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.
Everything a dentist needs to know about a periodontal abscess is here.
Along with all the relevant facts, references, definitions, classifications, and each and every statement is given with proper detail
Dental caries leads to changes in the enamel and dentin, including tubular sclerosis, reactionary dentine, and dead tracts formation. Left untreated, dental caries can cause pulpitis, which involves inflammation of the pulp and can be reversible, acute, or chronic. Pulpitis and pulp necrosis can further lead to apical periodontitis, periapical abscess, osteomyelitis, or cellulitis as the infection spreads. Advanced stages include formation of a periapical cyst, bone destruction, and soft tissue infection.
This document discusses various classifications and types of periapical diseases including symptomatic and asymptomatic apical periodontitis, acute alveolar abscess, phoenix abscess, persistent apical periodontitis, chronic alveolar abscess, radicular cyst, condensing osteitis, and different types of external and internal root resorption. It provides definitions, causes, symptoms, diagnostic features and treatment options for each condition.
This document discusses gingival inflammation and gingivitis. It begins by defining inflammation and describing the cardinal signs. It then outlines the stages of gingivitis from initial to established to advanced/periodontitis. Microorganisms attached to teeth secrete enzymes that damage tissues and widen junctional epithelium, allowing bacterial products to access connective tissue and activate immune cells. Studies showed that not practicing oral hygiene led to plaque buildup and gingivitis within 10-21 days. Gingivitis is characterized by redness, swelling, bleeding and is prevalent worldwide. The document discusses features, course, distribution and systemic influences of gingival inflammation.
This document provides an overview of pulp and periapical pathologies. It begins by defining the dental pulp and pulpitis. It then covers causes of pulp disease including physical, chemical, and bacterial factors. It classifies pulp disease and discusses factors affecting the pulp response. It details the pathways of bacterial invasion of the pulp and describes different types of reversible and irreversible pulpitis. It also discusses chronic hyperplastic pulpitis, gangrenous necrosis of the pulp, and diseases of the periapical tissues like acute and chronic apical periodontitis and periapical abscess.
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.
Everything a dentist needs to know about a periodontal abscess is here.
Along with all the relevant facts, references, definitions, classifications, and each and every statement is given with proper detail
Dental caries leads to changes in the enamel and dentin, including tubular sclerosis, reactionary dentine, and dead tracts formation. Left untreated, dental caries can cause pulpitis, which involves inflammation of the pulp and can be reversible, acute, or chronic. Pulpitis and pulp necrosis can further lead to apical periodontitis, periapical abscess, osteomyelitis, or cellulitis as the infection spreads. Advanced stages include formation of a periapical cyst, bone destruction, and soft tissue infection.
This document discusses various classifications and types of periapical diseases including symptomatic and asymptomatic apical periodontitis, acute alveolar abscess, phoenix abscess, persistent apical periodontitis, chronic alveolar abscess, radicular cyst, condensing osteitis, and different types of external and internal root resorption. It provides definitions, causes, symptoms, diagnostic features and treatment options for each condition.
This document discusses gingival inflammation and gingivitis. It begins by defining inflammation and describing the cardinal signs. It then outlines the stages of gingivitis from initial to established to advanced/periodontitis. Microorganisms attached to teeth secrete enzymes that damage tissues and widen junctional epithelium, allowing bacterial products to access connective tissue and activate immune cells. Studies showed that not practicing oral hygiene led to plaque buildup and gingivitis within 10-21 days. Gingivitis is characterized by redness, swelling, bleeding and is prevalent worldwide. The document discusses features, course, distribution and systemic influences of gingival inflammation.
This document provides an overview of pulp and periapical pathologies. It begins by defining the dental pulp and pulpitis. It then covers causes of pulp disease including physical, chemical, and bacterial factors. It classifies pulp disease and discusses factors affecting the pulp response. It details the pathways of bacterial invasion of the pulp and describes different types of reversible and irreversible pulpitis. It also discusses chronic hyperplastic pulpitis, gangrenous necrosis of the pulp, and diseases of the periapical tissues like acute and chronic apical periodontitis and periapical abscess.
The document discusses dental stains, which can be extrinsic or intrinsic in nature. Extrinsic stains are located on the tooth surface and caused by external factors like plaque, foods/beverages, tobacco, and medications. Intrinsic stains are within the tooth structure due to conditions, materials, medications, and genetic/hereditary factors. Treatment depends on the specific cause and may include cleaning, bleaching, restorations, or consulting medical experts in case of underlying systemic issues. Maintaining good oral hygiene can help prevent extrinsic staining.
