Description :
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
This document provides an overview of the differential diagnosis of keratotic white lesions in the oral cavity. It begins with an introduction and classification of keratotic white lesions. The main part of the document discusses specific lesions such as white sponge nevus, leukoedema, frictional keratosis, linea alba, smokeless tobacco-induced keratosis, nicotine stomatitis, oral hairy leukoplakia, candidiasis, and oral lichen planus. Each lesion is described in terms of etiology, clinical features, differential diagnosis from other lesions, and examples. The document concludes with a reference section.
This document summarizes fibro-osseous lesions (FOLs), which are characterized by the replacement of bone by a benign connective tissue matrix displaying varying degrees of mineralization. FOLs include fibrotic dysplasia, cemental lesions arising from the periodontal ligament, and fibro-osseous neoplasms. Fibrotic dysplasia is caused by a GNAS1 gene mutation and can be monostotic (single bone) or polyostotic (multiple bones). Polyostotic fibrotic dysplasia can occur with skin pigmentation and endocrine disorders. Treatment depends on symptoms and may include observation, medication such as bisphosphonates, surgical remodeling, or radical excision.
an overview of muscle pain disorder which regularly create some discomfort for patient to live a normal life as well as to the doctor regarding diagnosis of the problem.
This document discusses osteomyelitis, including its pathogenesis and management. It defines osteomyelitis as an infection of the bone marrow and describes how local and systemic predisposing factors can lead to decreased bone vitality and impaired host defense. The main types of osteomyelitis covered are suppurative, focal sclerosing, diffuse sclerosing, and proliferative perositis. For each type, the document discusses pathogenesis, clinical features, histology, radiology, and management. Key points include how acute suppurative osteomyelitis can progress to chronic form if inadequately treated, and how eliminating infection sources is important but bone changes may persist radiographically for some types.
This document provides an overview of fibro-osseous lesions and focuses on fibrous dysplasia. It discusses the classification, etiology, clinical features, radiographic features, histologic features, treatment and prognosis of fibrous dysplasia. Fibrous dysplasia is a benign bone lesion caused by a mutation in the GNAS1 gene. It can present as monostotic, polyostotic or craniofacial lesions. Radiographically, it appears as radiolucent or radiopaque areas with a "ground glass" appearance. Histologically, it is characterized by fibrous tissue and irregular woven bone trabeculae. Treatment involves surgery or bisphosphonates and the prognosis is generally good
Fibro-osseous lesions of the jaws
Fibrous dysplasia
Cemento-osseous dysplasia
Focal cemento-osseous dysplasia
Periapical cemento-osseous dysplasia
Florid cemento-osseous dysplasia
Ossifying fibroma
Juvenile aggressive ossifying fibroma
Cherubism
Fibro-osseous lesions (FOL) are characterized by replacement of normal bone architecture by collagen fibers and fibroblasts containing calcified tissue.
They include a wide variety of lesions of developmental, dysplastic and neoplastic origins with clinical and radiographic presentation and behavior.
Because of the histological similarities between diverse diseases, proper diagnosis requires correlation of history, clinical and radiographic findings.Fibrous Dysplasia
2. Reactive (dysplastic lesions arising in the tooth-bearing area (presumably of periodontal origin).
a. Periapical cemento-osseous dysplasia
b. Focal cemento-osseous dysplasia
c. Florid cemento-osseous dysplasia
3. Fibro-osseous neoplasms (widely designated as cementifying fibroma, ossifying fibroma or cemento-ossifying fibroma.Bone dysplasias
a. Fibrous dyspla i. Monostoticii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasia
b. Osteitis deformansc. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
2. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia b. Florid cemento-osseous dysplasia
3.Inflammatory/reactive processes
a. Focal sclerosing osteomyelitisb. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
4. Metabolic Disease: hyperparathyroidism
5. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibromab. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma i. Trabecular typeii. Psammomatoid type
d. Gigantiform cementomas
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.
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.
This document provides an overview of the differential diagnosis of keratotic white lesions in the oral cavity. It begins with an introduction and classification of keratotic white lesions. The main part of the document discusses specific lesions such as white sponge nevus, leukoedema, frictional keratosis, linea alba, smokeless tobacco-induced keratosis, nicotine stomatitis, oral hairy leukoplakia, candidiasis, and oral lichen planus. Each lesion is described in terms of etiology, clinical features, differential diagnosis from other lesions, and examples. The document concludes with a reference section.
This document summarizes fibro-osseous lesions (FOLs), which are characterized by the replacement of bone by a benign connective tissue matrix displaying varying degrees of mineralization. FOLs include fibrotic dysplasia, cemental lesions arising from the periodontal ligament, and fibro-osseous neoplasms. Fibrotic dysplasia is caused by a GNAS1 gene mutation and can be monostotic (single bone) or polyostotic (multiple bones). Polyostotic fibrotic dysplasia can occur with skin pigmentation and endocrine disorders. Treatment depends on symptoms and may include observation, medication such as bisphosphonates, surgical remodeling, or radical excision.
an overview of muscle pain disorder which regularly create some discomfort for patient to live a normal life as well as to the doctor regarding diagnosis of the problem.
This document discusses osteomyelitis, including its pathogenesis and management. It defines osteomyelitis as an infection of the bone marrow and describes how local and systemic predisposing factors can lead to decreased bone vitality and impaired host defense. The main types of osteomyelitis covered are suppurative, focal sclerosing, diffuse sclerosing, and proliferative perositis. For each type, the document discusses pathogenesis, clinical features, histology, radiology, and management. Key points include how acute suppurative osteomyelitis can progress to chronic form if inadequately treated, and how eliminating infection sources is important but bone changes may persist radiographically for some types.
This document provides an overview of fibro-osseous lesions and focuses on fibrous dysplasia. It discusses the classification, etiology, clinical features, radiographic features, histologic features, treatment and prognosis of fibrous dysplasia. Fibrous dysplasia is a benign bone lesion caused by a mutation in the GNAS1 gene. It can present as monostotic, polyostotic or craniofacial lesions. Radiographically, it appears as radiolucent or radiopaque areas with a "ground glass" appearance. Histologically, it is characterized by fibrous tissue and irregular woven bone trabeculae. Treatment involves surgery or bisphosphonates and the prognosis is generally good
Fibro-osseous lesions of the jaws
Fibrous dysplasia
Cemento-osseous dysplasia
Focal cemento-osseous dysplasia
Periapical cemento-osseous dysplasia
Florid cemento-osseous dysplasia
Ossifying fibroma
Juvenile aggressive ossifying fibroma
Cherubism
Fibro-osseous lesions (FOL) are characterized by replacement of normal bone architecture by collagen fibers and fibroblasts containing calcified tissue.
They include a wide variety of lesions of developmental, dysplastic and neoplastic origins with clinical and radiographic presentation and behavior.
Because of the histological similarities between diverse diseases, proper diagnosis requires correlation of history, clinical and radiographic findings.Fibrous Dysplasia
2. Reactive (dysplastic lesions arising in the tooth-bearing area (presumably of periodontal origin).
a. Periapical cemento-osseous dysplasia
b. Focal cemento-osseous dysplasia
c. Florid cemento-osseous dysplasia
3. Fibro-osseous neoplasms (widely designated as cementifying fibroma, ossifying fibroma or cemento-ossifying fibroma.Bone dysplasias
a. Fibrous dyspla i. Monostoticii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasia
b. Osteitis deformansc. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
2. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia b. Florid cemento-osseous dysplasia
3.Inflammatory/reactive processes
a. Focal sclerosing osteomyelitisb. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
4. Metabolic Disease: hyperparathyroidism
5. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibromab. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma i. Trabecular typeii. Psammomatoid type
d. Gigantiform cementomas
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.
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.
This document discusses odontomas, which are benign odontogenic tumors composed of dental tissue like enamel, dentin, and pulp. There are two main types: compound odontomas, which appear like small tooth structures, and complex odontomas, which have a disorganized appearance. Odontomas are usually asymptomatic and discovered incidentally on x-rays during dental exams. On x-rays, they appear as radiopaque masses surrounded by a radiolucent rim. Treatment involves simple surgical removal, with an excellent prognosis and no recurrence.
Fibrous dysplasia is a benign bone lesion characterized by the replacement of normal bone by fibrous tissue containing irregularly shaped bone trabeculae. It can involve single bones (monostotic) or multiple bones (polyostotic). The lesion is caused by a mutation in the GNAS1 gene leading to abnormal bone formation. Clinically, it presents as swelling or deformity and radiographically as a "ground-glass" opacity. Histologically, there are irregular bone trabeculae in a cellular fibrous stroma. Treatment involves surgery for functional or cosmetic reasons, while some severe cases may be treated with bisphosphonates. Malignant transformation is rare.
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.
Jaw bone cysts are fluid-filled cavities lined by epithelium that are commonly found in the jaw. The most common types are radicular (periapical) cysts and dentigerous cysts. Radicular cysts form in response to non-vital teeth and are usually asymptomatic, while dentigerous cysts form by fluid accumulation between the reduced enamel epithelium and an unerupted tooth. Diagnosis involves history, imaging like x-rays, and sometimes biopsy. Treatment options depend on size and include observation, marsupialization, or surgical removal.
A 36-year-old female presented with a 3-year history of a painless mass in her left buccal mucosa. Examination found a 1cm red-white firm nodule. Biopsy revealed stratified squamous epithelium overlying dense collagen bundles and fibroblasts, consistent with fibroma. Fibromas are common benign tumors of the oral cavity occurring most often in the buccal mucosa of females in the third to fourth decade of life. Histopathological examination is needed to differentiate fibromas from other similar lesions and confirm the diagnosis.
This document provides information on trismus, TMJ ankylosis, their causes and management. It discusses that trismus is the inability to open the mouth, and normal opening is 40-60mm. Trismus can be caused by infections, trauma, dental procedures, tumors, drugs, radiation and congenital issues. TMJ ankylosis is a stiffness of the joint resulting in limited or no mobility. It discusses the classification, clinical manifestations, diagnosis and management of TMJ ankylosis, whether conservative or surgical. The goals of surgical management are to release the ankylosed mass, create a gap for mobility, reconstruct the joint and prevent re-ankylosis.
The document discusses the dentinogenic concept introduced by John P. Frush and Roland D. Fisher. This concept states that the form of one's teeth is determined by factors like sex, age, and personality. Masculine features include prominent, square teeth while feminine features include smaller, rounded teeth. Personality is also a factor, with vigorous people having squarer teeth and delicate people having smaller, symmetrically arranged teeth. Age affects features like shade, wear, and the shape of the smiling line and canines. Dentinogenic restorations aim to incorporate these factors to create natural-looking teeth according to one's sex, personality, and age.
The document discusses various bone diseases that can affect the jaw bone, including inflammatory, hereditary, metabolic, and neoplastic diseases. It provides details on osteomyelitis, describing acute and chronic suppurative osteomyelitis as well as specific types like alveolar ostitis. It also discusses chronic osteomyelitis with proliferative periostitis, chronic sclerosing osteomyelitis, osteoradionecrosis, and fibro-osseous diseases like fibrous dysplasia. Histopathological features of many of these conditions are also summarized.
This document discusses fibro-osseous lesions, which replace normal bone with fibrous tissue containing newly formed mineralized structures. It describes several types of fibro-osseous lesions including fibrous dysplasia, cemento-osseous dysplasias like periapical cemental dysplasia, and fibro-osseous neoplasms like ossifying fibroma. For each type, it covers definitions, clinical features, radiographic appearances, differential diagnosis, and treatment approaches.
This document discusses causes and management of delayed tooth eruption. Common causes include retained primary teeth, supernumerary teeth, cysts, and trauma. Management involves removing the cause, assessing the impacted tooth's eruptive potential, and determining if sufficient space exists. For local causes, treatment may include extracting retained primary teeth or unerupted supernumerary teeth, and using orthodontics to create space or erupt impacted teeth if needed.
