Regional odontodysplasia is a developmental anomaly affecting the ectodermal and mesodermal components of tooth development, causing teeth to be small, mottled brown, and hypocalcified. It most commonly impacts the central and lateral incisors. Radiographically, affected teeth appear ghost-like with reduced density and large pulp chambers. While the etiology is uncertain, factors like trauma, infection, and vascular defects have been suggested. Clinical diagnosis is based on irregular tooth shape and brown discoloration, while radiographs reveal a shell-like appearance. Treatment typically involves early extraction and prosthetic replacement, though restorative procedures like root canals may attempt to save affected teeth.
Developmental disturbances of LIP,PALATE and ORAL MUCOSAaanchalshruti
This document summarizes several developmental disturbances of the lip, palate, and oral mucosa. It describes congenital lip and commissural pits/fistulas, which can occur alone or with clefts. It also discusses Van der Woude syndrome, cleft lip and palate, cheilitis glandularis, cheilitis granulomatosa, hereditary intestinal polyposis syndrome, labial and oral melanotic macules, Fordyce's granules, and focal epithelial hyperplasia. For each condition, it provides information on etiology, clinical features, histological features if applicable, differential diagnosis, and treatment approaches.
DEVELOPMENTAL DISTURBANCES OF GINGIVA
1) Fibromatosis Gingivae(Elephantiasis gingivae, hereditary gingival fibromatosis, congenital macrogingivae)
Fibromatosis gingivae is a diffuse fibrous overgrowth of the gingival tissues.
This condition is manifested as a dense, diffuse, smooth, or nodular overgrowth of the gingival tissues of one or both arches, usually appearing about the time of eruption of the permanent incisors.
Even seen in very young children
It is not painful and shows no tendency for hemorrhage.
The extent of the tissue overgrowth may be such that the crowns of the teeth are nearly hidden even though they are fully erupted with respect to the alveolar bone .
2) Retrocuspid Papilla
It is a small, elevated nodule located on the lingual mucosa of the mandibular cuspids.
Clinical Features
This soft, well-circumscribed, sessile, mucosal nodule, commonly bilateral, is located lingual to the mandibular cuspid, between the free gingival margin and the mucogingival junction.
It is exceedingly common in children.
Found a greater occurrence bilaterally than unilaterally.
The structure appears as an elevated mucosal tag often showing mild hyperorthokeratosis or hyperparakeratosis, with or without acanthosis.
The underlying connective tissue is sometimes highly vascularized and may exhibit large stellate fibroblasts as well as occasional epithelial rests.
Because of its frequency of occurrence, the retrocuspid papilla is often considered to be a ‘normal’ anatomic structure which regresses with age and requires no treatment.
This document provides information about calcifying odontogenic cysts (COCs). It defines COCs and classifies them according to the WHO. COCs are rare jaw lesions characterized by ghost cells and calcifications. They are thought to arise from odontogenic epithelial remnants. Clinically, they typically present in the second decade of life with lesions more common in the maxilla than mandible. Radiographically, COCs appear well-defined with variable calcifications. Histologically, they contain ghost cells and basal cell layer with hyperchromatic nuclei. Prognosis is generally good when treated with surgical removal.
This document discusses several pathologies that can affect the jaws, including:
1. The adenomatoid odontogenic tumor, which presents as a swelling in young patients around unerupted teeth and consists of epithelial cells and calcifications.
2. The calcifying epithelial odontogenic tumor, which occurs in the mandible or maxilla as a radiolucent lesion containing radiopacities from calcification.
3. Odontomas, which are hamartomas containing dental tissues like enamel and dentin that appear as radiopaque masses and require conservative excision.
This document discusses various developmental disturbances that can affect the tongue, including microglossia (small tongue), macroglossia (large tongue), ankyloglossia (tongue tie), cleft tongue, fissured tongue, median rhomboid glossitis (reddish patch on dorsal tongue), benign migratory glossitis (geographic tongue), hairy tongue, lingual varices (dilated veins on tongue), and lingual thyroid nodule (thyroid tissue on tongue). Many of these conditions can cause difficulties with speech, swallowing, or irritation of the tongue. Treatment may include surgery, antifungal medications, or thyroid hormone supplements.
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.
This document provides an overview of enamel hypoplasia, including its definition, classification, etiology, clinical features, radiographic features, and management. Enamel hypoplasia is defined as an incomplete or defective formation of the enamel matrix of teeth. It can be hereditary or environmental in origin. Common causes include nutritional deficiencies, infections like syphilis, and dental fluorosis from excess fluoride intake. Clinical features range from mild pitting to severe absence of enamel. Treatment depends on severity and location, and may include desensitizing agents, composite restoration, crowns, or extractions for severely malformed teeth.
Regional odontodysplasia is a developmental anomaly affecting the ectodermal and mesodermal components of tooth development, causing teeth to be small, mottled brown, and hypocalcified. It most commonly impacts the central and lateral incisors. Radiographically, affected teeth appear ghost-like with reduced density and large pulp chambers. While the etiology is uncertain, factors like trauma, infection, and vascular defects have been suggested. Clinical diagnosis is based on irregular tooth shape and brown discoloration, while radiographs reveal a shell-like appearance. Treatment typically involves early extraction and prosthetic replacement, though restorative procedures like root canals may attempt to save affected teeth.
Developmental disturbances of LIP,PALATE and ORAL MUCOSAaanchalshruti
This document summarizes several developmental disturbances of the lip, palate, and oral mucosa. It describes congenital lip and commissural pits/fistulas, which can occur alone or with clefts. It also discusses Van der Woude syndrome, cleft lip and palate, cheilitis glandularis, cheilitis granulomatosa, hereditary intestinal polyposis syndrome, labial and oral melanotic macules, Fordyce's granules, and focal epithelial hyperplasia. For each condition, it provides information on etiology, clinical features, histological features if applicable, differential diagnosis, and treatment approaches.
DEVELOPMENTAL DISTURBANCES OF GINGIVA
1) Fibromatosis Gingivae(Elephantiasis gingivae, hereditary gingival fibromatosis, congenital macrogingivae)
Fibromatosis gingivae is a diffuse fibrous overgrowth of the gingival tissues.
This condition is manifested as a dense, diffuse, smooth, or nodular overgrowth of the gingival tissues of one or both arches, usually appearing about the time of eruption of the permanent incisors.
Even seen in very young children
It is not painful and shows no tendency for hemorrhage.
The extent of the tissue overgrowth may be such that the crowns of the teeth are nearly hidden even though they are fully erupted with respect to the alveolar bone .
2) Retrocuspid Papilla
It is a small, elevated nodule located on the lingual mucosa of the mandibular cuspids.