The document discusses different types of cysts that can occur in the oral region, dividing them into odontogenic cysts and non-odontogenic cysts. Odontogenic cysts include radicular, dentigerous, primordial, odontogenic keratocyst, and lateral periodontal cysts. Non-odontogenic cysts include globulomaxillary, nasolabial, median palatal, and nasopalatine canal cysts. Each cyst type is described in terms of etiology, clinical features, radiographic appearance, histology, and treatment.
This document provides an overview of periodontal instruments, including their classification, parts, materials used, and specific uses. It describes various assessment instruments like mouth mirrors and probes, as well as therapeutic instruments such as scalers, curettes, files, chisels, and surgical tools. The key instruments discussed in detail include mirrors, probes, explorers, sickle scalers, and curettes. It explains the design and uses of each instrument in assessing and treating periodontal disease.
This document outlines the components of a case history for prosthodontic treatment planning. It discusses collecting patient information such as name, age, sex, occupation, etc. It also describes examining the patient extraorally and intraorally, including assessing facial form, lip support, the temporomandibular joint, and neuromuscular function. Taking a thorough case history and clinical examination allows the clinician to determine the patient's diagnosis and develop an appropriate treatment plan.
This document discusses various dental conditions including attrition, abrasion, erosion, abfraction, fractures, enamel hypoplasia, and discoloration. It provides details on the causes, clinical features, and characteristics of each condition. Attrition is defined as wear from tooth-to-tooth contact, while abrasion is caused by direct friction from external objects. Erosion involves chemical dissolution of tooth structure from acids. Abfraction results from biomechanical forces causing flexure and fatigue away from the point of loading. Enamel hypoplasia occurs when enamel formation is disrupted, resulting in pits or grooves in the enamel surface.
Odontogenic keratocyst (OKC) is the cyst arising from the cell rests of dental lamina. It can occur anywhere in the jaw, but commonly seen in the posterior part of the mandible. Radiographically, most OKCs are unilocular when presented at the periapex and can be mistaken for radicular or lateral periodontal cyst.
This document discusses several conditions related to abnormalities in dentin formation, including dentinogenesis imperfecta and dentin dysplasia. It describes the genetic basis, clinical and radiographic features, classifications, and histopathological characteristics of these inherited disorders. The key features include opalescent or discolored teeth, bulbous crowns, thin dentin, enlarged pulp chambers, shortened roots, and premature tooth loss. Classification systems include those proposed by Shields and Witkop. Treatment may involve extraction and dental prosthetics due to poor cosmetic outcomes and functional complications.
The periodontium consists of the gingiva, periodontal ligament, root cementum, and alveolar bone. The gingiva is pink, firm, and resilient with a stippled surface. It consists of masticatory mucosa and protects the underlying periodontal tissues. The periodontal ligament is a soft, vascular connective tissue that surrounds tooth roots and connects the cementum to alveolar bone. It provides support, absorbs shock, senses function, and facilitates nutrient exchange between the tooth and bone.
This document discusses various pulpal diseases, their causes, symptoms and treatment. It covers reversible and irreversible pulpitis caused by physical, chemical and bacterial factors. It also covers chronic hyperplastic pulpitis, characterized by a fleshy pulpal mass filling the pulp chamber. Internal resorption is discussed as an idiopathic resorptive process in the dentin and root canals, often asymptomatic with a history of trauma. Classification schemes and histopathological features of different pulpal conditions are also presented.
Radicular cysts originate from epithelial cell rests of Malassez and form through three phases: initiation, cyst formation, and growth/enlargement. They are usually painless unless infected and associated with nonvital teeth. Calcifying odontogenic cysts contain ghost cells, which represent abnormal keratinization and have an affinity for calcification. They may also induce dental tissue formation. Keratocystic odontogenic tumors initiate from dental lamina proliferation and enlarge through factors like osmolality, inflammatory exudate, glycosaminoglycans, and collagenolytic/bone resorbing molecules. Their thin fragile linings and intrinsic growth potential contribute to high recurrence rates.
Definition of pulpitis, Factors causing injury to the pulp, aerodontalgia, classification of pulpitis, clinical features of various types of pulpitis, histopathology and its treatment are inlisted in this presentation.
The document discusses various conditions that can affect the tooth pulp and surrounding structures. It describes the normal anatomy of the pulp and defines different types of pulpitis. It then outlines several pathological conditions such as pulp necrosis, pulp polyps, periapical abscess, granuloma, and cysts. For each condition, it provides details on clinical features and radiographic appearances seen on dental imaging.