Pulpotomy is the removal of the coronal portion of the pulp while preserving the radicular pulp. It is indicated for cariously exposed primary teeth when extraction is less advantageous than retention. There are various techniques for pulpotomy including devitalization with formocresol or other chemicals to fix the pulp, preservation techniques using less harmful chemicals to maintain pulp vitality, and regeneration techniques aiming to stimulate reparative dentin formation. The goal of pulpotomy is to disinfect the exposed pulp, maintain pulp vitality, and avoid periapical issues.
TMJ is a ginglymo-diarthroidal joint that is freely mobile with superior and inferior joint spaces separated by articular disc.
The type of imaging technique depends upon the clinical problems associated, so either imaging of hard tissue (OSSEOUS) or soft tissue is desired.
Certain protocols are to be taken care before the imaging procedure:
the amount of diagnostic information available from particular imaging modality.
The cost of examination
The radiation dose
This document discusses odontogenic tumors, specifically ameloblastoma. It provides details on the classification, clinical features, histologic features, treatment and prognosis of ameloblastoma. Key points include:
- Ameloblastoma is the most common odontogenic tumor and occurs most often in the mandible. It is typically benign but locally invasive.
- Radiographically, it appears as a well-circumscribed radiolucent lesion that can be unilocular or multilocular.
- Treatment options range from curettage to marginal resection, with the goal of obtaining clear margins of at least 1cm. Wide excision is necessary in the maxilla due to risk of local invasion.
Dentigerous cysts are odontogenic cysts that surround the crown of an impacted tooth. They are the most common type of developmental jaw cyst, making up 20% of all jaw cysts. Dentigerous cysts typically occur in males in the second and third decades of life, with the most common sites being the mandibular and maxillary third molars and maxillary cuspid areas. Radiographically, dentigerous cysts can appear as central, lateral, or circumferential expansions surrounding the crown of an unerupted tooth. Small cysts are usually treated with enucleation, while larger cysts involving bone loss require marsupialization.
This document describes vesiculo-bullous lesions, which present clinically as vesicles or bullae that often rupture early, appearing as ulcerated or erosive areas. Some key points:
- Vesicles are fluid-filled lesions less than 1 cm, while bullae contain fluid and are over 1 cm.
- Causes include trauma, infection, autoimmunity, and genetic factors.
- Examples described include herpes simplex infection, varicella zoster infection, and hand foot and mouth disease. Clinical features, pathogenesis, management are provided for each. Classification is discussed based on acute vs chronic presentation, clinical presentation, and histopathological location.
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.
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
Dr. Gaurav S. Salunkhe presented on oral and maxillofacial pathology. The document discussed the classification, development, diseases and conditions that affect bone, including the alveolar bone. Specific conditions discussed in detail include cherubism, osteogenesis imperfecta, osteopetrosis, and cleidocranial dysplasia. Cherubism is a rare hereditary condition causing bilateral jaw swelling in children that typically resolves after puberty.
This document discusses various entities that can produce pericoronal radiolucencies, including both those without and with opacities. It describes normal follicular spaces and several pathologies that appear as radiolucencies surrounding unerupted teeth, such as dentigerous cysts, odontogenic keratocysts, and ameloblastic fibromas. It also provides details on inflammatory paradental cysts and pericoronitis. Differential diagnoses and typical management approaches are provided for each condition.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
This document describes cherubism, a rare genetic condition characterized by bilateral swelling of the jaws causing a cherubic facial appearance. It results from mutations in the SH3BP2 gene in most cases, causing excess bone growth in the jaws during childhood that typically resolves by adulthood. Symptoms range from mild jaw enlargement to severe issues with vision, breathing, speech or swallowing depending on the severity.
This document discusses odontomas, which are benign odontogenic tumors composed of dental tissue like enamel, dentin, and pulp. There are two main types: compound odontomas, which appear like small tooth structures, and complex odontomas, which have a disorganized appearance. Odontomas are usually asymptomatic and discovered incidentally on x-rays during dental exams. On x-rays, they appear as radiopaque masses surrounded by a radiolucent rim. Treatment involves simple surgical removal, with an excellent prognosis and no recurrence.
Fibrous dysplasia is a benign bone lesion characterized by the replacement of normal bone by fibrous tissue containing irregularly shaped bone trabeculae. It can involve single bones (monostotic) or multiple bones (polyostotic). The lesion is caused by a mutation in the GNAS1 gene leading to abnormal bone formation. Clinically, it presents as swelling or deformity and radiographically as a "ground-glass" opacity. Histologically, there are irregular bone trabeculae in a cellular fibrous stroma. Treatment involves surgery for functional or cosmetic reasons, while some severe cases may be treated with bisphosphonates. Malignant transformation is rare.
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.
Jaw bone cysts are fluid-filled cavities lined by epithelium that are commonly found in the jaw. The most common types are radicular (periapical) cysts and dentigerous cysts. Radicular cysts form in response to non-vital teeth and are usually asymptomatic, while dentigerous cysts form by fluid accumulation between the reduced enamel epithelium and an unerupted tooth. Diagnosis involves history, imaging like x-rays, and sometimes biopsy. Treatment options depend on size and include observation, marsupialization, or surgical removal.
A 36-year-old female presented with a 3-year history of a painless mass in her left buccal mucosa. Examination found a 1cm red-white firm nodule. Biopsy revealed stratified squamous epithelium overlying dense collagen bundles and fibroblasts, consistent with fibroma. Fibromas are common benign tumors of the oral cavity occurring most often in the buccal mucosa of females in the third to fourth decade of life. Histopathological examination is needed to differentiate fibromas from other similar lesions and confirm the diagnosis.
This document provides information on trismus, TMJ ankylosis, their causes and management. It discusses that trismus is the inability to open the mouth, and normal opening is 40-60mm. Trismus can be caused by infections, trauma, dental procedures, tumors, drugs, radiation and congenital issues. TMJ ankylosis is a stiffness of the joint resulting in limited or no mobility. It discusses the classification, clinical manifestations, diagnosis and management of TMJ ankylosis, whether conservative or surgical. The goals of surgical management are to release the ankylosed mass, create a gap for mobility, reconstruct the joint and prevent re-ankylosis.
The document discusses the dentinogenic concept introduced by John P. Frush and Roland D. Fisher. This concept states that the form of one's teeth is determined by factors like sex, age, and personality. Masculine features include prominent, square teeth while feminine features include smaller, rounded teeth. Personality is also a factor, with vigorous people having squarer teeth and delicate people having smaller, symmetrically arranged teeth. Age affects features like shade, wear, and the shape of the smiling line and canines. Dentinogenic restorations aim to incorporate these factors to create natural-looking teeth according to one's sex, personality, and age.
The document discusses various bone diseases that can affect the jaw bone, including inflammatory, hereditary, metabolic, and neoplastic diseases. It provides details on osteomyelitis, describing acute and chronic suppurative osteomyelitis as well as specific types like alveolar ostitis. It also discusses chronic osteomyelitis with proliferative periostitis, chronic sclerosing osteomyelitis, osteoradionecrosis, and fibro-osseous diseases like fibrous dysplasia. Histopathological features of many of these conditions are also summarized.
This document discusses fibro-osseous lesions, which replace normal bone with fibrous tissue containing newly formed mineralized structures. It describes several types of fibro-osseous lesions including fibrous dysplasia, cemento-osseous dysplasias like periapical cemental dysplasia, and fibro-osseous neoplasms like ossifying fibroma. For each type, it covers definitions, clinical features, radiographic appearances, differential diagnosis, and treatment approaches.
This document discusses causes and management of delayed tooth eruption. Common causes include retained primary teeth, supernumerary teeth, cysts, and trauma. Management involves removing the cause, assessing the impacted tooth's eruptive potential, and determining if sufficient space exists. For local causes, treatment may include extracting retained primary teeth or unerupted supernumerary teeth, and using orthodontics to create space or erupt impacted teeth if needed.
Pulpotomy is the removal of the coronal portion of the pulp while preserving the radicular pulp. It is indicated for cariously exposed primary teeth when extraction is less advantageous than retention. There are various techniques for pulpotomy including devitalization with formocresol or other chemicals to fix the pulp, preservation techniques using less harmful chemicals to maintain pulp vitality, and regeneration techniques aiming to stimulate reparative dentin formation. The goal of pulpotomy is to disinfect the exposed pulp, maintain pulp vitality, and avoid periapical issues.
TMJ is a ginglymo-diarthroidal joint that is freely mobile with superior and inferior joint spaces separated by articular disc.
The type of imaging technique depends upon the clinical problems associated, so either imaging of hard tissue (OSSEOUS) or soft tissue is desired.
Certain protocols are to be taken care before the imaging procedure:
the amount of diagnostic information available from particular imaging modality.
The cost of examination
The radiation dose
This document discusses odontogenic tumors, specifically ameloblastoma. It provides details on the classification, clinical features, histologic features, treatment and prognosis of ameloblastoma. Key points include:
- Ameloblastoma is the most common odontogenic tumor and occurs most often in the mandible. It is typically benign but locally invasive.
- Radiographically, it appears as a well-circumscribed radiolucent lesion that can be unilocular or multilocular.
- Treatment options range from curettage to marginal resection, with the goal of obtaining clear margins of at least 1cm. Wide excision is necessary in the maxilla due to risk of local invasion.
Dentigerous cysts are odontogenic cysts that surround the crown of an impacted tooth. They are the most common type of developmental jaw cyst, making up 20% of all jaw cysts. Dentigerous cysts typically occur in males in the second and third decades of life, with the most common sites being the mandibular and maxillary third molars and maxillary cuspid areas. Radiographically, dentigerous cysts can appear as central, lateral, or circumferential expansions surrounding the crown of an unerupted tooth. Small cysts are usually treated with enucleation, while larger cysts involving bone loss require marsupialization.
This document describes vesiculo-bullous lesions, which present clinically as vesicles or bullae that often rupture early, appearing as ulcerated or erosive areas. Some key points:
- Vesicles are fluid-filled lesions less than 1 cm, while bullae contain fluid and are over 1 cm.
- Causes include trauma, infection, autoimmunity, and genetic factors.
- Examples described include herpes simplex infection, varicella zoster infection, and hand foot and mouth disease. Clinical features, pathogenesis, management are provided for each. Classification is discussed based on acute vs chronic presentation, clinical presentation, and histopathological location.
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.
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
Dr. Gaurav S. Salunkhe presented on oral and maxillofacial pathology. The document discussed the classification, development, diseases and conditions that affect bone, including the alveolar bone. Specific conditions discussed in detail include cherubism, osteogenesis imperfecta, osteopetrosis, and cleidocranial dysplasia. Cherubism is a rare hereditary condition causing bilateral jaw swelling in children that typically resolves after puberty.
This document discusses various entities that can produce pericoronal radiolucencies, including both those without and with opacities. It describes normal follicular spaces and several pathologies that appear as radiolucencies surrounding unerupted teeth, such as dentigerous cysts, odontogenic keratocysts, and ameloblastic fibromas. It also provides details on inflammatory paradental cysts and pericoronitis. Differential diagnoses and typical management approaches are provided for each condition.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
This document describes cherubism, a rare genetic condition characterized by bilateral swelling of the jaws causing a cherubic facial appearance. It results from mutations in the SH3BP2 gene in most cases, causing excess bone growth in the jaws during childhood that typically resolves by adulthood. Symptoms range from mild jaw enlargement to severe issues with vision, breathing, speech or swallowing depending on the severity.
This document discusses various medical emergencies that may occur in a dental setting including altered consciousness, respiratory distress, seizures, chest pain, hypertension, and drug reactions. It provides details on the diagnosis, treatment, and management of conditions like hypoglycemia, asthma, myocardial infarction, vasovagal syncope, and drug overdoses. Prevention of medical emergencies is emphasized through thorough patient history, monitoring of vital signs, and minimizing stress on high risk individuals. Proper training of dental practitioners in emergency recognition and management is key to providing efficient treatment when complications arise.
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.