Clinical Features
This soft, well-circumscribed, sessile, mucosal nodule, commonly bilateral, is located lingual to the mandibular cuspid, between the free gingival margin and the mucogingival junction.
It is exceedingly common in children.
Found a greater occurrence bilaterally than unilaterally.
The structure appears as an elevated mucosal tag often showing mild hyperorthokeratosis or hyperparakeratosis, with or without acanthosis.
The underlying connective tissue is sometimes highly vascularized and may exhibit large stellate fibroblasts as well as occasional epithelial rests.
Because of its frequency of occurrence, the retrocuspid papilla is often considered to be a ‘normal’ anatomic structure which regresses with age and requires no treatment.
This document provides information about calcifying odontogenic cysts (COCs). It defines COCs and classifies them according to the WHO. COCs are rare jaw lesions characterized by ghost cells and calcifications. They are thought to arise from odontogenic epithelial remnants. Clinically, they typically present in the second decade of life with lesions more common in the maxilla than mandible. Radiographically, COCs appear well-defined with variable calcifications. Histologically, they contain ghost cells and basal cell layer with hyperchromatic nuclei. Prognosis is generally good when treated with surgical removal.
This document discusses several pathologies that can affect the jaws, including:
1. The adenomatoid odontogenic tumor, which presents as a swelling in young patients around unerupted teeth and consists of epithelial cells and calcifications.
2. The calcifying epithelial odontogenic tumor, which occurs in the mandible or maxilla as a radiolucent lesion containing radiopacities from calcification.
3. Odontomas, which are hamartomas containing dental tissues like enamel and dentin that appear as radiopaque masses and require conservative excision.
This document discusses various developmental disturbances that can affect the tongue, including microglossia (small tongue), macroglossia (large tongue), ankyloglossia (tongue tie), cleft tongue, fissured tongue, median rhomboid glossitis (reddish patch on dorsal tongue), benign migratory glossitis (geographic tongue), hairy tongue, lingual varices (dilated veins on tongue), and lingual thyroid nodule (thyroid tissue on tongue). Many of these conditions can cause difficulties with speech, swallowing, or irritation of the tongue. Treatment may include surgery, antifungal medications, or thyroid hormone supplements.
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.
This document provides an overview of enamel hypoplasia, including its definition, classification, etiology, clinical features, radiographic features, and management. Enamel hypoplasia is defined as an incomplete or defective formation of the enamel matrix of teeth. It can be hereditary or environmental in origin. Common causes include nutritional deficiencies, infections like syphilis, and dental fluorosis from excess fluoride intake. Clinical features range from mild pitting to severe absence of enamel. Treatment depends on severity and location, and may include desensitizing agents, composite restoration, crowns, or extractions for severely malformed teeth.
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.
Hypercementosis is characterized by the excessive deposition of cementum on tooth roots. It can be localized, affecting a single tooth due to conditions like periapical osteitis, or generalized, affecting many teeth as an age-related factor or due to diseases like Paget's disease of bone. Radiographically, it appears as thickening and blunting of roots with a bulbous or irregular apex. Diagnosis is clinical based on the bulbous root appearance. Treatment focuses on managing any underlying primary causes.
This document discusses squamous papilloma, a benign proliferation of stratified squamous epithelium that presents as a soft, painless, pedunculated nodule with cauliflower-like projections. It is caused by human papillomavirus (HPV) infection, most commonly HPV subtypes 6 and 11. Clinically, it appears as a white or slightly red exophytic lesion that is usually solitary and less than 0.5cm in size. Microscopically, it demonstrates papillary projections composed of epithelium with fibrovascular cores. Treatment is conservative surgical excision.
A cyst is an epithelium-lined sac containing fluid or semisolid material. In the formation of a cyst, the epithelial cells first proliferate and later undergo degeneration and liquefaction. The liquefied material exerts equal pressure on the walls of the cyst from within. Cysts grow by expansion and thus displace the adjacent teeth by pressure. May can produce expansion of the cortical bone. On a radiograph, the radiolucency of a cyst is usually bordered by a radiopaque periphery of dense sclerotic bone. The radiolucency may be unilocular or multilocular. Odontogenic cysts are those which arise from the epithelium associated with the development of teeth. The source of epithelium is from the enamel organ, the reduced enamel epithelium, the cell rests of Malassez or the remnants of the dental lamina.
Developmental disorders of tongue elvis chiramel davidDr. Elvis David
This document discusses various developmental disturbances that can occur in the tongue, including microglossia, macroglossia, ankyloglossia, cleft tongue, fissured tongue, median rhomboid glossitis, benign migratory glossitis, hairy tongue, lingual varices, and lingual thyroid nodule. It provides details on the etiology, clinical features, classification where relevant, and treatment for each of these conditions. Various tongue abnormalities can result in difficulties with speech, swallowing, or irritation and infection if debris gets trapped. Treatment may involve surgery, antifungal medications, or reducing long term antibiotic use depending on the specific condition.
This document discusses various types of red and white lesions that can occur in the oral mucosa. It describes hereditary lesions including leukodema, white sponge nevus, and hereditary benign intraepithelial dyskeratosis. It also covers reactive/inflammatory lesions such as frictional keratosis. Infectious lesions covered include oral hairy leukoplakia caused by Epstein-Barr virus and various forms of oral candidiasis. Idiopathic "true" leukoplakia and erythroplakia are also discussed. Treatment options are provided for many of the conditions.
This document discusses enamel defects including hereditary enamel dysplasia and enamel hypoplasia. It describes the three stages of enamel development and factors that can disrupt this process such as nutritional deficiencies, infections, trauma, and genetic conditions. Specific enamel defects are defined including pitted enamel hypoplasia and enamel discoloration seen in conditions like congenital syphilis and fluorosis. Classification systems for hereditary enamel dysplasia and clinical, radiographic, and genetic features are also summarized.
This document discusses different types of pulpitis, including acute reversible and irreversible pulpitis, chronic pulpitis, and chronic hyperplastic pulpitis. It describes the definition, etiology, clinical features, histopathological features, and treatment for each type. Acute reversible pulpitis involves mild pain from obvious causes like caries that can be treated by removing the cause. Acute irreversible pulpitis causes severe spontaneous pain and requires root canal treatment. Chronic pulpitis may cause mild intermittent pain from previous acute pulpitis or caries. Chronic hyperplastic pulpitis forms a red nodule in open cavities, usually in children's teeth.
Oral lichen planus is a common chronic mucocutaneous disease of unknown etiology that may undergo malignant transformation. It typically presents as white reticulated lines on the oral mucosa but can also appear as erosive, atrophic, bullous or other lesions. A confirmed diagnosis requires characteristic histopathology. While there is no cure, treatment focuses on managing symptoms like pain with topical or systemic corticosteroids and maintaining oral hygiene to reduce cancer risks.