This document discusses various non-carious lesions of teeth including attrition, abrasion, erosion, abfraction, dentinal sclerosis, dead tracts, secondary dentin, pulp stones, hypercementosis, and cementicles. It defines each lesion, describes the etiology and pathogenesis, and highlights key clinical features. Attrition is mechanical wear of teeth from tooth contact while abrasion is caused by external frictional forces. Erosion results from chemical dissolution of tooth structure by acids. Abfraction involves stress-induced cervical lesions. Dentinal sclerosis and dead tracts are age-related changes in dentin. Secondary dentin deposition occurs in response to stimuli. Pulp stones, hypercementosis and
Tooth wear can occur through abrasion, attrition, erosion, and abfraction. Abrasion involves foreign objects rubbing teeth, while attrition is tooth-to-tooth contact. Erosion is acid etching of teeth and abfraction involves microfractures from occlusal stresses. Diagnosis involves examining location, appearance, and progression of tooth wear. Management focuses on controlling factors, restoring function and aesthetics, and using materials like composites and night guards to minimize further wear. Ongoing maintenance appointments are needed to monitor wear and refurbish restorations as the condition is progressive.
The document discusses bone loss patterns in periodontal disease. It notes that the balance between bone formation and resorption maintains bone height and density under normal conditions. The most common cause of bone destruction in periodontal disease is the extension of gingival inflammation into the supporting bone and tissues. This can lead to horizontal bone loss when inflammation travels along the bone crest or vertical bone loss when it travels directly into the periodontal ligament space. Bone destruction patterns include osseous craters in the interdental bone, bulbous bone contours, reversed architecture with loss of interdental bone, and furcation involvement in multi-rooted teeth.
This document discusses pin-retained amalgam restorations for teeth with extensive caries or fractures. It describes the advantages as conserving tooth structure and providing increased resistance and retention compared to cast restorations. Potential disadvantages include dentinal microfractures, microleakage, and decreased amalgam strength. Factors that affect pin retention such as pin type, size, orientation, and number are examined. Guidelines for cavity preparation and pin placement based on tooth anatomy and pulp location are provided. Common problems and their solutions are also outlined.
Dr. Ahmed M. Adawy
Professor Emeritus, Dep. Oral & Maxillofacial Surg.
Former Dean, Faculty of Dental Medicine
Al-Azhar University. By definition, a cyst is a “pouch” or sac without an opening, provided with a distinct membrane, and containing fluid or semifluid material, abnormally developed in one of the natural cavities or in the substance of an organ. Cysts of the oral region may be epithelial or non-epithelial, odontogenic or non-odontogenic, developmental, or inflammatory in origin. The distribution of jaw cysts according to diagnosis in a general population is given. The treatment of choice is dependent on the size and localization of the lesion, the bone integrity of the cystic wall, its proximity to vital structures and patient age.Treatment modalities are discussed.
Burs, mirrors, probes and excavators are used to prepare the access cavity and remove pulp tissue. K-files, reamers, and Hedstrom files are used to shape the root canal in a twisting motion. NiTi files are used to initially flare canals. Gates Glidden drills and Peeso reamers further widen canals. Irrigation, paper points and gutta percha are used to clean canals and conduct root canal fillings. Spreaders and pluggers are used to condense gutta percha during filling.
The document summarizes information about periapical cysts, also known as radicular cysts or apical cysts. It defines a periapical cyst as an odontogenic cyst derived from cell rests of Malassez that proliferate in response to inflammation from pulpal necrosis. Periapical cysts typically present as round radiolucencies associated with the apex of a non-vital tooth. Histologically, they contain a lumen lined by stratified squamous epithelium and surrounded by a fibrous connective tissue wall. Treatment involves extraction of the involved tooth along with cyst enucleation or marsupialization.
This document discusses various developmental cysts that can occur in the oral and maxillofacial region. It provides details on the location, cause, clinical features, radiographic features, histological features, treatment and prognosis for different cysts such as palatal cyst of newborn, nasolabial cyst, globullomaxillary cyst, nasopalatine duct cyst, median palatal cyst, median mandibular cyst, epidermoid cyst, dermoid cyst, thyroglossal duct cyst, branchial cleft cyst, and oral lymphoepithelial cyst.
The document discusses dental stains, which can be extrinsic or intrinsic in nature. Extrinsic stains are located on the tooth surface and caused by external factors like plaque, foods/beverages, tobacco, and medications. Intrinsic stains are within the tooth structure due to conditions, materials, medications, and genetic/hereditary factors. Treatment depends on the specific cause and may include cleaning, bleaching, restorations, or consulting medical experts in case of underlying systemic issues. Maintaining good oral hygiene can help prevent extrinsic staining.
