in dentine caries.
25. • Collections of bacteria in adjacent tubules coalesce to form irregular
liquefaction foci. These in turn coalesce to form progressively more
widespread tissue destruction.
• In some areas bacteria also spread laterally, and, occasionally, large
bacteria-filled clefts form at right angles to the general direction of
the tubules.
26. Why does dentin caries has a rapid course
and more pain in young patients?
• In the teeth of younger patients the dentinal
tubules are less densely mineralized,
• shorter in length, and
• wider in diameter, allowing for ease of penetration
and progression of the invading microorganisms.
• In older patients, deposits of calcifying salts
usually narrow the dentinal tubules, making the
teeth less porous. In addition,
• the dentin will be thicker because of the
production of additional normal and abnormal
secondary dentin on the pulpal walls.
Dentinal caries in younger patients
often quickly involves the pulpal
tissue, which produces an acute
inflammatory reaction and intense
pain.
in older patients it
has a slower course with intermittent
mild pain
27. HISTOPATHOLOGY
• Five microscopic zones that reveal the stages of dentinal caries that
eventuates in a cavity:
Zone 1, fatty degeneration :
The deepest zone, reflects the earliest changes of caries
infection where bacterial enzymes have advanced ahead
of the bacteria in the dentinal tubules, causing a
breakdown of the cell membranes of the organic
component of the dentin-liberating lipid.
Zone 2, translucent zone :
is a band of hypermineralized dentin in which the
dentinal tubules are sclerotic because of the
redeposition of calcifying salts released from the
demineralized zone.
Zone 3,
demineralization:
is composed of dentin
that is softer than
normal because of the
initial action of the
bacterial enzymes
Zone 4, brown
discoloration :
is due to a reduction in the
mineral content and the presence
of distended dentinal tubules
packed with bacteria. This zone is
usually soft enough to be
removed with a hand instrument.
Zone 5, cavitation :
Differs from the previous zone, because no
mineralization is present and the organic component
is partially dissolved by the bacteria. This zone is the
clinically observed base of a large cavity. It also has a
brown coloration and easily peels away in layers
along the incremental lines of growth.
28.
29. • In Zone 5 the tubules
will contain focal, dense
accumulations of
bacteria that form
liquefaction foci,
referred to as beading
(Figure 3-12, A). These
foci fuse horizontally,
producing transverse
clefts.
a large area of liquefaction of dentin caused by the
horizontal fusion of the focal accumulations
of bacteria within individual tubules (“transverse clefts”)
30. PULPITIS
An inflammation of the pulpal tissue that
may be acute or chronic, with or without symptoms, and
reversible or irreversible.
31. Acute pulpitis
• In the early stages the tooth is hypersensitive.
Very cold or hot food causes a stab of pain
which stops as soon as the irritant is removed.
As inflammation progresses, pain becomes
more persistent and there may be prolonged
attacks of toothache.
• The pain may start spontaneously, often when
the patient is trying to get to sleep.
• The pain is partly due to the pressure on the
irritated nerve endings by inflammatory
infiltrate within the rigid pulp chamber and
partly due to release of pain-producing
substances from the damaged tissue. The pain
at its worst is excruciatingly severe, sharp and
stabbing in character. It is little affected by
simple analgesics.
Acute pulpitis may be confined to one horn of the
coronal pulp (focal acute pulpitis) or involve the whole
pulp (total acute pulpitis).
most commonly found in the teeth of children and
adolescents.
The exudate remains within the enclosed chamber,
builds pressure, and quickly extends to all parts of
the healthy pulp.
An acute pulpitis can arise when the pulp becomes
suddenly overheated to the extent that the blood
vessels rupture, causing focal areas of hemorrhage.
This may occur during crown preparation, when
inadequate cooling does not accompany the high-
speed removal of the tooth structure.
32.
33. Acute closed pulpitis
• There is initial hyperaemia limited to the area immediately beneath
the irritant.
• Infiltration by inflammatory cells and destruction of odontoblasts and
adjacent mesenchyme follow.
• A limited areas of necrosis may result in formation of a minute
abscess, localised by granulation tissue.
• Inflammation spreads until the pulp is obliterated by dilated blood
vessels and acute inflammatory cells.
• Necrosis follows.
34. Pulpal abscess
• The core is composed of a purulent exudate consisting of polymorphonuclear leukocytes
against a background of fibrin, necrotic tissue debris, and extravasated red blood cells.