This document discusses and compares different types of non-odontogenic (not related to teeth) cysts. It separates them into developmental and inflammatory cysts. Developmental cysts form due to epithelial cell remnants becoming trapped during embryonic development, while inflammatory cysts form due to duct obstruction or trauma. Some examples of developmental cysts mentioned are nasopalatine duct cysts, median palatal cysts, and dermoid cysts. Inflammatory cysts include mucoceles, ranulas caused by salivary gland duct obstruction, and retention cysts of the maxillary sinus. The document provides details on pathogenesis, clinical features, histopathology, diagnosis and treatment of several of these cyst types.
The document discusses different types of cysts that can occur in the oral and maxillofacial region. It defines cysts and classifies them based on their origin and location. It provides details on the pathogenesis, clinical features, radiographic appearance and histology of specific cysts such as dentigerous cysts and odontogenic keratocysts. Dentigerous cysts are defined as cysts originating from the separation of the dental follicle from around the crown of an unerupted tooth. Odontogenic keratocysts are distinctive cysts that arise from cell rests of the dental lamina and have more aggressive behavior than other cysts. Complications of cysts include recurrence, development of
Developmental disturbances of the TeethChelsea Mareé
This document discusses various developmental disturbances that can affect the teeth, including size, number and eruption, shape/form, and enamel and dentin defects. For size, it describes microdontia and macrodontia, covering true generalized, relative generalized, and focal/localized variations. For number and eruption, it discusses supernumerary teeth, anodontia (complete, partial, and other types), and impaction. Shape/form disturbances include crown variations like fusion, gemination, taurodontism, talon's cusp, and dens invaginatus, as well as root anomalies. Finally, it covers defects of enamel and dentin, focusing on amelogenesis imperfecta.
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.
Cavity varnish is a resin solution applied to prepared cavity walls that forms a protective film barrier between restorations and dentin. It is composed of natural or synthetic resins dissolved in solvents like alcohol or acetone, and sometimes contains fluorides or other agents. Cavity varnish is supplied in bottles and applied in thin layers to reduce sensitivity, seal dentin, and protect restorations from corrosion or dehydration. Proper application involves allowing layers to dry before adding more.
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.
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.
This document discusses different types of odontogenic tumors. It classifies them into three categories: tumors of odontogenic epithelium, mixed odontogenic tumors, and tumors of odontogenic ectomesenchyme. Key tumors discussed include ameloblastoma, adenomatoid odontogenic tumor (AOT), and calcifying epithelial odontogenic tumor (CEOT). Ameloblastoma is the most common odontogenic tumor and can be solid/multicystic, unicystic, or peripheral. AOT typically occurs in younger females in the anterior maxilla. CEOT accounts for less than 1% of odontogenic tumors and resembles cells of the enamel organ or dental lamina.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The document provides information about Pindborg tumor, also known as calcifying epithelial odontogenic tumor (CEOT). It defines CEOT as a locally invasive epithelial odontogenic neoplasm characterized by the presence of amyloid material that may become calcified. The document discusses the pathogenesis, histopathological features including epithelial cells, amyloid-like material and calcific deposits, immunohistochemical findings, differential diagnosis and treatment of CEOT. It also mentions the recurrence rate of CEOT is typically 10-15% but can be higher in certain variants.
This seminar consists of various cysts seen in the oral cavity alonh with various classifications and added case repots for better understanding and the various treatment protocols followed for treating various cysts.
1) Cysts are pathological cavities that can form in hard or soft tissues and may contain fluid, semisolid, or gaseous material.
2) Cysts are generally classified as intraosseous or soft tissue cysts, and epithelial or non-epithelial cysts.
3) Common intraosseous cysts include odontogenic cysts like dentigerous and radicular cysts arising from dental tissues, and non-odontogenic cysts such as nasopalatine duct cysts arising from other epithelial tissues.
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.
Hypercementosis is characterized by the excessive deposition of cementum on tooth roots. It can be localized, affecting a single tooth due to conditions like periapical osteitis, or generalized, affecting many teeth as an age-related factor or due to diseases like Paget's disease of bone. Radiographically, it appears as thickening and blunting of roots with a bulbous or irregular apex. Diagnosis is clinical based on the bulbous root appearance. Treatment focuses on managing any underlying primary causes.
This document discusses squamous papilloma, a benign proliferation of stratified squamous epithelium that presents as a soft, painless, pedunculated nodule with cauliflower-like projections. It is caused by human papillomavirus (HPV) infection, most commonly HPV subtypes 6 and 11. Clinically, it appears as a white or slightly red exophytic lesion that is usually solitary and less than 0.5cm in size. Microscopically, it demonstrates papillary projections composed of epithelium with fibrovascular cores. Treatment is conservative surgical excision.
A cyst is an epithelium-lined sac containing fluid or semisolid material. In the formation of a cyst, the epithelial cells first proliferate and later undergo degeneration and liquefaction. The liquefied material exerts equal pressure on the walls of the cyst from within. Cysts grow by expansion and thus displace the adjacent teeth by pressure. May can produce expansion of the cortical bone. On a radiograph, the radiolucency of a cyst is usually bordered by a radiopaque periphery of dense sclerotic bone. The radiolucency may be unilocular or multilocular. Odontogenic cysts are those which arise from the epithelium associated with the development of teeth. The source of epithelium is from the enamel organ, the reduced enamel epithelium, the cell rests of Malassez or the remnants of the dental lamina.
Developmental disorders of tongue elvis chiramel davidDr. Elvis David
This document discusses various developmental disturbances that can occur in the tongue, including microglossia, macroglossia, ankyloglossia, cleft tongue, fissured tongue, median rhomboid glossitis, benign migratory glossitis, hairy tongue, lingual varices, and lingual thyroid nodule. It provides details on the etiology, clinical features, classification where relevant, and treatment for each of these conditions. Various tongue abnormalities can result in difficulties with speech, swallowing, or irritation and infection if debris gets trapped. Treatment may involve surgery, antifungal medications, or reducing long term antibiotic use depending on the specific condition.
This document discusses various types of red and white lesions that can occur in the oral mucosa. It describes hereditary lesions including leukodema, white sponge nevus, and hereditary benign intraepithelial dyskeratosis. It also covers reactive/inflammatory lesions such as frictional keratosis. Infectious lesions covered include oral hairy leukoplakia caused by Epstein-Barr virus and various forms of oral candidiasis. Idiopathic "true" leukoplakia and erythroplakia are also discussed. Treatment options are provided for many of the conditions.