The document provides an overview of medical emergencies that can occur in dental practice. It begins with an introduction defining medical emergency and classifications of emergencies. It then discusses the dental office emergency team and basic actions for any emergency. Common emergencies like syncope, postural hypotension, acute adrenal insufficiency, hyperventilation, asthma, diabetes, epilepsy and anaphylaxis are explained. Emergency equipment, drugs, and camp management are reviewed. Recent Indian studies on emergency preparedness and knowledge are summarized. The document aims to increase awareness of medical emergencies and their appropriate management in dental settings.
This document summarizes various diseases that can affect the jaw bone. It discusses inherited conditions like osteogenesis imperfecta and achondroplasia. It also covers infections like osteomyelitis, inflammatory conditions like fibrous dysplasia, and tumors originating from bone or other tissues that can develop in the jaw. For each condition, it provides details on characteristics, clinical presentation, radiographic appearance, and other relevant information.
Major lung diseases are often caused by inhalation of irritants, infectious agents, or carcinogens. The lungs can be affected by diseases in other parts of the respiratory tract or body. Common lung diseases include infections like pneumonia, occupational diseases like black lung, and chronic conditions like COPD, lung cancer, and asthma. Loss of lung tissue cannot be recovered, so prevention and treatment of lung disease is important.
This document provides an overview of several common respiratory diseases and conditions, including their definitions, predisposing factors, clinical manifestations, nursing management, and medications. Some of the major topics covered include COPD, emphysema, chronic bronchitis, asthma, pulmonary embolism, cystic fibrosis, respiratory arrest, and pulmonary tuberculosis. Nursing interventions focus on airway clearance, breathing exercises, oxygen therapy, infection prevention, nutrition, and treating underlying causes.
Metabolic and genetic bone diseases dina pathodina hameed
This document contains radiographs and photomicrographs showing various bone diseases including:
- Osteogenesis imperfecta showing opaque dentin and thin enamel and dentin.
- Osteopetrosis showing dense bone replacing marrow in the infantile form with mandibular osteomyelitis.
- Cleidocranial dysplasia with unerupted teeth and ability to approximate shoulders.
- Paget's disease with cranial enlargement and dense new bone formation.
- Giant cell tumor showing large giant cells in destroyed maxilla.
- Massive osteolysis with extensive mandibular bone loss and pathologic fracture over 8 months.
Osteoporosis is a disease where bones become brittle and weak, increasing the risk of fractures. It is caused by low bone density due to lack of calcium and other minerals in bones. Symptoms include back pain and loss of height. Risk factors include age, gender, family history, and medications like corticosteroids. It is diagnosed through tests like DXA scans and treated through lifestyle changes, medications, and hormone therapy.
This document summarizes disorders of the respiratory system including respiratory infections, asthma, laryngitis, bronchitis, strep throat, pneumonia, emphysema, and tuberculosis. Respiratory infections can affect the upper or lower respiratory tract and are caused by bacteria, viruses, or fungi. The respiratory tract is protected by defense mechanisms but smoking and viruses can weaken these defenses. Common respiratory infections include the common cold caused by rhinoviruses and influenza. Asthma involves reversible airway obstruction from inflammation. Pneumonia is an infection of the lungs that can be treated with antibiotics. Emphysema and tuberculosis are also chronic lung diseases discussed.
Bone (2)/certified fixed orthodontic courses by Indian dental academyIndian dental academy
Description :
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 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.
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 discusses the structure and function of bones. It describes that bones are composed of cells embedded in a calcified matrix. The main cell types are osteoprogenitor cells, osteoblasts, osteoclasts and osteocytes. Bone has two types of osseous tissue - compact bone and spongy bone. Compact bone has concentric lamellae surrounding Haversian canals, while spongy bone has a more porous structure. Bones provide structure, protection, enable movement and store minerals. Remodeling and modeling allow bones to adapt throughout life.
Bone is a composite material formed mostly of calcium phosphate. There are two types of bone tissue: compact bone and spongy bone. Cortical bone accounts for 80% of the total bone mass in the adult skeleton. There are two processes of bone formation: intramembranous ossification which forms flat bones of the skull, and endochondral ossification which forms most other bones through a cartilage model. Bone is constantly remodeled through the actions of osteoblasts which build bone and osteoclasts which break it down.
The document summarizes key aspects of alveolar bone anatomy and physiology:
1. The alveolar process forms tooth sockets and provides osseous attachment to the periodontal ligament. It is made up of cortical plates and cancellous bone containing osteons and lamellae.
2. Alveolar bone remodeling is regulated by hormones like PTH and involves balanced bone resorption by osteoclasts and formation by osteoblasts.
3. The alveolar bone proper surrounds tooth roots and gives attachment to periodontal fibers, while supporting bone surrounds it. Disorders like fenestrations and dehiscences can result in root surface denudation.
Bone is a specialized connective tissue that forms the endoskeleton and provides strength and rigidity for muscle attachment. It acts as a calcium reservoir and is optimized for maximum strength with minimum weight. Bone is composed of cells embedded in a collagenous extracellular matrix that becomes mineralized with calcium hydroxyapatite, giving it rigidity and strength. Osteoblasts lay down bone matrix, osteocytes are trapped in the matrix, and osteoclasts resorb bone. Bone formation occurs through either intramembranous or endochondral ossification.
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
Physiology of tooth movement ii /certified fixed orthodontic courses by India...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Indian dental academy provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit www.indiandentalacademy.com ,or call
0091-9248678078
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
The document discusses alveolar bone and its relevance in prosthodontics. It defines alveolar bone and related terms, and describes the functions, composition, cells, classification, anatomy, development, histological structure, and influence of systemic diseases, vitamins, hormones, and drugs on alveolar bone. Alveolar bone supports teeth, distributes forces, provides attachment for muscles, acts as a reservoir for minerals, and works to maintain pH balance. Its microscopic structure consists of concentric lamellae that form Haversian systems. Conditions like hyperparathyroidism and diabetes can negatively impact alveolar bone through increased resorption.
This document discusses bone structure and fracture healing. It describes how bones are composed of minerals and store calcium, phosphate and magnesium. The periosteum and endosteum are important sources of bone forming cells. There are two types of bone tissue - compact bone which is dense and cortical, and sponge bone which is cancellous and located in the marrow cavity. Woven bone is immature bone tissue with randomly arranged collagen fibers, while lamellar bone is mature bone composed of concentric layers. Fractures heal through stimulation of the periosteum and endosteum, which results in new bone formation.
biological consideration for maxillary denture bearing areas / dental coursesIndian dental academy
Indian Dental Academy: will be one of the most relevant and exciting training
center with best faculty and flexible training programs for dental
professionals who wish to advance in their dental practice,Offers certified
courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry,
Prosthetic Dentistry, Periodontics and General Dentistry.
biological consideration for maxillary denture bearing areas / dental coursesIndian dental academy
Indian Dental Academy: will be one of the most relevant and exciting training
center with best faculty and flexible training programs for dental
professionals who wish to advance in their dental practice,Offers certified
courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry,
Prosthetic Dentistry, Periodontics and General Dentistry.
Alveolar bone and its relavance in prosthodontics / dental coursesIndian dental academy
This document discusses alveolar bone, its relevance in prosthodontics, and its development, composition, structure, and role in supporting teeth. Alveolar bone forms the sockets in the jawbones that hold the roots of teeth in place. It is composed of cortical plates, cribriform plates surrounding each tooth socket, and sometimes intervening spongy bone. The bone undergoes remodeling throughout life in response to tooth movement and forces from occlusion. Loss of teeth leads to residual ridge resorption that reduces the available bone for dental implants or dentures.
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 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 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
Description :
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
Opportunity for Dentists (BDS/MDS )to relocate to United kingdom -Register as a DENTAL HYGIENIST/ DENTAL THERAPIST without Board exams and after approval you can register in GDC as a DH/DT and start working as a DH/DT Immediately and get paid.
You can complete the whole process in 3-4 months.Salary range for DH/DT is around 2500-3500 Pounds per month.
Eligibility / requirements-
1. An International English Language Testing System (IELTS) certificate
at the appropriate level.(Within 2 yrs of application date )
2: A recent primary dental qualification that has been taught and examined in English..(Within 2 yrs of application date )
3: A recent pass in a language test for registration with a regulatory authority in a country where the first language is English.
If you are interested Please contact us for more details.
1ST, 2ND AND 3RD ORDER BENDS IN STANDARD EDGEWISE APPLIANCE SYSTEM /Fixed ort...Indian dental academy
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals
who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry,
Periodontics and General Dentistry.
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
I –Aligners are made with FDA approved transparent thermoplastic materials using 3D scanning, 3D Printing and finally Trays with Pressure vacuum formers.
Dear Doctor,
Indian Dental Academy Now offers comprehensive online Orthodontics course.
Course includes:
1.whiteboard lecture presentations
2.Case Discussions
3.with hundreds of pictures.
4.Demo on Models
5.Demo on Patients
6. subtitles in your own language
12 months unlimited access and support @350 USD only.
For Demo please visit :www.idalectures.com/preview/
For more details visit: www.idalectures.com
Please contact us for any clarifications:
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indiandentalacademy@gmail.com
Thanks & Regards
Indian Dental Academy
--
Indian Dental Academy
Leader in continuing dental education
www.indiandentalacademy.com
skype:indiandentalacademy
+919248678078
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 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
Cytotoxicity of silicone materials used in maxillofacial prosthesis / dental ...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Diagnosis and treatment planning in completely endntulous arches/dental coursesIndian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Properties of Denture base materials /rotary endodontic coursesIndian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Use of modified tooth forms in complete denture occlusion / dental implant...Indian dental academy
This document discusses dental occlusion concepts and philosophies for complete dentures. It introduces key terms like physiologic occlusion and defines different occlusion schemes like balanced articulation and monoplane articulation. The document discusses advantages and disadvantages of using anatomic versus non-anatomic teeth for complete dentures. It also outlines requirements for maintaining denture stability, such as balanced occlusal contacts and control of horizontal forces. The goal of occlusion for complete dentures is to re-establish the homeostasis of the masticatory system disrupted by edentulism.
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 Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
This document discusses dental casting investment materials. It describes the three main types of investments - gypsum bonded, phosphate bonded, and ethyl silicate bonded investments. For gypsum bonded investments specifically, it details their classification, composition including the roles of gypsum, silica, and modifiers, setting time, normal and hygroscopic setting expansion, and thermal expansion. It provides information on how the properties of gypsum bonded investments are affected by their composition. The document serves as a comprehensive overview of dental casting investment materials.
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 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 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 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 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
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
Chapter wise All Notes of First year Basic Civil Engineering.pptxDenish Jangid
Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
Main Java[All of the Base Concepts}.docxadhitya5119
This is part 1 of my Java Learning Journey. This Contains Custom methods, classes, constructors, packages, multithreading , try- catch block, finally block and more.
हिंदी वर्णमाला पीपीटी, hindi alphabet PPT presentation, hindi varnamala PPT, Hindi Varnamala pdf, हिंदी स्वर, हिंदी व्यंजन, sikhiye hindi varnmala, dr. mulla adam ali, hindi language and literature, hindi alphabet with drawing, hindi alphabet pdf, hindi varnamala for childrens, hindi language, hindi varnamala practice for kids, https://www.drmullaadamali.com
Beyond Degrees - Empowering the Workforce in the Context of Skills-First.pptxEduSkills OECD
Iván Bornacelly, Policy Analyst at the OECD Centre for Skills, OECD, presents at the webinar 'Tackling job market gaps with a skills-first approach' on 12 June 2024
1. Bone , itsBone , its
disorders anddisorders and
treatmenttreatment
INDIAN DENTAL ACADEMYINDIAN DENTAL ACADEMY
Leader in Continuing Dental EducationLeader in Continuing Dental Education
www.indiandentalacademy.com
2. AGENDAAGENDA
IntroductionIntroduction
EmbryologyEmbryology
Development of boneDevelopment of bone
Classification of boneClassification of bone
CompositionComposition
Gross histologyGross histology
Ultrastructure of boneUltrastructure of bone
Bone cellsBone cells
Bone remodellingBone remodelling
Bone disorders and treatmentBone disorders and treatment
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3. www.indiandentalacademy.com
INTRODUCTIONINTRODUCTION
Bone is a hard, specialized connective tissue with aBone is a hard, specialized connective tissue with a
calcified collagenous intercellular substancecalcified collagenous intercellular substance
Functions of bone includeFunctions of bone include
- skeletal support of the body- skeletal support of the body
- protection to internal organs- protection to internal organs
- increases efficiency of muscle action- increases efficiency of muscle action
- reservoir of minerals- reservoir of minerals
- hosts hematopoietic cells- hosts hematopoietic cells
8. DEVELOPMENT OF BONEDEVELOPMENT OF BONE
Bone development is calledBone development is called osteogenesis orosteogenesis or
ossificationossification
Two mechanisms -Two mechanisms - intramembranous
- endochondral
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13. Intramembranous ossification(cont..)Intramembranous ossification(cont..)