• A zone of granulation tissue consisting of newly formed capillary blood vessels, plump
fibroblasts, plasma cells, and lymphocytes surrounds this core.
The liberated autolytic
enzymes that result
from tissue destruction
and the exotoxins of the
invading bacteria quickly
spread to all parts of the
remaining healthy pulp
and eventually through
the apical foramen into
the adjacent periodontal
membrane.
Because of the
intenseness of the irritant
in the
form of virulent bacteria
and the lack of drainage
Purulent exudate
penetrates the cortical
bone surrounding
the apical periodontal
membrane and invades
the marrow
spaces of the medullary
bone
At this point the condition
represents a form of focal
acute suppurative
osteomyelitis.
35. Chronic pulpitis
• The pulps of individual teeth are not
precisely represented on the sensory
cortex.
• The pulp pain is therefore poorly
localized and may be felt in any of the
teeth of the upper or lower jaw of
the affected side. Rarely, pain may be
referred to a more distant site such
as the ear.
• Pulp pain is not provoked by pressure
on the tooth.
• Many pulps under large carious
cavities die painlessly.
• In other cases there are bouts of dull
pain, brought on by hot or cold
stimuli or coming on spontaneously.
There are often prolonged
remissions.
Chronic pulpitis occurs when there is little or no penetration into the
pulp by large numbers of the virulent types of bacteria.
Occurs often in older teeth, because they have restorations done or
sclerosis or reparative dentin.
On microscope: (Pulp fibrosis) presence of loose, delicate
connective tissue with bundles of dense collagen and a severe
reduction in both the size and number of the vascular structures and
peripheral nerves. A diffuse infiltrate of lymphocytes and plasma
cells exists throughout the pulp.
Pulp fibrosis pulp stones (spherical calcifications) or dystrophic
calcifications (linear calcifications) pulpal necrosis periapical
granuloma.
Periapical granuloma : indolent and asymptomatic, and it is composed
of a circumscribed nodule of fibrous tissue with a
mild infiltrate of lymphocytes and plasma cells.
36.
37. Chronic closed pulpitis
• Mononuclear cell infiltrate.
• A small area of pulpal necrosis and pus formation may be localised by
a well-defined wall of granulation tissue, and a minute abscess may
form.
• The remainder of the pulp may then appear normal.
• Partial calcific barrier forms beneath the lesion.
• Or reactionary dentine continue to form round the opening.
• This may allow preservation of the remainder of the pulp.
• Pulp death is the end result.
38.
39.
40. Open pulpitis
• The pulp survives but is chronically inflamed, beneath a wide
exposure, despite the heavy infection.
• Associated with open apices which allow an adequate blood supply.
42. • Chronic hyperplastic pulpitis
• a rare condition that is primarily confined
to the molars of children. result of
rampant acute caries in young teeth.
• The combination of an open chronic
pulpitis, an ample blood supply, and the
increased regenerative capacity of young
pulpal tissue appear, in some instances, to
stimulate the pulpal tissue to proliferate or
to produce granulation tissue.
• a surface layer of stratified squamous
epithelium.
• pulpal tissue may undergo excessive
overgrowth (hyperplasia) and project out
of the crown of the tooth.
Because this lesion clinically
projects from the pulpal chamber, it is
commonly referred to as a pulp polyp.
Clinically, a pulp polyp appears as a
dusky red or pinkish soft nodule
protruding into the cavity. It is
painless but may be tender and bleed
on probing
These lesions produce no symptoms
because they are said to be deficient
in nerve fibers.
The usual treatment of a tooth with a
pulp polyp is extraction.
43.
44. REVERSIBLE PULPITIS
The diagnosis of reversible pulpitis implies that the pulp is
capable of a full recovery if the irritating factors subside or are
removed.
Vasodilation, some transudation, a slight infiltrate of
lymphocytes, and disruption of the odontoblastic layer.
The pain of reversible pulpitis is sharp and intense and
responds to a sudden change in temperature.
The pain generally remains for 5 to 10 minutes and seldom lasts
longer than 20 minutes.
Changes in the position of the body, such as lying down, do not
generally affect the nature or the duration of the pain.
Treatment: prevention from further thermal stimulation, and
placing sedative dressings in the base of carious defect.
45.
46. IRREVERSIBLE PULPITIS
Pulp will most likely not recover
The pulpal tissue will exhibit a wide spectrum of acute
and chronic inflammatory changes.
The remaining pulp must be removed or the tooth
must be extracted.