The document discusses different types of cysts that can occur in the oral region, dividing them into odontogenic cysts and non-odontogenic cysts. Odontogenic cysts include radicular, dentigerous, primordial, odontogenic keratocyst, and lateral periodontal cysts. Non-odontogenic cysts include globulomaxillary, nasolabial, median palatal, and nasopalatine canal cysts. Each cyst type is described in terms of etiology, clinical features, radiographic appearance, histology, and treatment.
This document provides an overview of periodontal instruments, including their classification, parts, materials used, and specific uses. It describes various assessment instruments like mouth mirrors and probes, as well as therapeutic instruments such as scalers, curettes, files, chisels, and surgical tools. The key instruments discussed in detail include mirrors, probes, explorers, sickle scalers, and curettes. It explains the design and uses of each instrument in assessing and treating periodontal disease.
This document outlines the components of a case history for prosthodontic treatment planning. It discusses collecting patient information such as name, age, sex, occupation, etc. It also describes examining the patient extraorally and intraorally, including assessing facial form, lip support, the temporomandibular joint, and neuromuscular function. Taking a thorough case history and clinical examination allows the clinician to determine the patient's diagnosis and develop an appropriate treatment plan.
This document discusses various dental conditions including attrition, abrasion, erosion, abfraction, fractures, enamel hypoplasia, and discoloration. It provides details on the causes, clinical features, and characteristics of each condition. Attrition is defined as wear from tooth-to-tooth contact, while abrasion is caused by direct friction from external objects. Erosion involves chemical dissolution of tooth structure from acids. Abfraction results from biomechanical forces causing flexure and fatigue away from the point of loading. Enamel hypoplasia occurs when enamel formation is disrupted, resulting in pits or grooves in the enamel surface.
Odontogenic keratocyst (OKC) is the cyst arising from the cell rests of dental lamina. It can occur anywhere in the jaw, but commonly seen in the posterior part of the mandible. Radiographically, most OKCs are unilocular when presented at the periapex and can be mistaken for radicular or lateral periodontal cyst.
This document discusses several conditions related to abnormalities in dentin formation, including dentinogenesis imperfecta and dentin dysplasia. It describes the genetic basis, clinical and radiographic features, classifications, and histopathological characteristics of these inherited disorders. The key features include opalescent or discolored teeth, bulbous crowns, thin dentin, enlarged pulp chambers, shortened roots, and premature tooth loss. Classification systems include those proposed by Shields and Witkop. Treatment may involve extraction and dental prosthetics due to poor cosmetic outcomes and functional complications.
The periodontium consists of the gingiva, periodontal ligament, root cementum, and alveolar bone. The gingiva is pink, firm, and resilient with a stippled surface. It consists of masticatory mucosa and protects the underlying periodontal tissues. The periodontal ligament is a soft, vascular connective tissue that surrounds tooth roots and connects the cementum to alveolar bone. It provides support, absorbs shock, senses function, and facilitates nutrient exchange between the tooth and bone.
This document discusses various pulpal diseases, their causes, symptoms and treatment. It covers reversible and irreversible pulpitis caused by physical, chemical and bacterial factors. It also covers chronic hyperplastic pulpitis, characterized by a fleshy pulpal mass filling the pulp chamber. Internal resorption is discussed as an idiopathic resorptive process in the dentin and root canals, often asymptomatic with a history of trauma. Classification schemes and histopathological features of different pulpal conditions are also presented.
Radicular cysts originate from epithelial cell rests of Malassez and form through three phases: initiation, cyst formation, and growth/enlargement. They are usually painless unless infected and associated with nonvital teeth. Calcifying odontogenic cysts contain ghost cells, which represent abnormal keratinization and have an affinity for calcification. They may also induce dental tissue formation. Keratocystic odontogenic tumors initiate from dental lamina proliferation and enlarge through factors like osmolality, inflammatory exudate, glycosaminoglycans, and collagenolytic/bone resorbing molecules. Their thin fragile linings and intrinsic growth potential contribute to high recurrence rates.
Definition of pulpitis, Factors causing injury to the pulp, aerodontalgia, classification of pulpitis, clinical features of various types of pulpitis, histopathology and its treatment are inlisted in this presentation.
The document discusses various conditions that can affect the tooth pulp and surrounding structures. It describes the normal anatomy of the pulp and defines different types of pulpitis. It then outlines several pathological conditions such as pulp necrosis, pulp polyps, periapical abscess, granuloma, and cysts. For each condition, it provides details on clinical features and radiographic appearances seen on dental imaging.