This document discusses enamel defects including hereditary enamel dysplasia and enamel hypoplasia. It describes the three stages of enamel development and factors that can disrupt this process such as nutritional deficiencies, infections, trauma, and genetic conditions. Specific enamel defects are defined including pitted enamel hypoplasia and enamel discoloration seen in conditions like congenital syphilis and fluorosis. Classification systems for hereditary enamel dysplasia and clinical, radiographic, and genetic features are also summarized.
This document discusses different types of pulpitis, including acute reversible and irreversible pulpitis, chronic pulpitis, and chronic hyperplastic pulpitis. It describes the definition, etiology, clinical features, histopathological features, and treatment for each type. Acute reversible pulpitis involves mild pain from obvious causes like caries that can be treated by removing the cause. Acute irreversible pulpitis causes severe spontaneous pain and requires root canal treatment. Chronic pulpitis may cause mild intermittent pain from previous acute pulpitis or caries. Chronic hyperplastic pulpitis forms a red nodule in open cavities, usually in children's teeth.
Oral lichen planus is a common chronic mucocutaneous disease of unknown etiology that may undergo malignant transformation. It typically presents as white reticulated lines on the oral mucosa but can also appear as erosive, atrophic, bullous or other lesions. A confirmed diagnosis requires characteristic histopathology. While there is no cure, treatment focuses on managing symptoms like pain with topical or systemic corticosteroids and maintaining oral hygiene to reduce cancer risks.
This document discusses and compares different types of non-odontogenic (not related to teeth) cysts. It separates them into developmental and inflammatory cysts. Developmental cysts form due to epithelial cell remnants becoming trapped during embryonic development, while inflammatory cysts form due to duct obstruction or trauma. Some examples of developmental cysts mentioned are nasopalatine duct cysts, median palatal cysts, and dermoid cysts. Inflammatory cysts include mucoceles, ranulas caused by salivary gland duct obstruction, and retention cysts of the maxillary sinus. The document provides details on pathogenesis, clinical features, histopathology, diagnosis and treatment of several of these cyst types.
The document discusses different types of cysts that can occur in the oral and maxillofacial region. It defines cysts and classifies them based on their origin and location. It provides details on the pathogenesis, clinical features, radiographic appearance and histology of specific cysts such as dentigerous cysts and odontogenic keratocysts. Dentigerous cysts are defined as cysts originating from the separation of the dental follicle from around the crown of an unerupted tooth. Odontogenic keratocysts are distinctive cysts that arise from cell rests of the dental lamina and have more aggressive behavior than other cysts. Complications of cysts include recurrence, development of
Developmental disturbances of the TeethChelsea Mareé
This document discusses various developmental disturbances that can affect the teeth, including size, number and eruption, shape/form, and enamel and dentin defects. For size, it describes microdontia and macrodontia, covering true generalized, relative generalized, and focal/localized variations. For number and eruption, it discusses supernumerary teeth, anodontia (complete, partial, and other types), and impaction. Shape/form disturbances include crown variations like fusion, gemination, taurodontism, talon's cusp, and dens invaginatus, as well as root anomalies. Finally, it covers defects of enamel and dentin, focusing on amelogenesis imperfecta.
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.
Cavity varnish is a resin solution applied to prepared cavity walls that forms a protective film barrier between restorations and dentin. It is composed of natural or synthetic resins dissolved in solvents like alcohol or acetone, and sometimes contains fluorides or other agents. Cavity varnish is supplied in bottles and applied in thin layers to reduce sensitivity, seal dentin, and protect restorations from corrosion or dehydration. Proper application involves allowing layers to dry before adding more.
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.
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.
This document discusses different types of odontogenic tumors. It classifies them into three categories: tumors of odontogenic epithelium, mixed odontogenic tumors, and tumors of odontogenic ectomesenchyme. Key tumors discussed include ameloblastoma, adenomatoid odontogenic tumor (AOT), and calcifying epithelial odontogenic tumor (CEOT). Ameloblastoma is the most common odontogenic tumor and can be solid/multicystic, unicystic, or peripheral. AOT typically occurs in younger females in the anterior maxilla. CEOT accounts for less than 1% of odontogenic tumors and resembles cells of the enamel organ or dental lamina.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The document provides information about Pindborg tumor, also known as calcifying epithelial odontogenic tumor (CEOT). It defines CEOT as a locally invasive epithelial odontogenic neoplasm characterized by the presence of amyloid material that may become calcified. The document discusses the pathogenesis, histopathological features including epithelial cells, amyloid-like material and calcific deposits, immunohistochemical findings, differential diagnosis and treatment of CEOT. It also mentions the recurrence rate of CEOT is typically 10-15% but can be higher in certain variants.
This seminar consists of various cysts seen in the oral cavity alonh with various classifications and added case repots for better understanding and the various treatment protocols followed for treating various cysts.
1) Cysts are pathological cavities that can form in hard or soft tissues and may contain fluid, semisolid, or gaseous material.
2) Cysts are generally classified as intraosseous or soft tissue cysts, and epithelial or non-epithelial cysts.
3) Common intraosseous cysts include odontogenic cysts like dentigerous and radicular cysts arising from dental tissues, and non-odontogenic cysts such as nasopalatine duct cysts arising from other epithelial tissues.
This document discusses gingival enlargement from multiple perspectives. It begins by defining key terms like hyperplasia and hypertrophy. It then categorizes enlargement based on location, etiology, degree, and associated conditions. Chronic inflammatory enlargement and acute conditions like gingival abscesses are explained. Drug-induced, hereditary, and condition-associated enlargements are explored. Systemic diseases that can cause enlargement like leukemia and Wegener's granulomatosis are summarized. The document concludes with an overview of neoplastic enlargements.
Xerostomia is the diesease in which their is absence of saliva in mouth. The slide inlcudes all the helpful subjects about the topic. graphical representation for ease of understanding
This document summarizes different types of salivary gland disorders including developmental, functional, obstructive, cysts, infections, and autoimmune disorders. Developmental disorders include abnormalities like aplasia, hyperplasia, and atresia. Functional disorders involve increased or decreased salivary secretion known as sialorrhea and xerostomia. Obstructive disorders are due to blockages like sialolithiasis. Cysts include mucoceles and ranulas. Infections can be viral, bacterial, or mycotic. Autoimmune disorders include Sjogren's syndrome and Mikulicz's disease. The document also discusses diagnostic tools like sialography used to evaluate salivary gland
Burkitt's lymphoma is an undifferentiated B-cell lymphoma that commonly affects the jaws of children, particularly the maxilla. Histopathology shows sheets of small round tumor cells with prominent nuclei and minimal cytoplasm, giving a starry-sky appearance. Hyperparathyroidism is caused by increased PTH secretion or calcium demand, resulting in bone and joint issues. Primary hyperparathyroidism is due to parathyroid hyperplasia while secondary involves chronic renal disease. Mucous membrane pemphigoid is a rare autoimmune blistering disease of the mouth, eyes, and other mucosal surfaces causing blisters, erosions and vision impairment. Treatment requires systemic immunosuppression.