Pain is less intense.
Pain is spontaneously initiated, not the result of a
sudden temperature changes.
It lasts for a prolonged period, usually longer than 20
minutes.
The pain may be initiated or accentuated when the
patient reclines.
The pain from an irreversible pulpitis may be referred
to another nearby location
47.
48. PULPAL NECROSIS
• In pulpal necrosis the pulpal tissue may be infected with bacteria.
Infected pulpal necrosis is usually the result of dental decay, in which
case the infection can quickly extend into the apical areas of the tooth
and the surrounding bone. These occurrences produce a great deal of
pain and other systemic reactions.
• Noninfected (aseptic) pulpal necrosis usually occurs after a traumatic
incident and may not produce symptoms for many months. The first
sign of noninfected pulpal necrosis may be a change in the coloration
of the tooth.
49. • Change in tooth color due to pulpal necrosis:
• This is the result of the decomposing tissue debris and breakdown
products of the red blood cells entering the open ends of the empty
dentinal tubules and becoming distributed throughout the dentin.
This process alters the translucency of the tooth. After the tooth has
become nonvital, it loses its ability to rehydrate the dentin, making it
more brittle and subject to cracks and fractures.
50. • Pain due to inflammatory
response in the apical periodontal
membrane.
• Tooth may extrude from the
socket causing premature contact
with opposing teeth.
A diagnostic tool used to
determine if a tooth has
undergone pulpal necrosis
consists of gently tapping on
several teeth in the area with
a blunt instrument.
A tooth that has undergone
pulpal necrosis will be
identified, because the
pressure from the tapping will
produce intense pain. This is
referred to as the percussion
test.
51. COMMON DIAGNOSTIC TECHNIQUES
• The diagnostic procedures that are commonly used to assess the
status of a symptomatic tooth and pulp are as follows:
• 1. History and nature of pain
• 2. Reaction to thermal changes
• 3. Reaction to mild electric stimulation
• 4. Reaction to tooth percussion
• 5. Radiographic examination
• 6. Visual clinical examination
• 7. Palpation of surrounding area
53. The four major factors follow:
• 1. Presence of an open or
closed pulpitis
• 2. Virulence of the involved
microorganisms
• 3. Extent of sclerosis of the
dentinal tubules
• 4. Competency of the host
immune response
54. CHRONIC APICAL PERIODONTITIS
Extension of the inflammatory process from the pulpal chamber into
the adjacent periodontal membrane around the apical foramen.
A positive reaction to a percussion test.
A transitory phase between pulpitis and the more distinct forms of
periapical lesions.
55. PERIAPICAL GRANULOMA
a pulpitis progresses into a
periapical lesion, pulpal
necrosis
drainage of the exudate is
inhibited, a
periapical granuloma can
be transformed into an
acute
periapical abscess
transformation into a
periapical cyst
56. RADIOGRAPHIC
FEATURES
• An oval or rounded
radiolucency with a
welldemarcated outline located
at the apex of the tooth.
• Possible findings:
hypercementosis of the apical
third of the root and
• resorption resulting in blunting
of the root tip.
57. HISTOPATHOLOGY
• an outer capsule of dense
fibrous tissue and a central
zone of granulation tissue.
• The central zone will often
contain macrophages with a
foamy cytoplasm caused by
phagocytized cholesterol.
• Some cholesterol crystals
may be present, surrounded
by multinucleated giant cells.
• Throughout, the soft tissue
will be a diffuse infiltrate of
lymphocytes and plasma
cells.
58. PERIAPICAL CYST
• Develops from untreated granuloma.
• The cyst’s epithelial lining is derived from the rests of Malassez.
• The rests are stimulated to proliferate by the low-grade inflammation
of the preceding periapical granuloma.
• The cyst may become inflamed and symptomatic.
• It can result in the destruction of a large portion of the maxilla or
mandible.
59. RADIOGRAPHIC FEATURES
• The periapical cyst is well circumscribed, often with a
distinct thin line of cortication separating it from the
surrounding bone.
• It may be associated with resorption of the apices of the
teeth, displacement of the roots, or both.
• It is distinctly rounded and unilocular and may become
very large, resulting in erosion of the inferior border and
bulging of the buccal and lingual cortical plates.
60.
61. HISTOPATHOLOGY
• Outer dense fibrous connective tissue capsule that
surrounds a central lumen containing a thick,
proteinaceous fluid and cellular debris.