Deposition of calcium saltsDeposition of calcium salts
Layer of osteoid becomes lamellasLayer of osteoid becomes lamellas
of bone (trabeculae)of bone (trabeculae)
Anastomosing network of trabeculaeAnastomosing network of trabeculae
form spongy or cancellous boneform spongy or cancellous bone
Continuing appositional growth &Continuing appositional growth &
remodelling of bony trabeculae -remodelling of bony trabeculae -
convert cancellous bone intoconvert cancellous bone into
compact bonecompact bone
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14. Endochondral ossificationEndochondral ossification
Mesenchymal condensation –Mesenchymal condensation –
differentiation intodifferentiation into
chondroblasts – cartilagechondroblasts – cartilage
model with perichondriummodel with perichondrium
Capillaries grow intoCapillaries grow into
perichondrium – inner layerperichondrium – inner layer
differentiates into osteoblastsdifferentiates into osteoblasts
– thin collar of bone matrix– thin collar of bone matrix
formsforms
Perichondrium is now calledPerichondrium is now called
periosteumperiosteum
Thin collar of bone –Thin collar of bone –
subperiosteal bonesubperiosteal bone
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15. EndochondralEndochondral
ossification(cont..)ossification(cont..)
osteogenic cells & periosteal capillariesosteogenic cells & periosteal capillaries
invade cartilage model - periosteal budinvade cartilage model - periosteal bud
forms – initiate primary centre offorms – initiate primary centre of
ossification ( primary areolae)ossification ( primary areolae)
Osteogenic cells give rise toOsteogenic cells give rise to
osteoblasts- arranged along secondaryosteoblasts- arranged along secondary
areolaeareolae
Layer of ossein fibrils embedded inLayer of ossein fibrils embedded in
gelatinous intercellular substancegelatinous intercellular substance
Osteoid is calcified and a lamellae ofOsteoid is calcified and a lamellae of
bone is formedbone is formed
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16. ENDOCHONDRAL OSSIFICATIONENDOCHONDRAL OSSIFICATION
(cont..)(cont..)
At this stage, forming boneAt this stage, forming bone
consists ofconsists of
1. Elongating collar of bone1. Elongating collar of bone
along the midsectionalong the midsection
–– diaphysisdiaphysis
2. Cartilaginous ends –2. Cartilaginous ends –
epiphysesepiphyses
Secondary centre ofSecondary centre of
ossification develops inossification develops in
epiphyses – ossificationepiphyses – ossification
spreads from this centre in allspreads from this centre in all
directionsdirections
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18. ENDOCHONDRAL OSSIFICATIONENDOCHONDRAL OSSIFICATION
(cont..)(cont..)
Cartilage remains asCartilage remains as
1. Articular cartilage – covers1. Articular cartilage – covers
articular surfacearticular surface
2. Epiphyseal plate – transverse disc2. Epiphyseal plate – transverse disc
of hyaline cartilageof hyaline cartilage
Epihyseal plate enables bone toEpihyseal plate enables bone to
grow until full adult stature isgrow until full adult stature is
attainedattained
The zones of epiphyseal plate areThe zones of epiphyseal plate are
- zone of resting cartilage- zone of resting cartilage
- zone of proliferating cartilage- zone of proliferating cartilage
- zone of maturing cartilage- zone of maturing cartilage
- zone of calcifying cartilage- zone of calcifying cartilage
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19. MINERALIZATION OF BONEMINERALIZATION OF BONE
Bone tissue that is uncalcified is called osteoidBone tissue that is uncalcified is called osteoid
calcification front - interface between osteoid &calcification front - interface between osteoid &
surrounding calcified bone - calcification beginssurrounding calcified bone - calcification begins
Critical factor determining mineralization is localCritical factor determining mineralization is local
[Ca[Ca2+2+
] x [P] x [Pii
] ion into crystalline hydroxapatite] ion into crystalline hydroxapatite
[Ca[Ca55(PO(PO44))33OH]OH]
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20. MINERALIZATION OF BONEMINERALIZATION OF BONE
(cont..)(cont..)
Three theories of calcification are:Three theories of calcification are:
1. Phosphatase theory1. Phosphatase theory – by Robison– by Robison
- Alkaline phosphatase releases inorganic phosphate ionsAlkaline phosphatase releases inorganic phosphate ions
from organic phosphatesfrom organic phosphates
- Phosphate ions react with Ca ions in tissue fluids leadingPhosphate ions react with Ca ions in tissue fluids leading
to precipitation of insoluble calcium phosphateto precipitation of insoluble calcium phosphate
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21. MINERALIZATION OF BONEMINERALIZATION OF BONE (cont..)(cont..)
2. Seeding theory2. Seeding theory - by Glimcher et al- by Glimcher et al
-- Certain substances like collagen & chondroitin sulfateCertain substances like collagen & chondroitin sulfate
acts as a seed which induce crystallization ofacts as a seed which induce crystallization of
hydroxyapatitehydroxyapatite
- Regions in these molecules might have distribution of- Regions in these molecules might have distribution of
electric charges or spatial configuration for attachment ofelectric charges or spatial configuration for attachment of
ionsions
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22. MINERALIZATION OF BONEMINERALIZATION OF BONE
(cont..)(cont..)
3. Matrix vesicle theory3. Matrix vesicle theory – by Anderson– by Anderson
-- Matrix vesicles are membrane bound structures, 25nm toMatrix vesicles are membrane bound structures, 25nm to
250nm in diameter250nm in diameter
- Rounded outgrowths of cell membrane that bud from- Rounded outgrowths of cell membrane that bud from
chondrocytes, osteoblasts & odontoblastschondrocytes, osteoblasts & odontoblasts
- Contain alkaline phosphatase & ATPase- Contain alkaline phosphatase & ATPase
- Act as calcification initiators- Act as calcification initiators
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23. Decalcification:Decalcification:
Nitric acid – 5 -10%, rapid but damage to tissueNitric acid – 5 -10%, rapid but damage to tissue
and inhibit nuclear staining.and inhibit nuclear staining.
Formic acid – 10-30%, slow but less damage toFormic acid – 10-30%, slow but less damage to
tissue structures and staining.tissue structures and staining.
EDTA – 20%, slow but superior to other agentsEDTA – 20%, slow but superior to other agents
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24. CLASSIFICATION OF BONECLASSIFICATION OF BONE
BasedBased on shapeon shape
FlatFlat - skull- skull
Tubular /longTubular /long - femur, humerus- femur, humerus
IrregularIrregular - facial bones- facial bones
Based on locationBased on location
Axial skeleton - skull, vertebral columnAxial skeleton - skull, vertebral column
Appendicular skeleton - pectoral, pelvisAppendicular skeleton - pectoral, pelvis
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25. CLASSIFICATION OF BONECLASSIFICATION OF BONE (cont..)(cont..)
Based on MatrixBased on Matrix
arrangementarrangement
Lamellar boneLamellar bone
woven bonewoven bone
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26. CLASSIFICATION OF BONECLASSIFICATION OF BONE (cont..)(cont..)
Based on cross sectionBased on cross section
compact bonecompact bone
spongy bonespongy bone
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27. CLASSIFICATION OF BONECLASSIFICATION OF BONE (cont..)(cont..)
Based onBased on
developmental origindevelopmental origin
intramembraneousintramembraneous
intracartilagenousintracartilagenous
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28. COMPOSITION OF BONECOMPOSITION OF BONE
Bone : 67% inorganicBone : 67% inorganic
33% organic – 28% collagen33% organic – 28% collagen
- 5% noncollagen- 5% noncollagen
Inorganic mineral:Inorganic mineral:
- consists of calcium phosphate salt in form of- consists of calcium phosphate salt in form of
hydroxapatitehydroxapatite
--
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29. COMPOSITION OF BONECOMPOSITION OF BONE (cont..)(cont..)
Organic matrix:Organic matrix:
1. Collagen – primarily type I1. Collagen – primarily type I
trace amounts of type III,V,XI,XIIItrace amounts of type III,V,XI,XIII
2. Noncollagenous ground substance:2. Noncollagenous ground substance:
I.I. Structural components:Structural components:
a. proteoglycans – chondroitin sulfate, heparan sulfatea. proteoglycans – chondroitin sulfate, heparan sulfate
- incorporated as decorin & biglycan- incorporated as decorin & biglycan
- organizes collagen fibres- organizes collagen fibres
- seed for mineralization- seed for mineralization
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30. COMPOSITION OF BONECOMPOSITION OF BONE (cont..)(cont..)
b. gylcoproteins – fibronectin, thrombospondin,b. gylcoproteins – fibronectin, thrombospondin,
osteonectin, osteopontin,osteonectin, osteopontin,
bone sialoproteinbone sialoprotein
c.c. γγ carboxy glutamic acid containing proteins – matrix glacarboxy glutamic acid containing proteins – matrix gla
proteins, osteocalcinproteins, osteocalcin
II.II. Non structural components:Non structural components:
a. enzymes – alkaline phosphatase, collagenasea. enzymes – alkaline phosphatase, collagenase
b. growth factors – FGF, GF, TGFb. growth factors – FGF, GF, TGFββ
c. bone morphogenetic proteins – BMP-2, BMP-7c. bone morphogenetic proteins – BMP-2, BMP-7
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31. GROSS HISTOLOGY OF BONEGROSS HISTOLOGY OF BONE
DenseDense outer sheet of compact bone & aouter sheet of compact bone & a
central medullary cavitycentral medullary cavity
Medullary cavityMedullary cavity filled with yellow or redfilled with yellow or red
marrow – interrupted by network of bonymarrow – interrupted by network of bony
trabeculae (cancellous/spongy bone)trabeculae (cancellous/spongy bone)
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33. GROSS HISTOLOGY OF BONEGROSS HISTOLOGY OF BONE
(cont..)(cont..)
Mature bones consist of microscopic layers ofMature bones consist of microscopic layers of
calcified bone matrixcalcified bone matrix – lamellae– lamellae
3 distinct types of lamellae are:3 distinct types of lamellae are:
Circumferential lamellaeCircumferential lamellae ::
- circular lamallae lining external surface of- circular lamallae lining external surface of
cortex adjacent to periosteum & innercortex adjacent to periosteum & inner
surface of cortex next to endosteumsurface of cortex next to endosteum
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35. GROSS HISTOLOGY OF BONEGROSS HISTOLOGY OF BONE (cont..)(cont..)
Concentric lamellae :Concentric lamellae :
- make up bulk of compact bone- make up bulk of compact bone
- form basic unit of bone (osteon)- form basic unit of bone (osteon)
Interstitial lamellaeInterstitial lamellae ::
- interspersed between adjacent concentric- interspersed between adjacent concentric
lamellae & fill spaces between themlamellae & fill spaces between them
- represent fragments of preexisting concentric- represent fragments of preexisting concentric
lamellaelamellae
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39. GROSS HISTOLOGY OF BONEGROSS HISTOLOGY OF BONE (cont..)(cont..)