This document discusses various developmental disorders, dysfunctions, and diseases that can affect the salivary glands. It covers conditions such as aplasia, agenesis, hypoplasia, and accessory ducts as developmental disorders. Dysfunctions like xerostomia and its causes are explained. Inflammatory and reactive lesions including necrotizing sialometaplasia and radiation-induced pathology are outlined. Viral diseases like mumps and bacterial infections are also summarized, along with treatments for various conditions.
This document provides an overview of developmental disturbances of teeth. It begins with an introduction that defines development and discusses genetic and environmental factors that can disrupt odontogenesis. It then classifies and describes various developmental disturbances affecting the size, number, shape, structure, and eruption of teeth. Specific disturbances covered in detail include microdontia, macrodontia, gemination, fusion, taurodontism, talon cusp, dens invaginatus, and shovel-shaped incisors. The document discusses causes, clinical features, classifications, and treatments for each disturbance. Radiographic features are also described for some conditions.
Soft tissue sarcomas are rare cancers accounting for less than 1% of oral cancers. This document lists and describes 10 common types of soft tissue sarcomas that can occur in the oral cavity including fibrosarcoma, liposarcoma, neurofibrosarcoma, and rhabdomyosarcoma. For each type, the document outlines clinical features, radiographic features, diagnosis, and treatment options. Metastatic cancers spreading to the oral soft tissues from primary tumors like breast cancer are also discussed.
This document discusses various medical conditions and oral symptoms, including pregnancy, osteoporosis, diabetes, heart disease, and others. It also discusses bruxism (tooth grinding), its causes and complications, and treatments. Additional topics covered include tooth wear, xerostomia (dry mouth), pulp reactions, and more. Medical conditions can manifest oral symptoms, and conditions affecting the mouth like bruxism and xerostomia can impact overall health. Maintaining good oral hygiene is important for general well-being.
The document discusses the diagnostic imaging of jaw lesions. Radiologists perform various imaging studies to evaluate known or suspected jaw lesions, assess dental arches for implants, and examine the temporomandibular joint. Jaw lesions are often classified based on their radiographic appearance and borders on plain films. Important parameters for diagnosis include location, relationship to surrounding structures, and associated changes. Common well-circumscribed radiolucent lesions discussed include periapical lesions, dentigerous cysts, and odontogenic keratocysts.
DENTIGEROUS CYST- an odontogenic cyst that surrounds the crown of impacted tooth , develops by fluid accumulation between REE(reduced enamel epithelium) and the enamel surface , resulting in a cyst which the crown located within the lumen.
Premature exfoliation of primary teeth can be caused by toxicities, metabolic disorders, malignancies, dental causes, and miscellaneous conditions. Specific etiologies include acrodynia from mercury exposure, radiation-induced xerostomia, acatalasia, hypophosphatasia, leukemia-associated gingival enlargement, localized aggressive periodontitis, Papillon-Lefevre syndrome, cherubism, aplastic anemia, and dentin dysplasia. Diagnostic testing may involve blood tests, imaging, biopsies, and microbial cultures to identify the underlying condition leading to premature tooth loss.
This document discusses several benign oral lesions that can be mistaken for tumours, including tori, fibromas, pyogenic granulomas, peripheral ossifying fibromas, and lipomas. It provides details on the clinical features, locations, appearances, diagnoses, and typical treatment for each condition, emphasizing that they are non-cancerous structural variants or reactive lesions of the oral soft tissues and bones. Conservative surgical excision is usually sufficient to treat these common benign growths of the oral cavity.
Eruption problems /certified fixed orthodontic courses by Indian dental academy Indian dental academy
This document discusses dental eruption and problems with eruption from the Indian Dental Academy website. It provides information on the mechanisms, etiology, diagnosis, and treatment of eruption problems. The key points are:
- Tooth eruption is a complex process involving root development, periodontium establishment, and functional occlusion.
- Problems can occur at any phase of eruption due to ectopic tooth position, obstacles in the eruption path, or failures in the eruption mechanisms.
- Common causes of delayed eruption are local factors like scarring, supernumerary teeth, and systemic factors such as nutrition deficiencies, endocrine disorders, cerebral palsy, and genetic syndromes.
- Accurate
Dr. Abdelhady provides a lecture on odontogenic tumors. The lecture aims to help students classify and diagnose odontogenic tumors, examine patients presenting with facial swellings, and determine differential diagnoses and management techniques for mandibular and maxillary swellings. Specific odontogenic tumors discussed include cementoblastoma, odontogenic fibroma, central giant cell granuloma, cherubism, fibrous dysplasia, and ossifying fibroma. Radiographic features, histology, treatment options and prognosis are described for each tumor type.
This document provides an overview of a student presentation on pediatric oral pathology. It discusses various developmental conditions like orofacial clefts, palatal cysts of newborns, congenital epulis, natal/neonatal teeth, ankyloglossia, and congenital absence of teeth. It also covers odontogenic conditions, reactive lesions, infections, and developmental abnormalities seen in pediatric oral pathology. Treatment approaches for many of these conditions are mentioned as well.
This document discusses different types of gingival enlargement, including inflammatory, drug-induced, conditioned by systemic factors, idiopathic, neoplastic, and false enlargement. Inflammatory enlargement is usually caused by chronic inflammation from poor oral hygiene. Drug-induced enlargement can be caused by anticonvulsants, immunosuppressants, and calcium channel blockers. Conditioned enlargement is exacerbated by hormonal, allergic or nutritional factors. Neoplastic enlargement involves benign or malignant tumors of the gingiva. False enlargement is due to underlying dental or bone anomalies rather than issues with the gingiva.
Similar to DEVELOPMENTAL DISTURBANCES OF SALIVARY GLAND.pptx (20)
Lymphomas are primary malignancies of lymph nodes and the peripheral lymphatics.
Neoplastic proliferative process of the lymphopoietic portion of the lymphoid system that involves cells of either the lymphocytic or histiocytic series in varying degrees of differentiation & occurs in an essentially homogenous population of a single cell type.
The first lymphoma type recognised was by Dr Thomas Hodgkin in 1832. In 1865 Dr Samuel Wilks recognised additional cases, rediscovered the report by Hodgkin, and designated this neoplasm as ‘Hodgkin disease’.
Hodgkin lymphoma (HL) represents about 10% of all lymphomas.