• The lumen is lined by a nonkeratinized, stratified
squamous epithelium containing rete pegs that are
generally elongated and branched.
• Collections of cholesterol-laden macrophages are
commonly present.
• A diffuse infiltration of plasma cells and lymphocytes in
capsule and epithelial lining.
• Cholesterol crystals surrounded by foreign-body giant
cells.
• The presence of eosinophilic refractile hyaline bodies,
65. • The factors leading to the development of acute lesions at the apex
of a tooth:
• 1. Young tooth with open tubules
• 2. Rampant caries
• 3. Closed acute pulpitis
• 4. Presence of highly virulent microorganisms
• 5. Weakened host defense system
66. Inflammatory events happen quickly and
cause a great deal of pain
If unchecked, infection and
purulent exudate rapidly
spread throughout the
affected jaw into the
adjacent structures and
the systemic circulation
Emboli of the infection
could lodge in the small
capillaries of a number of
distant organs or anatomic
locations
67. PERIAPICAL ABSCESS
• It is a progression of an
acute pulpitis in which
exudate extends into the
adjacent soft and hard
tissues.
• Internal pressure causes
extrusion of the tooth from
the socket and rapid
extension of the exudate
throughout the underlying
medullary bone.
CLINICAL FEATURES
Pain, Temperature elevation and malaise are common.
The tooth associated with the abscess will extrude from
the socket.
Swelling and redness of the area
Although the tooth is relatively insensitive or
unresponsive to hot, cold, and electrical stimulation,
gently tapping on it produces intense pain.
Percussion test for diagnosis.
68. RADIOGRAPHIC FEATURES
• A slight widening of the apical periodontal space, with a gradual loss
of the distinctness of the adjacent alveolar bone (lamina dura).
• bone loss by exhibiting a faintness of the trabecular pattern and an
increased radiolucency.
69. HISTOPATHOLOGY
• An outer thin capsule of fibrous tissue is infiltrated with lymphocytes
and plasma cells.
• A wide zone of granulation tissue,
• containing a mixture of neutrophils, lymphocytes, plasma cells, and
macrophages,
• surrounds a
• central core of tissue that has undergone disintegration and
liquefaction and is composed of purulent exudate.
70. OSTEOMYELITIS
• An inflammatory
process within
medullary (trabecular)
bone that involves the
marrow spaces.
ACUTE OSTEOMYELITIS: A rapidly
destructive inflammatory
process within bone that consists of
granulation tissue,
purulent exudate, and islands of
nonvital bone (sequestra).
71. ACUTE OSTEOMYELITIS
• Acute osteomyelitis is a destructive lesion of the trabecular bone and
bone marrow of an acute inflammatory origin and usually contains
virulent strains of bacteria.
• Causes:
an untreated periapical abscess
osteoradionecrosis
72. CLINICAL FEATURES
intense pain and physical
illness.
a lack of drainage of
purulent exudate produces
a rapid increase in pain
with accompanying pyrexia
and malaise.
an alteration in the
conductivity of the inferior
alveolar nerve.
paresthesia of the lower lip
of the affected side.
73. RADIOGRAPHIC FEATURES
Initially the area is faintly visible and
eventually appears diffusely blotchy or
mottled with indistinct margins.
Islands of apparently intact bone are
often visible in central locations.
In reality, these fragments are dead,
nonresorbed bone surrounded by
wide zones of purulent exudate. An
island of dead bone is referred to as a
sequestrum.
74. CELLULITIS: A painful swelling of the
soft tissue of the mouth and face
resulting from a diffuse spreading of
purulent exudate along the fascial
planes that separate the muscle
bundles.
SINUS TRACT: A drainage pathway
from a deep focus
of acute infection through tissue,
bone, or both to an
opening on the surface.
PARULIS: A sessile nodule
on the gingiva at the site
where a draining sinus
tract reaches the surface.
FISTULA: A drainage
pathway or abnormal
communication between
two epithelium-lined
surfaces because of
destruction of the
intervening tissue.
75.
76.
77. • LUDWIG ANGINA: Cellulitis involving fascial spaces
• between muscles and other structures of the posterior floor
• of the mouth that can compromise the airway.
78. CELLULITIS
• Cellulitis is an acute condition in which purulent exudate, usually
accompanied by virulent forms of bacteria, involves the fascial planes
between the bundles of facial and perioral muscles.
• most commonly the result of extension of a periapical abscess into the soft
tissue.
exudate erodes through
the cortical plate of the
mandible or the maxilla
The erosion pathway
reaches the gingival
surface, it results in a
small nodule that
enlarges until it
ruptures.