Functions of periosteumFunctions of periosteum are :are :
- provides a medium for attachment of- provides a medium for attachment of
muscles, tendons & ligamentsmuscles, tendons & ligaments
- nutritive function- nutritive function
- form bone when required- form bone when required
- fibrous layer is a limiting membrane- fibrous layer is a limiting membrane
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40. GROSS HISTOLOGY OF BONEGROSS HISTOLOGY OF BONE
(cont..)(cont..)
Internal surfaces of compact & cancellous boneInternal surfaces of compact & cancellous bone
covered bycovered by endosteumendosteum
Consists of a layer of loose connective tissue withConsists of a layer of loose connective tissue with
osteogenic cellsosteogenic cells
Physically separates bone surface from thePhysically separates bone surface from the
marrow withinmarrow within
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41. CANCELLOUS BONE
CANCELLOUS BONE:CANCELLOUS BONE:
- large volume of soft tissue- large volume of soft tissue
space than bonespace than bone
matrixmatrix
- made up of bony plates or- made up of bony plates or
rods calledrods called
trabeculaetrabeculae
- trabeculae enclose wide- trabeculae enclose wide
spaces filled by bonespaces filled by bone
marrowmarrow
- lamellae, osteocytes &- lamellae, osteocytes &
canalicules similar tocanalicules similar to
compact bonecompact bone
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42. GROSS HISTOLOGY OF BONEGROSS HISTOLOGY OF BONE
(cont..)(cont..)
BONE MARROW:BONE MARROW:
- F- Fills the medullary cavity in living boneills the medullary cavity in living bone
- Framework of reticular tissue- Framework of reticular tissue
- Reticular cell turn into osteoprogenitor cell- Reticular cell turn into osteoprogenitor cell
- Red marrow in child- Red marrow in child
- Yellow in adult - more of fat cells- Yellow in adult - more of fat cells
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43. BONE CELLSBONE CELLS
Two cell lineages each withTwo cell lineages each with
specific functions:specific functions:
1. Osteogenic cells – form &1. Osteogenic cells – form &
maintain bonemaintain bone
- osteoprogenitors,- osteoprogenitors,
preosteoblasts,preosteoblasts,
osteoblasts, osteocytes, boneosteoblasts, osteocytes, bone
lining cellslining cells
2. Osteoclasts – resorb bone2. Osteoclasts – resorb bone
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44. BONE CELLSBONE CELLS (cont..)(cont..)
BONE LINING CELLS:BONE LINING CELLS:
- inactive/postproliferative osteoblasts- inactive/postproliferative osteoblasts
- flat cells extending along bone surfaces- flat cells extending along bone surfaces
- primary site for mineral exchange- primary site for mineral exchange
between blood & bonebetween blood & bone
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45. BONE CELLSBONE CELLS (cont..)(cont..)
OSTEOBLASTS:OSTEOBLASTS:
- large, nondividing cells that is polygonal or- large, nondividing cells that is polygonal or
slightly flattened in shapeslightly flattened in shape
- cytoplasm is deeply basophilic- cytoplasm is deeply basophilic
- nucleus is ovoid & eccentrically placed- nucleus is ovoid & eccentrically placed
- cytoplasmic processes are in contact with one- cytoplasmic processes are in contact with one
another & with processes of osteocytesanother & with processes of osteocytes
Functions:Functions:
- synthesize organic- synthesize organic
constituents of boneconstituents of bone
- participate in mineralisation- participate in mineralisation
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46. BONE CELLSBONE CELLS (cont..)(cont..)
OSTEOCYTES:OSTEOCYTES:
- osteoblasts entrapped within- osteoblasts entrapped within
bone matrixbone matrix
Functions:Functions:
- maintain bone matrix- maintain bone matrix
- release calicum ions from- release calicum ions from
bone matrix during demandbone matrix during demand
- participate in local- participate in local
degradation of bonedegradation of bone
(osteocytic osteolysis)(osteocytic osteolysis)
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47. BONE CELLSBONE CELLS (cont..)(cont..)
OSTEOCLASTS:OSTEOCLASTS:
- derived from monocyte-- derived from monocyte-
macrophage systemmacrophage system
- large, multinucleated- large, multinucleated
nondividing cellnondividing cell
- present within Howship’s- present within Howship’s
lacuna or resorptionlacuna or resorption
baysbays
- ruffled border & sealing zone- ruffled border & sealing zone
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48. BONE CELLSBONE CELLS (cont..)(cont..)
OSTEOCLASTSOSTEOCLASTS - resorb bone- resorb bone
Sequence of resorptive events are:Sequence of resorptive events are:
1.1. Attachment of osteoclasts to bone surface viaAttachment of osteoclasts to bone surface via
integrinsintegrins
2.2. Creation of sealed acidic microenvironment – protonCreation of sealed acidic microenvironment – proton
pump – demineralizationpump – demineralization
3.3. Degradation of exposed matrix – acid phosphataseDegradation of exposed matrix – acid phosphatase
& cathepsin B& cathepsin B
4.4. Endocytosis of degradation products at ruffledEndocytosis of degradation products at ruffled
borderborder
5.5. Translocation & extracellular releaseTranslocation & extracellular release
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49. BONE CELLSBONE CELLS (cont..)(cont..)
Regulators of bone resorption are:Regulators of bone resorption are:
1.1. Stimulators:Stimulators:
- parathyroid harmone- parathyroid harmone
- vitamin D- vitamin D
- interleukin 1, TNF- interleukin 1, TNF
- thyroid harmones- thyroid harmones
- TGF, EGF, FGF- TGF, EGF, FGF
- bacterial endotoxin- bacterial endotoxin
- thrombin, heparin- thrombin, heparin
- bradykinin- bradykinin www.indiandentalacademy.com
50. BONE CELLSBONE CELLS (cont..)(cont..)
2. Inhibitors:2. Inhibitors:
- calcitonin- calcitonin
- interferon- interferon γγ
- glucocorticoids- glucocorticoids
- estrogen, androgens- estrogen, androgens
3. Possible agonits3. Possible agonits – effects not established– effects not established
- interleukin 6- interleukin 6
- M-CSF- M-CSF
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51. Effect of hormones on boneEffect of hormones on bone
Androgens, estrogens, and somatotrophin exert a definiteAndrogens, estrogens, and somatotrophin exert a definite
influence on growing boneinfluence on growing bone
Parathyroid hormone has a direct action on bone it is responsibleParathyroid hormone has a direct action on bone it is responsible
for the maintenance of normal blood calciumfor the maintenance of normal blood calcium
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52. 1. Androgens, estrogens, and1. Androgens, estrogens, and
somatotrophin exert a definitesomatotrophin exert a definite
influence on growing boneinfluence on growing bone
2.2. Parathyroid hormone has aParathyroid hormone has a
direct action on bone it isdirect action on bone it is
responsible for theresponsible for the
maintenance of normal bloodmaintenance of normal blood
calciumcalcium
3.3. PTH secretion is controlledPTH secretion is controlled
by a negative feedbackby a negative feedback
mechanism.mechanism.
4. A fall in serum calcium4. A fall in serum calcium
stimulates the cells in thestimulates the cells in the
parathyroid gland to increaseparathyroid gland to increase
secretion of PTH, which insecretion of PTH, which in
turn stimulates target cells.turn stimulates target cells.
SystemicSystemic factors in alveolar bone lossfactors in alveolar bone loss ;; david.j.baylink jpd 1974 vol 31david.j.baylink jpd 1974 vol 31
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53. Effect of vitamin on boneEffect of vitamin on bone
Vitamin A( not proved totally)Vitamin A( not proved totally)
Vitamin C; calcification depends on collagenVitamin C; calcification depends on collagen
production, deficiency is characterized by a decreasedproduction, deficiency is characterized by a decreased
activity of fibroblasts, osteoblasts, and odontoblastsactivity of fibroblasts, osteoblasts, and odontoblasts
Vitamin D; the maintenance of normal plasma levels ofVitamin D; the maintenance of normal plasma levels of
calcium and phosphoruscalcium and phosphorus
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54. BONE CELLSBONE CELLS (cont..)(cont..)
OSTEOCLASTOSTEOCLAST
DIFFERENTIATION:DIFFERENTIATION:
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55. BONE REMODELLINGBONE REMODELLING
Replacement of old bone by new is called boneReplacement of old bone by new is called bone
turnover or remodellingturnover or remodelling
In healthy individual, this turnover is in a steadyIn healthy individual, this turnover is in a steady
state – amount of bone lost is balanced bystate – amount of bone lost is balanced by
formationformation
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58. BONE REMODELLINGBONE REMODELLING (cont..)(cont..)
Cemental/reversal lines:Cemental/reversal lines:
- deeply basophilic straight lines which- deeply basophilic straight lines which
indicate normal bone turnoverindicate normal bone turnover
- acts as cohesive mineralized layer- acts as cohesive mineralized layer
betweenbetween
old & new boneold & new bone
- indented cemental lines seen in- indented cemental lines seen in
acceleratedaccelerated
remodellingremodelling
e.g. Paget’s diseasee.g. Paget’s disease
In osteoporosis & old age, resorptionIn osteoporosis & old age, resorption
exceeds formation – overall loss ofexceeds formation – overall loss of
bonebone
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59. The most common form of osteoporosis isThe most common form of osteoporosis is
known as “known as “primary osteoporosis.”primary osteoporosis.”
It is the result of the cumulative impact of boneIt is the result of the cumulative impact of bone
loss and deterioration of bone structure asloss and deterioration of bone structure as
people age.people age.
This bone loss can be minimized andThis bone loss can be minimized and
osteoporosis prevented through adequateosteoporosis prevented through adequate
nutrition, physical activity, and, if necessary,nutrition, physical activity, and, if necessary,
appropriate treatment.appropriate treatment.
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61. Bone disordersBone disorders
OsteodystrophyOsteodystrophy is defined as convenient term for boneis defined as convenient term for bone
diseases which are neither inflammatory nor neoplastic in nature,diseases which are neither inflammatory nor neoplastic in nature,
but which are genetic, metabolic or are of unknown cause.but which are genetic, metabolic or are of unknown cause.
Normal bone development requiresNormal bone development requires
Formation of collagenous organic matrixFormation of collagenous organic matrix
Deposition of bone salts (Calcium and phosphorus)Deposition of bone salts (Calcium and phosphorus)
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62. Introduction…Introduction…
Normal bone development can be disturbed byNormal bone development can be disturbed by
Intrinsic DefectsIntrinsic Defects
Defect in bone matrix formation (scurvy)Defect in bone matrix formation (scurvy)
Defect in mineralisation (rickets)Defect in mineralisation (rickets)
Extrinsic DefectsExtrinsic Defects
Deficiency diseases (calcium and phosphorous)Deficiency diseases (calcium and phosphorous)
Endocrine disturbances (parathyroid)Endocrine disturbances (parathyroid)
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64. Classification of OsteodystrophyClassification of Osteodystrophy
A. Genetic Disorders of BoneA. Genetic Disorders of Bone
1.1. Osteogenesis ImperfectaOsteogenesis Imperfecta
2.2. Marfan syndromeMarfan syndrome
3.3. OsteopetrosisOsteopetrosis
4.4. Cleidocranial DysplasiaCleidocranial Dysplasia
5.5. CherubismCherubism
6.6. Treacher Collins syndromeTreacher Collins syndrome
7.7. Tricho-dento-osseous syndromeTricho-dento-osseous syndrome
8.8. AchondroplasiaAchondroplasia
B. CraniosynostosisB. Craniosynostosis
1.1. Crouzon syndromeCrouzon syndrome
2.2. Apert syndromeApert syndrome www.indiandentalacademy.com
65. Classification of Osteodystrophy…Classification of Osteodystrophy…
C. Fibro-osseous LesionsC. Fibro-osseous Lesions
1.1. Fibrous DysplasiaFibrous Dysplasia
2.2. Cemento-osseous DysplasiaCemento-osseous Dysplasia
D. Metabolic Disorders of BoneD. Metabolic Disorders of Bone
1.1. RicketsRickets
2.2. ScurvyScurvy
3.3. HypophosphatasiaHypophosphatasia
E. Endocrine DisturbancesE. Endocrine Disturbances
1.1. HyperparathyriodismHyperparathyriodism
2.2. DwarfismDwarfism
3.3. GigantismGigantism
4.4. AcromegalyAcromegaly
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66. Classification of Osteodystrophy…Classification of Osteodystrophy…
F. MucoploysaccharidosisF. Mucoploysaccharidosis
1.1. Hurler syndromeHurler syndrome
2.2. Hunter syndromeHunter syndrome
G. Renal OsteodystrophyG. Renal Osteodystrophy
1.1. OsteomalaciaOsteomalacia
2.2. OsteosclerosisOsteosclerosis
3.3. Osteitis FibrosaOsteitis Fibrosa
H. Bone pathology of unknown etiologyH. Bone pathology of unknown etiology
1.1. Paget’s DiseasePaget’s Disease
2.2. Massive OsteolysisMassive Osteolysis
3.3. Idiopathic OsteosclerosisIdiopathic Osteosclerosis
4.4. Pierre Robin syndromePierre Robin syndrome
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68. Osteogenesis ImperfectaOsteogenesis Imperfecta
Heterogeneous group of heritable disordersHeterogeneous group of heritable disorders
characterized by impairment of collagen maturation,characterized by impairment of collagen maturation,
resulting in thin cortex, fine trabeculation and diffuseresulting in thin cortex, fine trabeculation and diffuse
osteoporosis.osteoporosis.