HL is distinct from other non-Hodgkin lymphomas, clinically by the contiguous spread of tumour along the lymphoid system, and morphologically by the presence of a spectrum of neoplastic cells, including mononuclear Hodgkin (H) cells, classic multinucleated Reed–Sternberg (RS) cells, and mummified (degenerating) cells against an inflammatory background.
The background inflammatory cells actively attracted by HL tumour cells may include T cells, B cells, histiocytes, plasma cells, neutrophils, eosinophils and mast cells.
The etiology of HD is unknown. Infectious agents, especially the Epstein-Barr virus (EBV), may be involved in the pathogenesis.
In as many as 50% of HD cases, the tumor cells are EBV-positive. EBV positivity is higher with mixed cellularity Hodgkin disease (60–70%) than the nodular sclerosis Hodgkin disease (15–30%).
Epstein–Barr virus (EBV), also called human herpes virus 4 (HHV-4), is a member of the herpes family and is one of the most common viruses in humans.
In immunocompetent hosts, EBV-infected B cells are in a resting state under host T-cell immune surveillance.
In hosts with immune dysfunction, EBV-infected cells in the reservoir may be reactivated and proliferate.
In EBV-infected cells, based on the viral proteins expressed, three latency transcription programs of EBV are designated: growth program (latency III) with expression of EBV nuclear antigens 1–6 (EBNA1-6), latent membrane proteins (LMP1, 2A and 2B); default program (latency II) expressing EBNA1, LMP1 and LMP2A; and latency program (latency I), with none or only expression of LMP2A.
In EBV-positive cases, usually all HRS cells are positive, indicating that the infection was an early event in lymphoma development.
The EBV+ HRS cells typically show an EBV latency II gene expression profile, meaning expression of the viral proteins EBV nuclear antigen 1 (EBNA1) and latent membrane proteins 1 and 2a (LMP1 and LMP2a).
EBNA1 is essential for replication of the episomal viral genome in proliferating cells. LMP1 mimics an active CD40 receptor and hence stimulates NF- B and PI3K/AKT activity.
As BCR and CD40 signalling are main survival signals for GC B cells, EBV infection of GC B cells may be a way how GC B cells with destructive mutations survive and become HRS precursor cells.
The non-Hodgkin lymphomas include a diverse and complex group of malignancies of lymphoreticular histogenesis and differentiation.
In most instances, they initially arise within lymph nodes and tend to grow as solid masses.
The non-Hodgkin lymphomas most commonly originate from cells of the B-lymphocyte series, with an estimated 85% of European and American lymphoid neoplasms having this derivation.
Tumors with a T-lymphocyte derivation are less common, whereas true histiocyte-derived lymphomas are even rarer.
Genetic abnormalities like nonrandom chromosomal and molecular rearrangements play an important role in the pathogenesis of many lymphomas and correlate with histology and immunophenotype.
Most lymphomas do not have a familial pattern; however, coexistence of multiple breast cancers, ovarian cancer, sarcomas, and lymphomas in a family may suggest an inherited abnormality in tumor suppressor genes.
Environmental factors also seem to play a role in the development of NHL. Certain chemicals have been linked to the development of NHL include a variety of pesticides and herbicides (e.g. organophosphates, chlorophenols), solvents and organic chemicals (e.g. benzene, carbon tetrachloride), and wood preservatives.
Thus certain workers like pesticide applicators, workers in the petroleum, rubber, plastics, and synthetic industries have a slightly increased risk of NHL.
Patients who receive cancer chemotherapy and/or radiation therapy are at increased risk of developing NHL.
Several viruses have been implicated in the pathogenesis of NHL, including the Epstein-Barr virus in Burkitt’s lymphoma (especially in endemic areas of Africa), sinonasal lymphoma in Asia and South America, and lymphomas in immunocompromised patients; HTLV-1 Human T-lymphotropic Virus in adult T-cell lymphoma/leukemia; and human herpesvirus 8 (HHV 8) in body cavity-based lymphomas in patients with HIV infection.
Immunodeficiency states that seem to predispose to NHL include congenital immunodeficiency states (e.g. ataxia telangiectasia, Wiskott–Aldrich syndrome, common variable hypogammaglobulinemia, severe combined immunodeficiency (SCID) as well as acquired immunodeficiency states (e.g. HIV infection, iatrogenic immunosuppression for solid organ or bone marrow transplant recipients).
Connective-tissue disorders, including Sjögren syndrome, rheumatoid arthritis, chronic lymphocytic thyroiditis, and systemic lupus erythematosus (SLE) are also associated with increased risk of NHL.
The microscopic appearance of the lesional cells was used in the past to classify the tumors as either lymphocytic or histiocytic.
With the development of modern immunologic techniques, however, it is now known that many of the lesions that had been classified as histiocytic were in fact neoplasms composed of transformed B lymphocytes. In the early 1980s, a group of American pathologists devised a classification scheme, known as the Working Formulation for Clinical Use.
S. mutans was originally isolated from carious human teeth by Clarke in 1924.
Little attention was paid to this species until the 1960s when it was demonstrated that caries could be experimentally-induced and transmitted in animals artificially-infected with strains resembling S. mutans.
Besides functioning as a resistant structural matrix, insoluble extracellular polysaccharides can act as a diffusion barrier.
The transport of metabolites and salivary buffers into the plaque and the diffusion of acid out of the plaque may be affected by glucan.
Fructans, on the other hand, unlike the mutan homopolymer of glucan, are generally soluble and can be degraded by plaque bacteria, thus serving as a reservoir of fermentable sugars for oral bacteria.
A group of fructans produced by bacteria or created by breaking down other kinds of plant fructans are called levan .
Levans are both more soluble and more readily catabolized than glucans.
Since levan hydrolysis is rapid, it may function as a short-term reservoir for the sustenance of bacterial anaerobic glycolysis in times of relative unavailability of dietary carbohydrate.
Lipoteichoic acid is another extracellular polymer that is found in cultures of S. mutans. These highly negatively charged compounds might contribute to the adhesiveness of bacteria.
In addition to this, S. mutans strains have an ability to store intracellular glycogen amylopectin type polysaccharide, which provides a reservoir of substrate and enables prolonged periods of increased metabolic activity.
Intracellular glycogen and extracellular polysaccharides serve as substrate reservoirs, which the organism may utilize for energy production, as the exogenous supplies of readily metabolized carbohydrate are depleted. In this fashion, both types of polysaccharides may play a role in the survival of organisms and in their potential to prolong acid production via glycolysis well beyond meal time.
It is known that sucrose-adapted S. mutans strains possess significant levels of invertase activity, and this enzyme isknown to hydrolyze sucrose intracellularly to free glucose and fructose.