The site of the opening
(stoma) of a sinus tract
on the gingiva is
commonly termed a
parulis
79. • Occasionally the exudate tracks onto the palate, producing a large
tumorlike mass.
80. Oroantral fistula
• When a periapical abscess erodes into the
maxillary sinus, destroying the intervening bone and
lining, and the offending tooth is extracted, a
communication between the floor of the sinus and the
oral cavity may result.
81. • When purulent exudate emanating from a periapical abscess
penetrates the alveolar bone and enters the muscle layers, the lytic
enzymes from the microorganisms and the acute inflammatory
process break down the fascia that normally surrounds and binds the
muscle bundles.
• This breakdown of the fascia allows the exudate to spread throughout
the immediate region, greatly increasing the magnitude of the
infection.
• These patients exhibit extensive swelling of the affected facial region,
have considerable discomfort or pain, and develop signs and
symptoms of systemic involvement such as elevated temperature,
malaise, lethargy, and lymphadenopathy.
82. Involvement of the soft tissue and
muscle overlying the maxilla usually
results in periocular swelling and
temporary loss of sight on the
affected side.
When the muscle layers overlying the body of
the mandible are involved, patients experience a
puffy, pendulous swelling on the left side of the
face, closely resembling mumps.
Exudate may extend lingually into the muscle
spaces of the posterior floor of the mouth. Such
a posterior progression can result in the swelling
of the structures in and around the epiglottis.
Tissue swelling in this area is life
threatening, because it can
restrict the airway and result in
suffocation if emergency
measures
are not undertaken immediately.
The presence of cellulitis
in these locations has historically
been referred
to as Ludwig angina.
83. Another serious complication of cellulitis is the
extension
of the exudate into the maxillary cavernous sinus
area, resulting in thrombophlebitis.
From this location
fatal forms of brain abscess or acute meningitis are
possible unless rapid intervention is undertaken.
84. CHRONIC OSTEOMYELITIS
• It occurs in response to a low-grade inflammatory process
rather than the intense and destructive inflammation caused by
virulent bacteria.
• Induces bone to form and become denser.
• little or no pain is felt.
• a reduction of the marrow spaces.
• The area will radiographically appear mottled and more
radiopaque than normal. This process is histologically referred
to as osteosclerosis.
85. • Location It may be confined
to an area around the root of
a tooth or be present where a
tooth previously existed.
• These localized changes in the
bone are referred to as focal
chronic sclerosing
osteomyelitis.
• In other instances the
osteosclerosis may involve
larger areas of bone or
edentulous areas in one or
more quadrants. These
conditions are referred to as
diffuse chronic sclerosing
88. • Garré osteomyelitis is an unusual hyperplastic reaction of the
periosteum to a chronic osteomyelitis of the posterior mandible that is
unique to young patients.
• Also known as chronic osteomyelitis with proliferative periostitis.
89. • Associated with advanced acute caries in young patients that has
progressed to pulpitis and a periapical lesion.
• Periosteum is stimulated to thicken and lay down excess layers of
new bone.
• Cause: food impaction of the deepened gingival sulcus; a constant
lowgrade infection persists that stimulates the periosteum.
• Patients are in the age group that occurs shortly before the mixed
dentition stage or immediately afterward.
• The other common cause of this unique process is a molar that is
unable to fully erupt.
90. Upon palpation the area will be as hard as the normal surrounding bone,
and the patient will not exhibit pain when the area is slightly palpated.
The area is usually asymptomatic.
91. • RADIOGRAPHIC FEATURES
• The characteristic multiple thin layers of new bone, referred to as an
“onion skin” appearance.
• The trabecular bone will also exhibit the characteristic diffuse mottling of
mottling of a chronic osteomyelitis.
• HISTOPATHOLOGY
• The microscopic features of the reactive bone that forms in response
to the stimulated periosteum is less dense than normal cortical bone
and deposited in a layered pattern.
• The trabecular spaces are wide and occupied with a cellular
connective tissue.
92.
93. TREATMENT
The condition slowly reverts to normal after the source of infection is
identified and resolved.
Sometimes extraction of the offending tooth.
Surgical recontouring of the tissue in the molar area is necessary.
94. References
• Contemporary Oral and Maxillofacial Pathology - 2nd Edition
• Cawson's Essentials of Oral Pathology and Oral Medicine