This document discusses various non-carious lesions of teeth including attrition, abrasion, erosion, abfraction, dentinal sclerosis, dead tracts, secondary dentin, pulp stones, hypercementosis, and cementicles. It defines each lesion, describes the etiology and pathogenesis, and highlights key clinical features. Attrition is mechanical wear of teeth from tooth contact while abrasion is caused by external frictional forces. Erosion results from chemical dissolution of tooth structure by acids. Abfraction involves stress-induced cervical lesions. Dentinal sclerosis and dead tracts are age-related changes in dentin. Secondary dentin deposition occurs in response to stimuli. Pulp stones, hypercementosis and
Tooth wear can occur through abrasion, attrition, erosion, and abfraction. Abrasion involves foreign objects rubbing teeth, while attrition is tooth-to-tooth contact. Erosion is acid etching of teeth and abfraction involves microfractures from occlusal stresses. Diagnosis involves examining location, appearance, and progression of tooth wear. Management focuses on controlling factors, restoring function and aesthetics, and using materials like composites and night guards to minimize further wear. Ongoing maintenance appointments are needed to monitor wear and refurbish restorations as the condition is progressive.
The document discusses bone loss patterns in periodontal disease. It notes that the balance between bone formation and resorption maintains bone height and density under normal conditions. The most common cause of bone destruction in periodontal disease is the extension of gingival inflammation into the supporting bone and tissues. This can lead to horizontal bone loss when inflammation travels along the bone crest or vertical bone loss when it travels directly into the periodontal ligament space. Bone destruction patterns include osseous craters in the interdental bone, bulbous bone contours, reversed architecture with loss of interdental bone, and furcation involvement in multi-rooted teeth.
This document discusses pin-retained amalgam restorations for teeth with extensive caries or fractures. It describes the advantages as conserving tooth structure and providing increased resistance and retention compared to cast restorations. Potential disadvantages include dentinal microfractures, microleakage, and decreased amalgam strength. Factors that affect pin retention such as pin type, size, orientation, and number are examined. Guidelines for cavity preparation and pin placement based on tooth anatomy and pulp location are provided. Common problems and their solutions are also outlined.
Dr. Ahmed M. Adawy
Professor Emeritus, Dep. Oral & Maxillofacial Surg.
Former Dean, Faculty of Dental Medicine
Al-Azhar University. By definition, a cyst is a “pouch” or sac without an opening, provided with a distinct membrane, and containing fluid or semifluid material, abnormally developed in one of the natural cavities or in the substance of an organ. Cysts of the oral region may be epithelial or non-epithelial, odontogenic or non-odontogenic, developmental, or inflammatory in origin. The distribution of jaw cysts according to diagnosis in a general population is given. The treatment of choice is dependent on the size and localization of the lesion, the bone integrity of the cystic wall, its proximity to vital structures and patient age.Treatment modalities are discussed.
Burs, mirrors, probes and excavators are used to prepare the access cavity and remove pulp tissue. K-files, reamers, and Hedstrom files are used to shape the root canal in a twisting motion. NiTi files are used to initially flare canals. Gates Glidden drills and Peeso reamers further widen canals. Irrigation, paper points and gutta percha are used to clean canals and conduct root canal fillings. Spreaders and pluggers are used to condense gutta percha during filling.
The document summarizes information about periapical cysts, also known as radicular cysts or apical cysts. It defines a periapical cyst as an odontogenic cyst derived from cell rests of Malassez that proliferate in response to inflammation from pulpal necrosis. Periapical cysts typically present as round radiolucencies associated with the apex of a non-vital tooth. Histologically, they contain a lumen lined by stratified squamous epithelium and surrounded by a fibrous connective tissue wall. Treatment involves extraction of the involved tooth along with cyst enucleation or marsupialization.
This document discusses various developmental cysts that can occur in the oral and maxillofacial region. It provides details on the location, cause, clinical features, radiographic features, histological features, treatment and prognosis for different cysts such as palatal cyst of newborn, nasolabial cyst, globullomaxillary cyst, nasopalatine duct cyst, median palatal cyst, median mandibular cyst, epidermoid cyst, dermoid cyst, thyroglossal duct cyst, branchial cleft cyst, and oral lymphoepithelial cyst.
Mediastinal cysts are uncommon and comprise 15-20% of mediastinal masses. Common cysts include thymic, parathyroid, pericardial, foregut duplication (bronchogenic, esophageal), neuroenteric, teratoma, cystic lymphangiomas, and meningoceles. Cysts are evaluated based on age, location, radiological findings, gross appearance, microscopy, and epithelium/tissue presence. Thymic cysts are the most common and can be unilocular or multilocular. Parathyroid cysts are derived from the third/fourth pharyngeal pouch. Foregut cysts contain respiratory epithelium and cartilage. Ter
Osteomyelitis is an inflammatory process of bone caused by microbial infection. It can be acute, subacute, or chronic depending on duration. Common causes include hematogenous spread from other infections as well as direct introduction through open fractures or wounds. In acute osteomyelitis, infection starts in the metaphysis and can spread through bone canals, potentially crossing the growth plate in children. Chronic osteomyelitis results from inadequate treatment of acute infection and is characterized by persistent infection, bone necrosis, and sinus tract formation. Staging systems help classify osteomyelitis based on extent of bone and soft tissue involvement.