Invertase is activated by inorganic phosphate and since phosphate accumulation is coupled with acid production, it is probable that one of the several mechanisms by which sucrose degradation is regulated in S. mutans is the activation of invertase by inorganic phosphate.
Cariogenic features of mutans streptococci - Binding to and colonization of teeth
Accumulation on tooth surfaces & participation in the formation of dental plaque.
Production of acid at a high rate.
Tolerance of high concentration of sugar, high ionic strength & highly acidic conditions
Association with dental caries in humans
Causation of dental caries in animals
Transmissible in animals & apparently in man
Reduction or elimination of mutans results in reduction or elimination of dental caries
Epithelial – Mesenchymal Interactions in Tooth Development.pptxDrPurvaPihulkar
Epithelial mesenchymal interactions (EMIs) are a series of programmed, sequential and reciprocal (complex and multiphase) communications between the epithelium and the mesenchyme with its heterotypic cell population, that result in the differentiation of one or both cell populations.
Odontogenesis is the process of tooth development, which involves both ectodermal and mesenchymal components, being the key elements in the development of teeth.
In order for the tooth to form, an interactive mechanism between these heterotypic cellular populations is required.
For these interactions to occur there should be some or other form of messenger system between epithelium and mesenchyme, further underlining the importance of cell signaling networks and intricacies of physiological growth of an individual.
In the process of embryonic development the ectoderm is composed of surface ectoderm, neural crest and neural tube.
This document discusses sterilization and disinfection in dentistry. It defines sterilization as removing all microorganisms and disinfection as removing pathogens. It describes various sterilization methods like heat, radiation, filtration and chemicals. Heat methods include dry heat using devices like hot air ovens and moist heat using autoclaves. Proper sterilization of dental instruments and impressions is important to prevent infection.
The initiation of tooth development begins at 37 days of development
with formation of a continuous horseshoe-band of thickened epithelium
in the location of upper and lower jaws – Primary Epithelial Band
Dental lamina appears as a thickening
of the oral epithelium adjacent to
condensation of ectomesenchyme
20 areas of enlargement or knobs
appear, which will form tooth buds
for the 20 primary teeth
Not all will appear at the same time.
The first to develop are those of the
anterior mandible region
At this early stage the tooth buds
have already determined their crown morphology
Successional lamina: lamina from
which permanent teeth develop
The dental lamina begins to function
at 6th prenatal week and continues to
15th year of birth (3rd molar)
Tooth development is a continuous process, however can be
divided into 3 stages:
1. Bud Stage
2. Cap Stage
3. Bell Stage
4. Hertwigs epithelial root sheath and root formation
The bud stage is represented by the first epithelial incursion into the ectomesenchyme of the jaw.
The epithelial cells show little if any change in shape or function.
The supporting ectomesenchymal cells are packed closely beneath and around the epithelial bud. As the epithelial bud continues to proliferate into the ectomesenchyme, cellular density increases immediately adjacent to the epithelial outgrowth.
This process is classically referred to as a condensation of the ectomesenchyme.
The epithelium of the dental lamina separated from the underlying ectomesenchyme by basement membrane.
Bud stage is characterized by rounded, localized growth of
epithelium surrounded by proliferating mesenchymal cells,which are packed closely beneath and around the epithelial buds
The transition from bud to cap marks the onset of morphologic differences between tooth germs that give rise to different types of teeth.
Differential cellular division in the epithelial bud initiates a change in shape so that now the epithelial outgrowth assumes a more complex outline with a flattened internal portion along which the mesenchymal condensation densifies.
As the tooth bud grows larger, it drags along with it part of the dental lamina; thus from that point on, the developing tooth is tethered to the dental lamina by an extension called the lateral lamina.
At this early stage of tooth development, identifying the formative elements of the tooth and its supporting tissues is already possible.
The epithelial outgrowth, which superficially resembles a cap sitting on a ball of condensed ectomesenchyme , is still referred to widely as the dental organ but actually should be called the enamel organ, because it eventually will form the enamel of the tooth. Henceforth, the term enamel organ is used.
Condensation of the ectomesenchyme immediately subjacent to the tooth bud caused by lack of extracellular matrix secretion by the cells thus preventing separation.
DISEASES OF NERVES AND MUSCLES
Pain is defined as an “unpleasant sensory and emotional
experience that is associated with actual or potential
tissue damage, or described in such terms even in the
absence of any obvious damage.”
Nociceptive pain
on the one hand, is caused by actual tissue injury and inflammation, such as seen with pulpal involvement of a tooth secondary to dental caries, and is an important physiological protective mechanism
Neuropathic pain
on the other hand, is caused by dysfunction of the central and/or peripheral nervous system in the absence of active injury or inflammation, such as post-herpetic neuralgia, that results in neurosensory signs and symptom
CLSSIFICATION
Trigeminal neuralgia
Glossopharyngeal neuralgia
Sphenopalatine ganglion neuralgia
Raeder’s paratrigeminal
Atypical pain/neuralgia
Postherpetic facial neuralgia
Migrainous neuralgia
Occipital neuralgia
Geniculate neuralgia
Superior laryngeal neuralgia
Tympanic plexus neuralgia
Trigeminal neuralgia –Etiology
Dental pathosis—dental pathosis is believed by some investigators to be involved with the onset of trigeminal neuralgia.
Excessive traction—secondary to excessive traction on the various divisions of the fifth nerve, being influenced by maxillo-mandibular relationship.
3 .• Allergic—it can be secondary to an allergic and hypersensitivity reaction causing edema of the trigeminal nerve root.
4• Ischemia—Wolf thought that ischemia at various portions of the trigeminal pathway might be responsible for the paroxysms of pain.
5. Compression distortion phenomenon—Jannetta and others have shown subtle changes of a compression- distortion phenomenon which is usually caused by arterial loops of atherosclerotic vessels. Vessels become elongated with advancing age and withatherosclerotic involvement gain abnormal positions by wedging into the spacebetween the pons and trigeminal nerve. It is postulated that with progressive material elongation, fascicles of adjacent nerves later suffer myelin injury and pain results.
6• Mechanical factors—like pressure due to aneurysms of the intrapetrous portion of the internal carotid artery that may erode through the floor of the intracranial fossa to exert a pulsatile irritation on the ventral side of the trigeminal ganglion.
7• Anomalies of superior cerebellar artery—it is the most recently blamed cause for trigeminal neuralgia. It lies in contact with the sensory root of the nerve and implicated as a cause of demyelination. Surgical elevation of artery or decompression of the sensory root has high success rate in relieving paroxysmal pain in case of idiopathic trigeminal neuralgia.