Mainly inherited as AD (AR and sporadic cases hasMainly inherited as AD (AR and sporadic cases has
been reported).been reported).
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69. Osteogenesis Imperfecta…Osteogenesis Imperfecta…
Mutations in one of two genes that guide formation of type IMutations in one of two genes that guide formation of type I
collagen.collagen.
COL1A1 = 17q21.3-q22.COL1A1 = 17q21.3-q22.
COL1A2 = 7q22.1.COL1A2 = 7q22.1.
Defect in cross linking of collagen molecules resulting in failureDefect in cross linking of collagen molecules resulting in failure
of fetal collagen to be transformed into mature collagen.of fetal collagen to be transformed into mature collagen.
Calcification proceeds normally.Calcification proceeds normally.
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70. Osteogenesis Imperfecta…Osteogenesis Imperfecta…
Clinical FeaturesClinical Features
Angulations and shortening of long bones – multiple fractures.Angulations and shortening of long bones – multiple fractures.
Large head size with frontal and temporal bossngLarge head size with frontal and temporal bossng
Blue scleraBlue sclera
Xray of long bones show thin cortex with fine trabeculation andXray of long bones show thin cortex with fine trabeculation and
micro fractures.micro fractures.
Wormian bonesWormian bones
Oral ManifestationsOral Manifestations
Class III malocclusion – maxillary hypoplasiaClass III malocclusion – maxillary hypoplasia
Impacted teeth – 1Impacted teeth – 1stst
and 2and 2ndnd
molarsmolars
Opalescent teethOpalescent teeth
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71. Sillence, Senn and Danks classificationSillence, Senn and Danks classification
(1979)(1979)
Type IType I Type IIType II Type IIIType III Type IVType IV
Most common and mildestMost common and mildest
formform
Type I AType I A withoutwithout
opalescent teeth;opalescent teeth; Type I BType I B
associated with opalescentassociated with opalescent
teeth (DI is due to mutationteeth (DI is due to mutation
of DSPP gene 4q21.3)of DSPP gene 4q21.3)
Moderate bone fragilityModerate bone fragility
with 10% showingwith 10% showing
fracturesfractures at birth; 10%at birth; 10%
never show any fracture;never show any fracture;
frequency of fracture reducesfrequency of fracture reduces
after puberty.after puberty.
Blue scleraBlue sclera
Hearing lossHearing loss before thebefore the
age of 30age of 30
Hypermobility ofHypermobility of
JointsJoints (TMJ dysarthrosis)(TMJ dysarthrosis)
Easy bruisingEasy bruising
Most severeMost severe
form; 90% die atform; 90% die at
birth, rest withinbirth, rest within
4 weeks of age.4 weeks of age.
Extreme boneExtreme bone
fragility withfragility with
all casesall cases
showingshowing inin
uteroutero fractures.fractures.
Blue sclera.Blue sclera.
Moderately severe boneModerately severe bone
fragility; 50% showfragility; 50% show inin
uteroutero fractures.fractures.
Normal to pale blueNormal to pale blue
sclera; fades as the childsclera; fades as the child
grows.grows.
Hearing loss,Hearing loss,
hypermobility of joints,hypermobility of joints,
easy bruising.easy bruising.
Opalescent teeth may orOpalescent teeth may or
may not be present.may not be present.
Majority of affectedMajority of affected
individuals die duringindividuals die during
childhood due tochildhood due to
cardiopulmonarycardiopulmonary
complications.complications.
Mild to moderatelyMild to moderately
severe bone fragility.severe bone fragility.
50% show no50% show no
fractures at any timefractures at any time
of life.of life.
Normal to pale blueNormal to pale blue
sclera; fades as thesclera; fades as the
child grows.child grows.
Hearing loss and easyHearing loss and easy
bruising are rare.bruising are rare.
Opalescent teeth mayOpalescent teeth may
or may not be present.or may not be present.
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72. Osteogenesis Imperfecta…Osteogenesis Imperfecta…
Type V, VI, VII has been reported, but theType V, VI, VII has been reported, but the
genetic causes has not been identified.genetic causes has not been identified.
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74. •Bone graft augmentation and dental implant treatment in a
patient with osteogenesis imperfecta: review of the literature
with a case report.
Lee CY, Ertel SK.
Implant Dent. 2003;12(4):291-5
•Dentofacial rehabilitation by osteodistraction,
augmentation and implantation despite
osteogenesis imperfecta.
Binger T, Rucker M, Spitzer WJ.
Int J Oral Maxillofac Surg. 2006 Jun;35(6):559-62.
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76. OsteopetrosisOsteopetrosis
Marble bone disease; Albers-Schonberg disease (GermanMarble bone disease; Albers-Schonberg disease (German
radiologist)radiologist)
Exact molecular defect or site of mutation is not known.Exact molecular defect or site of mutation is not known.
Marked increase in bone density due to failure of osteoclast toMarked increase in bone density due to failure of osteoclast to
resorb bone. Osteoclast number is normal but bone remodelingresorb bone. Osteoclast number is normal but bone remodeling
doesn't occur due to failure of osteoclast function.doesn't occur due to failure of osteoclast function.
Clinically classified intoClinically classified into
Infantile (malignant) osteopetrosisInfantile (malignant) osteopetrosis
Adult (benign) osteopetrosisAdult (benign) osteopetrosis
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77. Infantile (malignant)Infantile (malignant)
osteopetrosisosteopetrosis
Adult (benign) osteopetrosisAdult (benign) osteopetrosis
ARAR
At birth or early infancyAt birth or early infancy
Nasal stuffiness due toNasal stuffiness due to
mastoid and paranasalmastoid and paranasal
sinus malformation maysinus malformation may
be the earliest presentingbe the earliest presenting
complaint.complaint.
Diffuse sclerosis ofDiffuse sclerosis of
bone with growthbone with growth
retardation.retardation.
ADAD
Less severe manifestations; discovered later in life.Less severe manifestations; discovered later in life.
40% are asymptomatic; discovered as increased bone opacity on routine40% are asymptomatic; discovered as increased bone opacity on routine
radiographs.radiographs.
IntermediateIntermediate
OsteopetrosisOsteopetrosis
TransientTransient
OsteopetrosisOsteopetrosis
Less severe variant ofLess severe variant of
infantile osteopetrosisinfantile osteopetrosis
Asymptomatic atAsymptomatic at
birthbirth
Frequent fracturesFrequent fractures
after the 1after the 1stst
decade ofdecade of
lifelife
Marrow failure isMarrow failure is
AsymptomaticAsymptomatic
Diffuse sclerosis withDiffuse sclerosis with
marrow failuremarrow failure
Resolve withoutResolve without
specific therapyspecific therapy
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78. Osteopetrosis…Osteopetrosis…
Clinical FeaturesClinical Features
Defective bone remodeling leads to obliteration ofDefective bone remodeling leads to obliteration of
marrow space, resulting in marrow failure andmarrow space, resulting in marrow failure and
pancytopenia.pancytopenia.
Anemia leads to compensatory hepatosplenomegalyAnemia leads to compensatory hepatosplenomegaly
Recurrent infections due to granulocytopeniaRecurrent infections due to granulocytopenia
Easy bruising and bleeding due to thrombocytopeniaEasy bruising and bleeding due to thrombocytopenia
Even though bone is thickened and sclerotic it has poorEven though bone is thickened and sclerotic it has poor
mechanical properties, and is fragile leading to frequentmechanical properties, and is fragile leading to frequent
pathological fractures (40%).pathological fractures (40%).www.indiandentalacademy.com
79. Osteopetrosis…Osteopetrosis…
Cranial nerve neuropathies due to compressionCranial nerve neuropathies due to compression
(narrowing of foramina) leads to blindness, deafness or(narrowing of foramina) leads to blindness, deafness or
facial palsy.facial palsy.
Facial deformity – broad face, frontal bossing,Facial deformity – broad face, frontal bossing,
hypertelorism, snub nose.hypertelorism, snub nose.
Delayed tooth eruption due to bone sclerosis.Delayed tooth eruption due to bone sclerosis.
Osteomyelitis common after tooth extraction (10%).Osteomyelitis common after tooth extraction (10%).
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80. RadiographicRadiographic
FeaturesFeatures
LaboratoryLaboratory
DiagnosisDiagnosis
HistopathologicHistopathologic
al Featuresal Features
Skull and jaws showSkull and jaws show
dense diffuse radiopacity.dense diffuse radiopacity.
Due to increasedDue to increased
density the roots of thedensity the roots of the
teeth are nearly invisible.teeth are nearly invisible.
Rugger-jersey sign –Rugger-jersey sign –
alternate bands ofalternate bands of
radio-dense and normalradio-dense and normal
bone densitybone density
appearance ofappearance of
vertebrae.vertebrae.
RBCs <1 millionRBCs <1 million
cmmcmm
Serum calcium,Serum calcium,
phosphorous andphosphorous and
alkaline phosphatasealkaline phosphatase
levels are normal;levels are normal;
acid phosphatase andacid phosphatase and
creatinine kinasecreatinine kinase
(CK-BB) are(CK-BB) are
elevated.elevated.
Abnormal endosteal boneAbnormal endosteal bone
formation.formation.
Cancellous bone is replaced byCancellous bone is replaced by
torturous lamellar bone.torturous lamellar bone.
Marrow spaces show globularMarrow spaces show globular
amorphous bone deposition.amorphous bone deposition.
Persistence of cartilaginousPersistence of cartilaginous
core in endochondrial bones.core in endochondrial bones.
Numerous osteoclast are seenNumerous osteoclast are seen
with no evidence of Howship’swith no evidence of Howship’s
lacunae.lacunae.
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82. Osteopetrosis…Osteopetrosis…
TreatmentTreatment
Bone marrow transplantBone marrow transplant
Interferon gamma 1b along with calcitriolInterferon gamma 1b along with calcitriol
Corticosteriods; PTH; MCSFCorticosteriods; PTH; MCSF
Administer antibiotics (lincomycin,Administer antibiotics (lincomycin,
fluoroquinolone) before extraction.fluoroquinolone) before extraction.