Osteomyelitis is an inflammation of bone and bone marrow caused by an infecting organism. It can be classified based on duration, mechanism of infection, anatomical involvement, and host factors. Acute hematogenous osteomyelitis most commonly affects the metaphysis of long bones in children under 2 years old. It is caused by hematogenous spread from another infection and presents with fever, pain, and swelling as the infection destroys bone and spreads. Proper classification and treatment is important to prevent complications like bone deformity, joint involvement, and chronic infection.
- Cysts are fluid-filled cavities lined by epithelium that form in the body. They commonly occur in the jaws.
- The pathogenesis of cysts is often uncertain, but they may form from cell rests left over from tooth development that proliferate in response to inflammation or other stimuli.
- Cysts enlarge through cellular proliferation, accumulation of fluid secretions, and bone resorption in response to increased internal fluid pressure.
The document discusses several types of non-odontogenic cysts that develop in the oral cavity. It describes nasopalatine duct cysts, which originate from remnants of the nasopalatine duct in the maxilla. These cysts typically appear as well-defined radiolucencies between the central incisors. Median palatal cysts and globulomaxillary cysts are also discussed, which develop from epithelial remnants during fusion of facial processes. Palatal cysts of newborns are extraosseous cysts that commonly appear on the hard palate of infants.
This document discusses and classifies various cysts of the jaws and neck. It describes 9 main odontogenic cysts including radicular, lateral periodontal, dentigerous, and calcifying odontogenic cysts. It also discusses non-odontogenic cysts such as nasolabial and nasopalatine canal cysts as well as pseudocysts like aneurysmal bone cyst and traumatic bone cyst. Finally, it summarizes 3 main soft tissue cysts of the neck - branchial, dermoid, and thyroglossal tract cysts.
This document provides an overview of salivary gland diseases. It discusses the major and minor salivary glands and their secretions. Functional disorders and diseases that can affect salivary gland secretion include xerostomia (dry mouth) and ptyalism (excessive salivation). Causes and classifications of salivary gland diseases are described, including developmental disorders, inflammatory conditions like sialadenitis, obstructive diseases, autoimmune disorders like Sjogren's syndrome, and neoplastic diseases. Specific conditions discussed in more detail include acute and chronic bacterial sialadenitis, viral sialadenitis, salivary calculi, cysts, ranula, and Sjogren's syndrome
This document summarizes various intestinal and tissue parasites that can infect humans through contaminated food or water. It describes the clinical presentations, locations of infection, and histopathological findings for parasites such as Giardia lamblia, Strongyloides stercoralis, hookworm, Trichuris trichura, Cryptosporidium, Enterobius vermicularis, Entamoeba histolytica, Anisakis, Trichinella spiralis, Dracunculus medinensis, Schistosoma species, Echinococcus granulosus, Taenia saginata, cysticercosis, and filarial worms. Definitive diagnosis of many parasitic infections requires identification of eggs,
This document discusses cysts of the jaw, beginning with definitions and classifications. It describes Shear's classification system for cysts, as well as the WHO 1992 classification system, which categorizes cysts as epithelial, non-epithelial, odontogenic, non-odontogenic, and soft tissue cysts. The pathogenesis section explains the processes of cyst initiation, formation, and enlargement, which involves cell proliferation, increased fluid volume and pressure, and bone resorption. Signs and symptoms include pain, swelling, tooth displacement, and pathological bone changes visible on radiographs.
This document provides an overview of cysts of the oral facial region, including:
- Definitions of cysts and their growth mechanisms.
- Classification systems based on location, pathogenesis, cell type, epithelial tissues. The main types discussed are radicular cysts, dentigerous cysts, and keratocysts.
- Clinical features such as swelling, tooth displacement, pain, and effects on bone. Diagnosis involves radiographic and microscopic examination of cyst contents.
- Management typically involves enucleation or marsupialization. Additional techniques like cryosurgery are used for keratocysts due to their high recurrence rate.