8• Secondary lesion—conditions such as carcinoma of the maxillary antrum, nasopharyngeal carcinoma, tumors of peripheral nerve root, intracranial vascular anomalies,and multiple sclerosis may be presented with trigeminal pain.
2.Glossopharyngeal neuralgia
The most common causes of glossopharyngeal neuralgia are
intracranial or extracranial
MANDIBULAR LATERAL INCISOR
INTRODUCTION
Lateral incisors generally appear in the oral cavity after central incisors.
Lateral incisors usually erupts during the seventh year of life .
Roots complete: 9 – 10 years
FDI SYSTEM (Federation Dentaire Internationalae)-
Mandibular RIGHT lateral incisor- 42
Mandibular LEFT lateral incisor- 32
UNIVERSAL SYSTEM-
Mandibular RIGHT lateral incisor- 26
Mandibular LEFT lateral incisor- 23
Zsigmondy-palmar system
Mandibular RIGHT central incisor-
2
Mandibular LEFT central incisor-
2
ARCH TRAITS
Lingual fossa are less pronounced on mandibular incisors.
Mandibular lateral incisors have roots that are more triangular in cross section.
Labio-lingual diameter is wider than mesio-distal diameter.
CLASS TRAITS-
Crown shapes are rectangular, longer inciso-gingivally than mesio-distally.
Mesial & distal marginal ridge converge toward the lingual cingulum.
SET TRAIT
There are depression or perikymata on the labial surface of the crown of the incisors.
Mammelons are seen on the incisal edge of newly erupted incisors.
Cervical ridges of anterior permanant teeth are prominent than primary teeth.
TYPE TRAIT
Lateral incisors have distal proximal contact more apical than the mesial contact.
Lateral incisors have disto-incisal angle more rounded than the mesio-incisal angle.
Labial Aspect
Crown is trapezoidal from labial aspect.
Mesial outline is almost straight in line with mesial outline of root.
Distal outline is straight near cervix and become slightly convex as it reaches distoincisal angle.
Distoincisal angle more rounded than mesioincisal angle
Incisal outline formed by incisal ridge is straight but has tendency to slope cervically in distal direction.
Cervical line is curved apically.
Crown is not bilaterally symmetrical
Distal half is slightly larger.
lingual aspect
Its shape is trapezoidal like labial surface.
Crown tapers lingually making lingual surface narrower than labial surface.
Shallow lingual fossa
Lingual surface is smooth devioid of developmental grooves, and is convex near cingulum.
Distal surface bulges from the incisal view
incisal aspect
It is oval labiolingually.
Labiolingual dimension is greater than mesiodistal.
Incisal ridge is at an angle to the line bisecting the tooth labiolingually rather than being perpendicular.
Slightly twisted on its root base from this aspect.
Cingulum twisted (off-center) to the distal
mesial aspect
Mesial aspect is triangular
Labial outline is convex near cervical line
Lingual outline is straight in incisal 3rd
Incisal edge lingual to root axis line
CEJ is curved more on the mesial than the distal
Mesial contact area is at incisal 3rd of crown
Mesial surface is longer than distal surface
Genetics in Tooth Development
Introduction
The Molecular Program of Tooth Development
Primary Epithelial Band
Dental Lamina
Vestibular Lamina
Initiation of the Tooth
Genes expressed during tooth development
Developmental signals controlling the position and the number of tooth germs along the oral surface
Homeobox code model
Instructive Signals for Patterning
Tooth Type Determination
Regionalization of Oral and Dental Ectoderm
Bud Stage
Bud-to-Cap Transition
Signaling centres
Applied aspects
developmental disturbances of teeth
DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH
DEVELOPMENTAL DISTURBANCES IN SIZE OF TEETH
DEVELOPMENTAL DISTURBANCES IN SHAPE OF TEETH
Anodontia
Supernumerary teeth
Predeciduous dentition
Post permanent dentition
Microdontia
Macrodontia
Gemination
Fusion
Concrescence
Dilaceration
Talon cusp
Taurodontism
Supernumerary roots
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
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.
3. Aplasia (Agenesis)
Any one or group of salivary glands may be absent,
unilaterally or bilaterally.
The CT scan or MRI will indicate the gland’s absence and
its replacement by fat and fibrous tissue.
4. Aplasia occurs for unknown reasons as an isolated
finding or in conjunction with other developmental
defects such as hemifacial microsomia, the LADD
syndrome and mandibulofacial dysostosis (Treacher
Collins).
Salivary loss leads to increased caries, burning
sensations, oral infections, taste aberrations and
difficulty with denture retention.
5. Xerostomia
(Dry mouth)
Xerostomia is not a disease but can be a symptom of
certain diseases.
It can produce serious negative effects on the patient’s
quality of life, affecting dietary habits, nutritional
status, speech, taste, tolerance to dental prosthesis and
increased susceptibility to dental caries.
7. Clinical features
Increase thirst
Dry leathery tongue
Difficulty in speech, swallowing & eating dry food
Burning sensation
Blurred vision
Fissuring of tongue.
8. Hyperplasia of Palatal Glands
An unusual localized hyperplasia or hypertrophy of minor
accessory salivary glands in the palate
Clinical Features
Palatal gland hyperplasia presents as a small localized
swelling, measuring from several millimeters to 1 cm or more
in diameter, usually on the hard palate or at the junction of
the hard and soft palates.
9. The lesion has an intact surface and is firm, sessile,
and normal in color.
It is usually asymptomatic and the patient may be
unaware of the lesion.
10. Histologic Features
The mass appears microscopically as closely packed
collections of normal-appearing mucous acini with
the usual intermingling of normal ducts. There is no
inflammation, no spillage of mucin, and no fibrosis.
Treatment
Surgical excision
11. Atresia
Congenital occlusion or absence of one or more of the
major salivary gland ducts is an exceedingly rare
condition.
When it does occur, it may result in the formation of a
retention cyst or produce a relatively severe
xerostomia.
12. Developmental Lingual Mandibular Salivary
Gland Depression
(Static bone cavity or defect of the mandible, lingual mandibular bone cavity,
static bone cyst, latent bone cyst, Stafne cyst or defect)
A Stafne bone cyst is an unusual form of slightly aberrant
salivary gland tissue wherein a developmental inclusion of
glandular tissue is found within or, more commonly.
13. It is adjacent to the lingual surface of the body of
the mandible within a deep and well-
circumscribed depression.
Predilection for males.
14. Radiographically, the lesion usually appears as an
ovoid radiolucency located between the inferior
alveolar canal and the inferior border of the mandible
in the region of the second or third molars.
Although the classic Stafne cyst is described in the
posterior mandible, an anterior variant presenting as a
round or ovoid radiolucency in the area between the
central incisors and first premolars exists; however, it
is far less common.