Acute appendicitis is caused by obstruction of the appendix lumen, which increases intraluminal pressure and leads to ischemic injury and bacterial proliferation. On gross examination, early appendicitis shows swelling and redness while advanced cases show necrosis, ulceration and gangrenous changes. Microscopically, early appendicitis is characterized by neutrophilic infiltration of the muscularis propria, while late stages show mucosal sloughing, wall necrosis, and thrombosed vessels. Acute appendicitis is commonly caused by obstruction from fecaliths or lymphoid hyperplasia and presents as abdominal pain.
Acute appendicitis is caused by obstruction of the appendix lumen, usually by a fecalith, which increases intraluminal pressure and compromises blood flow. This leads to ischemic injury and bacterial proliferation, causing inflammation. Clinically, it presents with abdominal pain that starts around the umbilicus and later localizes to the right lower quadrant, along with nausea, fever, and tenderness. Without treatment, complications can include perforation leading to peritonitis or abscess formation. Pathologically, acute appendicitis is characterized by neutrophilic infiltration of the muscularis propria. Rare tumors of the appendix include carcinoid tumors and adenocarcinomas.
This document summarizes the structure and function of cartilage and bone. It describes the main types of cartilage, including hyaline cartilage, elastic cartilage, and fibrocartilage. It also discusses the cells, matrix, and growth of cartilage. Regarding bone, it outlines the organic and inorganic components of bone matrix, and the cells involved in bone formation and resorption, including osteoblasts, osteocytes, and osteoclasts. It also summarizes the different types of bone and bone growth processes.
This document provides an overview of normal breast anatomy and histology, as well as benign and pre-malignant breast lesions. It begins with the definition and etiology of the breast. The normal histology includes two epithelial cell types that line ducts and lobules, as well as the basement membrane and stromal tissue. Common benign breast conditions are then described, such as fibrocystic changes, adenosis, papillomas, and radial scars. Proliferative breast disease and atypical hyperplasias are covered as pre-malignant lesions. Risk factors for breast cancer and the lifetime risk associated with different lesion types are also summarized.
Hydatid cyst disease of the liver الدكتور طارق المنيزل Tariq Al munaizel
Echinococcus granulosus is a parasitic tapeworm that causes hydatid disease (hydatidosis) in humans. Its life cycle involves carnivores as definitive hosts and herbivores as intermediate hosts. Humans can be infected by ingesting E. granulosus eggs from a definitive host. The larvae develop into hydatid cysts, most commonly in the liver. Hydatid cysts can cause symptoms from pressure or complications like rupture. Diagnosis involves imaging and serology. Treatment depends on cyst type and complications but may include surgery, percutaneous drainage, or antiparasitic drugs.
This document discusses cysts of the jaws. It defines cysts and provides classifications including the WHO and Robinson systems. It describes the pathogenesis of cyst formation in 3 stages: initiation, cyst formation, and enlargement. Signs include bone expansion and percussion sound. Radiographs can reveal size and extent. Diagnosis is based on aspirate characteristics. Treatment involves enucleation or marsupialization. Enucleation removes all tissue but has risks, while marsupialization has recurrence risks but preserves structures.
Investigations for the spleen include ultrasound, CT scan and MRI which can detect size, consistency and any masses or cysts. Congenital abnormalities include accessory spleens. Splenic artery aneurysms are prone to rupture and require surgery. Splenic infarcts may require splenectomy if abscess forms. Ruptured spleens mandate emergency surgery. Hypersplenism from splenomegaly causes cytopenias and may need splenectomy. Splenic abscesses are treated with antibiotics and sometimes surgery. Tuberculosis, tropical diseases and leukemia may cause splenomegaly requiring splenectomy. Idiopathic thrombocytop
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
1. University of Benghazi
Faculty of Dentistry
Department of Oral Pathology
Radicular cyst (Periapical cyst)
By:Hager Mohammed
Alfakhri
2. A cyst is defined as a pathological cavity lined wholly or in
part by epithelium ,having fluid or semi-fluid content.
3. Classification of cysts of the jaw
Epithelial cyst Non-epithelialized
primary bone cyst
Odontogenic cyst Non- odontogenic
cyst
Developmental
-Odontogenic
keratocyst
-Dentigerous cyst
-Eruption cyst
-Lateral periodontal
cyst
-Gingival cyst
-Glandular cyst
Inflammatory
-Radicular cyst
-Paradental cyst
-Nasopalatine
-Nasolabial cyst
-Median cyst
-Solitary bone cyst
-Aneurysmal bone cyst
-Stafnés idiopathic
bone cavity.
4. Odontogenic cyst
Periapical(radicular cyst)
Lateral periodontal cyst
Gingival cyst of the newborn
Dentigerous cyst
Eruption cyst
Glandular cyst
Odontogenic keratocyst
Calcifying odontogenic cyst
Nonodontogenic cyst
Globulomaxilary lesion
Nasolabial cyst
Median mandibular cyst
Nasopaltine canal cyst
Psedocyst
Aneurysmal bone cyst
Traumatic (simple )bone test
Static bone cyst(Stafnésbone cyst)
Focal osteoporosis bone marrow defect
5.
6. Periapical cyst
-An epithelial cyst, odontogenic cyst ,inflammatory cyst
derived from cell Rest of Malassez , that proliferation
in response to inflammation.
-Odontogenic cyst
A cyst in which lining of the lumen derived from epithelium
in tooth development.
-Non-odontogenic cyst
The epithelial lining is derived from sources other than the
tooth organ.
7. Periapical cyst/Radicular cyst
-Types of Radicular cyst (periapical cyst)
1.Apical 70%
2.Lateral 20%
3.Residual
Most common location:
1.Maxillary anterior region
2.Maxillary posterior region
3.Mandibularposterior region
4.Mandibular anterior region
8. Periapical cyst-Epidemiology
-Worldwide
-Common-constitutes approx one half to three fourth of all cyst in the
jaw
-Relative frequency :60-70%
-Frequent in age between 20-60years(rarely in <10 years Ago)
(Peak in third through six decades)
-M/F ratio 3:2
-Maxilla is 3 times more affected than mandible
9. Periapical cyst-clinical features
-Usually asymptomatic
-Slowly progressive
If infection enters, the swelling painful and
rapidly expands
(partly due to inflammatory edema)
-Initially swelling round and hard
-Later, part of wall is resorbed…leaving a soft
fluctuant swelling ,blush in color ,beneath the
mucous membrane .
11. Periapical cyst-Pathogenesis
(PHASE1)phase of initiation:
-Stimulation of cell rest of Malassez in response to INFLAMMATION elicited by
.Bacterial infection of pulp
.Direct response to necrotic pulp tissue.
(PHASE2)phase of cyst formation:
-Epithelial cells derive their nutrient by diffusion from adjacent C.T
,progressive growth of an epithelial island moves the innermost cells of the
island away from the nutrients.
-Ultimately these innermost cell undergo ischemic liquefactive necrosis
,establishing central cavity (lumen)surrounding by viable epithelium.
(PHASE3)phase of cyst expansion:
-Breakdown of cellular debris within cyst lumen.
-the protein concentration ..increased osmotic pressure
-in fluid transport into the lumen from the C.T side.
-Ingress thus assist in outward growth of a cyst.
12. Periapical cyst-Pathogenesis
Major factors in the Pathogenesis of cyst formation
.Epithelial proliferation
.Hydrostatic effects cyst fluid
.Bone resorbing factors
-Infection from pulp chamber induces inflammation .
-Cyst fluid contain protein which exert osmotic pressure.
-Hydrostatic pressure within cyst is about 70cm of
water(higher than capillary pressure).
-Bone resorption factors PGE2,PGE3 with osteoclast bone
resorption ,the cyst expand.
13.
14. Periapical cyst -Histopathology
.Lumen(cavity):
-Contains cyst fluid ;which is usually watery ,straw -color and
opalescent.
-Sometimes more viscid and yellowish.
-sometime shimmers with cholesterol crystals.
-Protein content of fluid .
.Epithelial Lining:
-Non-keratinized stratified squamous
epithelium.
-Lack a well-defined basal cell layer.
-Thick,irregular,hyperplastic or net like forming
rings and arcades.
-Hyaline Bodies(Rushton Bodies)may be found.
-Transmigration of inflammatory cells through
epithelium is common with neutrophils and less
lymphocyte.
15. Periapical cyst -Histopathology
.Wall/capsule:
-Composed of collagenous fibrous connective tissue .
-Capsule is vascular and infiltrated by chronic inflammatory cell.
-Plasma cell are prominent or often predominate.
-Russell bodies are often found.
-Cholesterol crystal associated with multinucleate giant
cells(foreign body type).they may erode through epithelial lining
and extrude into cyst lumen.
-Foam cells(lipid-filled macrophages)
16. Early radicular cyst showing
variation in thickness of the
epithelial lining
Periapical granuloma
containing proliferation
arcades of squamous
epithelium derived
from the rest of
Malassez showing early
cystic break down
19. Periapical cyst –Radiology
-Periapical cyst is well circumscribed
-Distinct line of cortication separating it from surrounding bone.
-May be associated with resorption of apices of teeth, displacement of
teeth or both.
20. References
-Cawson's essentials of oral pathology and oral medicine-8th edition
-Contemporary oral and maxillofacial pathology-2nd edition
-Oral pathology clinical pathologic correlations regezi-5th edition
-Soames and southam oral pathology-4th edition