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84. Cleidocranial DysplasiaCleidocranial Dysplasia
AD; 40% cases represent spontaneous mutationAD; 40% cases represent spontaneous mutation
Mutation in CBFa1 (core binding factor alpha -1) located on 6p21Mutation in CBFa1 (core binding factor alpha -1) located on 6p21
Rearrangement in 8q22 and 6q has also been reportedRearrangement in 8q22 and 6q has also been reported
Clinical FeaturesClinical Features
Short statureShort stature
10% shows absence of clavicle – unilateral or bilateral; 90% have10% shows absence of clavicle – unilateral or bilateral; 90% have
clavicle showing varying degree of hypoplasia and malformationclavicle showing varying degree of hypoplasia and malformation
Narrow drooping shoulders with long neck; can approximateNarrow drooping shoulders with long neck; can approximate
shoulders in frontshoulders in front
Arnold head – large globular head with frontal, parietal and occipitalArnold head – large globular head with frontal, parietal and occipital
bossingbossing
Frontanelles may remain open till adulthood; wormian bonesFrontanelles may remain open till adulthood; wormian bones
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85. Cleidocranial Dysplasia…Cleidocranial Dysplasia…
Oral ManifestationsOral Manifestations
Maxillary hypoplasiaMaxillary hypoplasia
Underdeveloped lacrimal and zygomatic bonesUnderdeveloped lacrimal and zygomatic bones
High arched narrow palateHigh arched narrow palate
Increased prevalence of cleft palateIncreased prevalence of cleft palate
Retention of deciduous teeth with delayed or failure of eruption ofRetention of deciduous teeth with delayed or failure of eruption of
permanent teethpermanent teeth
Radiographic FeaturesRadiographic Features
Numerous unerupted permanent and supernumerary teeth – lackNumerous unerupted permanent and supernumerary teeth – lack
cementumcementum
Mandible shows increased bone density with narrow ramus andMandible shows increased bone density with narrow ramus and
pointed coronoid processpointed coronoid process
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88. Bone grafting and osseointegratedBone grafting and osseointegrated implants in the treatment ofimplants in the treatment of
cleidocranial dysplasia.cleidocranial dysplasia.
Lombardas PLombardas P, Toothaker RW., Toothaker RW.
Bone grafts and endosseous implants were usedBone grafts and endosseous implants were used
in the maxillary arch in an attempt to provide ain the maxillary arch in an attempt to provide a
retentive and esthetic overdenture for a youngretentive and esthetic overdenture for a young
patientpatient
Compend Contin Educ Dent. 1997 May;18(5):509-12, 514.Compend Contin Educ Dent. 1997 May;18(5):509-12, 514.
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89. Cleidocranial dysplasia:
modern concepts of treatment and a report of an orthodontic resistant case
requiring a restorative solution.
- Butterworth C.
•A case is presented of a young boy with cleidocranial dysplasia,
whose multiple supernumerary teeth prevented the eruption of
most of his permanent teeth
• His maxillary incisor teeth failed to erupt following removal of
anterior supernumerary elements and orthodontic traction.
•Lack of abutment teeth and a difficult maxillary base made
prosthetic treatment almost impossible.
• A horseshoe acrylic denture retained by milled crowns bonded
to the deciduous canines and a maxillary first molar proved a
very successful restoration
Dent Update. 1999 Dec;26(10):458-62.
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90. Treatment of a patient with cleidocranial dysplasia using
osseointegrated implants: a patient report.
Petropoulos VC, Balshi TJ, Balshi SF, Wolfinger GJ.
•This patient report describes the treatment of a 42-year-old woman with
cleidocranial dysplasia.
•Endosseous implants were used to restore the mandibular and maxillary
arches with fixed prostheses.
•Six implants were placed in the mandible and immediately loaded with an
acrylic resin fixed prosthesis.
• In the maxillary arch, 10 implants were submerged for 4 months prior to
functional loading.
•A transitional denture was relined and placed in the maxilla 10 days after
implant placement.
•Three months later, a definitive mandibular prosthesis was fabricated.
•The definitive maxillary restoration was delivered 6 months after surgery.
The most recent follow-up, 6 months after delivery, confirmed a
satisfactory treatment result to date
Int J Oral Maxillofac
Implants. 2004 Mar-Apr;19(2):282-7
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92. Fibrous DysplasiaFibrous Dysplasia
Not a hereditary diseaseNot a hereditary disease
Mutation in GNAS1 (guanine nucleotide binding protein,Mutation in GNAS1 (guanine nucleotide binding protein, αα
stimulating activity polypeptide) located on 20q13.2stimulating activity polypeptide) located on 20q13.2
Cause continuous activation of G-protein leading to overCause continuous activation of G-protein leading to over
production of cAMP.production of cAMP.
Clinical severity depends on point in time mutation of GNAS1Clinical severity depends on point in time mutation of GNAS1
occursoccurs
Early embryological life – osteoblast, melanocytes, endocrine cells areEarly embryological life – osteoblast, melanocytes, endocrine cells are
affectedaffected
Later in life – osteoblast – multiple boneLater in life – osteoblast – multiple bone
Post natal – mutated cells confined to one site – single bonePost natal – mutated cells confined to one site – single bone
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93. Fibrous Dysplasia (FD)…Fibrous Dysplasia (FD)…
VariantsVariants
Monostotic Fibrous Dysplasia – 80%Monostotic Fibrous Dysplasia – 80%
Limited to a single boneLimited to a single bone
Polyostotic Fibrous DysplasiaPolyostotic Fibrous Dysplasia
Jaffe-Lichenstein syndrome – FD of bone + café-au-Jaffe-Lichenstein syndrome – FD of bone + café-au-
lait spotslait spots
McCune-Albright syndrome – FD + café-au-laitMcCune-Albright syndrome – FD + café-au-lait
spots + endocrine disturbancesspots + endocrine disturbances
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94. Monostotic Fibrous DysplasiaMonostotic Fibrous Dysplasia
Age: 2Age: 2ndnd
decade; mean age – 30yrsdecade; mean age – 30yrs
Gender: no predilectionGender: no predilection
Site: ribs, femur, tibia, craniofacial bones (25%)Site: ribs, femur, tibia, craniofacial bones (25%)
Maxilla along with zygoma, sphenoid or occiputMaxilla along with zygoma, sphenoid or occiput
Slow growing asymptomatic swelling causing facial deformity ofSlow growing asymptomatic swelling causing facial deformity of
varying degrees.varying degrees.
When maxilla involved obliteration of max. sinus is commonWhen maxilla involved obliteration of max. sinus is common
Radiographic FeaturesRadiographic Features
Ground glass appearanceGround glass appearance
Not well demarcated from normal adjacent boneNot well demarcated from normal adjacent bone
Narrowing of PDL space with ill-defined lamina duraNarrowing of PDL space with ill-defined lamina dura
Early lesion may appear radiolucent or mottledEarly lesion may appear radiolucent or mottled
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95. Polyostotic Fibrous DysplasiaPolyostotic Fibrous Dysplasia
Jaffe-Lichenstein syndromeJaffe-Lichenstein syndrome
Asymptomatic before 10yrs of ageAsymptomatic before 10yrs of age
Most commonly affected are long bones – leg length discrepancy dueMost commonly affected are long bones – leg length discrepancy due
to multiple pathological fractures; bowed legsto multiple pathological fractures; bowed legs
Upto 75% of the skeletal bones maybe involvedUpto 75% of the skeletal bones maybe involved
Facial asymmetry when jaws involvedFacial asymmetry when jaws involved
Café-au-lait spots – 50% casesCafé-au-lait spots – 50% cases
Increased melanocytes in basal layer of skin/mucosaIncreased melanocytes in basal layer of skin/mucosa
trunk, thighs, abdomen, buttocks, neck, oral mucosatrunk, thighs, abdomen, buttocks, neck, oral mucosa
Irregular outlineIrregular outline
Usually on same side as bone lesion and near midline of bodyUsually on same side as bone lesion and near midline of body
May occur at birth and precede development of skeletal and endocrineMay occur at birth and precede development of skeletal and endocrine
abnormalitiesabnormalities
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96. Polyostotic Fibrous DysplasiaPolyostotic Fibrous Dysplasia
McCune-Albright syndromeMcCune-Albright syndrome
Fuller Aibright 1Fuller Aibright 1stst
described this syndrome in 1937described this syndrome in 1937
Associated with endocrinopathies along with bone involvementAssociated with endocrinopathies along with bone involvement
and café-au-lait spotsand café-au-lait spots
Sexual precocity – menstrual bleeding, breast development and pubic hairSexual precocity – menstrual bleeding, breast development and pubic hair
growth within 1growth within 1stst
few yrs of lifefew yrs of life
Pituitary adenomasPituitary adenomas
HyperthyroidismHyperthyroidism
Maybe associated with intramuscular myxomas – Mazabraud’sMaybe associated with intramuscular myxomas – Mazabraud’s
syndromesyndrome
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97. Fibrous Dysplasia…Fibrous Dysplasia…
Histopathological FeaturesHistopathological Features
Irregularly shaped trabeculae of woven bone not connected toIrregularly shaped trabeculae of woven bone not connected to
each other in cellular, loosely arranged fibrous stroma –each other in cellular, loosely arranged fibrous stroma –
curvilinear or Chinese letter shapedcurvilinear or Chinese letter shaped
Lesionl bone fuses directly to normal bone at periphery of lesionLesionl bone fuses directly to normal bone at periphery of lesion
Bone trabeculae are not lined by osteoblast and are thought toBone trabeculae are not lined by osteoblast and are thought to
arise by metaplasiaarise by metaplasia
Tiny calcified spherules may be seen rarelyTiny calcified spherules may be seen rarely
Long standing lesion undergoes progressive maturation toLong standing lesion undergoes progressive maturation to
lamellar bonelamellar bone
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99. Fibrous Dysplasia…Fibrous Dysplasia…
TreatmentTreatment
Most stop enlarging when skeletal maturation is reachedMost stop enlarging when skeletal maturation is reached
Cosmetic surgery for large lesionsCosmetic surgery for large lesions
25-50% show re-growth after cosmetic shaving; especially25-50% show re-growth after cosmetic shaving; especially
in younger patientsin younger patients
ComplicationsComplications
0.1 - 4% has shown malignant transformation0.1 - 4% has shown malignant transformation
OsteosarcomaOsteosarcoma
FibrosarcomaFibrosarcoma
ChondrosarcomaChondrosarcoma
LiposarcomaLiposarcoma
Breast carcinomas (Females)Breast carcinomas (Females)
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100. Dental characteristics of fibrous dysplasia and McCune-AlbrightDental characteristics of fibrous dysplasia and McCune-Albright
syndrome.syndrome.
Akintoye SOAkintoye SO,, Lee JSLee JS,, Feimster TFeimster T,, Booher SBooher S,, Brahim JBrahim J,, Kingman AKingman A,,
Riminucci MRiminucci M,, Robey PGRobey PG,, Collins MTCollins MT..
((Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2003 Sep;96(3):275-82Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2003 Sep;96(3):275-82))
Malocclusion (81%) and other prevalent dental anomalies (41%)Malocclusion (81%) and other prevalent dental anomalies (41%)
included tooth rotation, oligodontia, and taurodontism. Theincluded tooth rotation, oligodontia, and taurodontism. The
expansion of the maxilla or mandible by FD did not distort theexpansion of the maxilla or mandible by FD did not distort the
dental arch curvature, anddental arch curvature, and routine dental therapies such as extractions,routine dental therapies such as extractions,
restorations, and orthodontic treatment did not exacerbate FD lesionsrestorations, and orthodontic treatment did not exacerbate FD lesions
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102. CherubismCherubism
AD inherited disease; sporadic cases have been reportedAD inherited disease; sporadic cases have been reported
Mutation in 4p16Mutation in 4p16
Clinical FeaturesClinical Features
Age: 2-5 yrsAge: 2-5 yrs
Gender: equal predilectionGender: equal predilection
Site: Posterior mandible; all four quadrants maybe affectedSite: Posterior mandible; all four quadrants maybe affected
Asymptomatic slow growing bilateral swelling in posteriorAsymptomatic slow growing bilateral swelling in posterior
mandible and / or maxilla – plump cheeked cherubsmandible and / or maxilla – plump cheeked cherubs
May develop within 6months; stabiles by 10-12yrs; slowly regressMay develop within 6months; stabiles by 10-12yrs; slowly regress
after pubertyafter puberty
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103. Cherubism…Cherubism…
Clinical Features…Clinical Features…
Eyes upturned to heaven appearanceEyes upturned to heaven appearance
eyeballs tilted upwards – involvement of infra orbital rim and flooreyeballs tilted upwards – involvement of infra orbital rim and floor
Rim of sclera seen beneath iris – stretching of upper facial skin pulls lowerRim of sclera seen beneath iris – stretching of upper facial skin pulls lower
eyelid downwardseyelid downwards
Cervical lymphadenopathyCervical lymphadenopathy
Loss of vision / hearingLoss of vision / hearing
Oral ManifestationsOral Manifestations
V shaped palate with widened alveolar ridgesV shaped palate with widened alveolar ridges
Premature loss of deciduous teeth and delayed or failure of eruptionPremature loss of deciduous teeth and delayed or failure of eruption
of teethof teeth
Displacement of teethDisplacement of teeth
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104. Cherubism…Cherubism…
Arnott (1978) grading systemArnott (1978) grading system
Grade I – involvement of both mandibular ramusGrade I – involvement of both mandibular ramus
Grade II – involvement of both mandibular ramus and maxillaryGrade II – involvement of both mandibular ramus and maxillary
tuberositiestuberosities
Grade III – involvement of whole maxilla and mandible exceptGrade III – involvement of whole maxilla and mandible except
coronoid and condylescoronoid and condyles
Radiographic FeaturesRadiographic Features
Bilateral multilocular radiolucencyBilateral multilocular radiolucency
Numerous unerupted teethNumerous unerupted teeth
Teeth appear floating because of alveolar bone lossTeeth appear floating because of alveolar bone loss
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105. Cherubism…Cherubism…
Histopathological FeaturesHistopathological Features
Fibro-vascular connective tissue with numerous small bloodFibro-vascular connective tissue with numerous small blood
vessels showing eosinophilic cuffingvessels showing eosinophilic cuffing
Multinucleated giant cells (osteoclast)Multinucleated giant cells (osteoclast)
Older resolving lesion show increased fibrous tissue, less giantOlder resolving lesion show increased fibrous tissue, less giant
cells, and new bone formationcells, and new bone formation
TreatmentTreatment
Tends to becom static,and shows regression as patientTends to becom static,and shows regression as patient
approaches puberty.approaches puberty.
Cosmetic surgery if deformity persists after growth completionCosmetic surgery if deformity persists after growth completionwww.indiandentalacademy.com
108. RicketsRickets
Rickets is common term for any disorder affecting Vit. DRickets is common term for any disorder affecting Vit. D
metabolism, leading to derangement of Vit. D-calcium-metabolism, leading to derangement of Vit. D-calcium-
phosphate axis, resulting in failure of endochondralphosphate axis, resulting in failure of endochondral
calcification.calcification.
Depending on derangement rickets can beDepending on derangement rickets can be
1.1. Vit. D Deficient RicketsVit. D Deficient Rickets
2.2. Adult Rickets (Osteomalacia)Adult Rickets (Osteomalacia)
3.3. Vit. D Resistant RicketsVit. D Resistant Rickets
4.4. Vit. D dependent Rickets (Renal Rickets)Vit. D dependent Rickets (Renal Rickets)
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109. Vit. D MetabolismVit. D Metabolism
Dietary ergosterol
from vegetables
7 dehydrocholestrol
from acetyl-CoA
UV Light UV Light
Ergocalciferol (Vit. D2) Cholecalciferol (Vit. D3)
25 hydoxycholecalciferol
Hepatic 25 hydroxylase
Renal 1 α hydroxylase
1, 25 dihydrocholecalceferol
Increased Ca absorption from gut
Increased Ca re-absorption from kidney
Increased Ca deposition in bone
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110. Vit. D deficient ricketsVit. D deficient rickets
Deficiency of Vit. D in children – 400IU daily requirementDeficiency of Vit. D in children – 400IU daily requirement
Clinical FeaturesClinical Features
Growth retardationGrowth retardation
Bowed legsBowed legs
Enlarged jointsEnlarged joints
Rachitic rosaryRachitic rosary
Oral ManifestationsOral Manifestations
Abnormal enamel & dentin formation – wide predentin zone,Abnormal enamel & dentin formation – wide predentin zone,
increased interglobular dentin; higher caries indexincreased interglobular dentin; higher caries index
Delayed eruption of teethDelayed eruption of teeth
MalocclusionMalocclusion
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111. Adult Rickets (Osteomalacia)Adult Rickets (Osteomalacia)
Deficiency of Vit. D in adults, leading toDeficiency of Vit. D in adults, leading to
reduced calcium absorptionreduced calcium absorption
Most common in postmenopausal womenMost common in postmenopausal women
Normal remodeling of bone, but due to CaNormal remodeling of bone, but due to Ca
deficiency bones are fragile – pelvisdeficiency bones are fragile – pelvis
Increased susceptibility to fracturesIncreased susceptibility to fractures
Radiographs of long bones may showRadiographs of long bones may show
longitudinal hairline fractureslongitudinal hairline fractureswww.indiandentalacademy.com
112. Vit. D resistant ricketsVit. D resistant rickets
Inherited as X-linked dominant traitInherited as X-linked dominant trait
Mutation in PHEX gene (phosphate regulating gene with endopeptidaseMutation in PHEX gene (phosphate regulating gene with endopeptidase
activity on X chromosome) which encodes for zinc metalloproteinase enzymeactivity on X chromosome) which encodes for zinc metalloproteinase enzyme
– precise mechanism unknown– precise mechanism unknown
Males more affectedMales more affected
Clinical symptoms of rickets but does not respond to therapeutic doses ofClinical symptoms of rickets but does not respond to therapeutic doses of
Vit. DVit. D
Hyocalcemia and hypophosphatemia due to decreased absorption from gutHyocalcemia and hypophosphatemia due to decreased absorption from gut
and renal re-absorptionand renal re-absorption
Short stature; bowed legsShort stature; bowed legs
Large pulp horns extending to DEJ causing pulp exposure and periapicalLarge pulp horns extending to DEJ causing pulp exposure and periapical
infection in otherwise normal appearing teeth.infection in otherwise normal appearing teeth.
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113. Vit.D dependent rickets (Renal Rickets)Vit.D dependent rickets (Renal Rickets)
Rare AR conditionRare AR condition
Chronic renal disease causing deficiency in 1Chronic renal disease causing deficiency in 1 αα
hydroxylase enzyme needed to convert 25hydroxylase enzyme needed to convert 25
hydoxycholecalciferol to 1,25hydoxycholecalciferol to 1,25
dihydoxycholecalciferoldihydoxycholecalciferol
Patients respond to replacement therapy withPatients respond to replacement therapy with
calcitriolcalcitriol
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115. HypophosphatasiaHypophosphatasia
Rare inherited metabolic disease of bone (AR / AD).Rare inherited metabolic disease of bone (AR / AD).
Deficiency of tissue-nonspecific alkaline phosphataseDeficiency of tissue-nonspecific alkaline phosphatase
(TNSALP).(TNSALP).
Mutation in ALPL gene located at 1p36.1Mutation in ALPL gene located at 1p36.1
VariantsVariants
PerinatalPerinatal
InfantileInfantile
ChildhoodChildhood
AdultAdult
Odonto-hypophosphatasiaOdonto-hypophosphatasia
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116. Hypophosphatasia…Hypophosphatasia…
PerinatalPerinatal
Most severeMost severe
Diagnosed at birth and infant dies within hours due toDiagnosed at birth and infant dies within hours due to
respiratory failurerespiratory failure
InfantileInfantile
Child appear normal till 6 months of age; show failure of growthChild appear normal till 6 months of age; show failure of growth
Skeletal malformationSkeletal malformation
Short bowed legs – short statureShort bowed legs – short stature
Rachitic chest – respiratory failureRachitic chest – respiratory failure
Craniosynostosis – increased intracranial pressureCraniosynostosis – increased intracranial pressure
Hypercalcemia – renal stones; failureHypercalcemia – renal stones; failure
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117. Hypophosphatasia…Hypophosphatasia…
ChildhoodChildhood
Child grows up to childhood without any symptomsChild grows up to childhood without any symptoms
Delayed milestones – walking, speech, motor skillsDelayed milestones – walking, speech, motor skills
CraniosynostosisCraniosynostosis
Short stature, bowed legs, enlarged jointsShort stature, bowed legs, enlarged joints
Premature loss of deciduous teeth – anterior teeth; alveolar bonePremature loss of deciduous teeth – anterior teeth; alveolar bone
loss; enlarged pulp chamberloss; enlarged pulp chamber
Skull radiograph – uniformly placed, poorly defined, smallSkull radiograph – uniformly placed, poorly defined, small
radiolucencies – beaten copper appearanceradiolucencies – beaten copper appearance
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118. Hypophosphatasia…Hypophosphatasia…
AdultAdult
Mildest form – symptom less till middle ageMildest form – symptom less till middle age
Foot pain / thigh pain due to pseudo-fractures of metatarsals /Foot pain / thigh pain due to pseudo-fractures of metatarsals /
femurfemur
Premature loss of deciduous and permanent teethPremature loss of deciduous and permanent teeth
Odonto-hypophosphatasiaOdonto-hypophosphatasia
AsymptomaticAsymptomatic
Premature loss of deciduous and permanent teethPremature loss of deciduous and permanent teeth
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119. Hypophosphatasia…Hypophosphatasia…
Laboratory DiagnosisLaboratory Diagnosis
Serum calcium and phosphorous – normalSerum calcium and phosphorous – normal
Serum alkaline phosphatase – decreasedSerum alkaline phosphatase – decreased
Serum and urine phosphoethanolamine – elevatedSerum and urine phosphoethanolamine – elevated
Histopathological FeaturesHistopathological Features
Normal bone or abundant woven boneNormal bone or abundant woven bone
Osteoblast and osteoclast appear morphologically normal; noOsteoblast and osteoclast appear morphologically normal; no
Howship’s lacunaeHowship’s lacunae
Increased width of proliferating cartilage; Numerous cartilageIncreased width of proliferating cartilage; Numerous cartilage
islands within marrowislands within marrow
Reduced or absence of cementumReduced or absence of cementum
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120. TreatmentTreatment
Therapeutic measures unsuccessful.Therapeutic measures unsuccessful.
High doses of phosphates results in moderateHigh doses of phosphates results in moderate
improvement.improvement.
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122. Paget’s DiseasePaget’s Disease
Abnormal resorption and deposition of bone, resulting inAbnormal resorption and deposition of bone, resulting in
distortion and weakening of affected bonesdistortion and weakening of affected bones
Exact cause is unknownExact cause is unknown
InflammatoryInflammatory
GeneticGenetic
EndocrineEndocrine
Slow virus infection – paramyxovirusSlow virus infection – paramyxovirus
VariantsVariants
MonostoticMonostotic
Polyostotic – most commonPolyostotic – most common
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123. Paget’s Disease…Paget’s Disease…
Clinical FeaturesClinical Features
Age: older people; rare in patients younger than 40yrsAge: older people; rare in patients younger than 40yrs
Gender: MaleGender: Male
Site: lumbar vertebrae, pelvis, skull, femur, skullSite: lumbar vertebrae, pelvis, skull, femur, skull
Jaws affected in 17% of casesJaws affected in 17% of cases
Bone painBone pain
Bowing deformity of weight bearing bones – simian stanceBowing deformity of weight bearing bones – simian stance
Pagetic bone forms near joints and promotes osteoarthriticPagetic bone forms near joints and promotes osteoarthritic
changes – joint pain, limited mobilitychanges – joint pain, limited mobility
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124. Paget’s Disease…Paget’s Disease…
Skull circumference will progressively increaseSkull circumference will progressively increase
Cranial nerve compression leads to deafness or visualCranial nerve compression leads to deafness or visual
disturbancesdisturbances
Maxilla more affected; cause enlargement of middle 3Maxilla more affected; cause enlargement of middle 3rdrd
of theof the
face – leontiasis osseaface – leontiasis ossea
Nasal obstruction, obliterated sinus, deviated nasal septumNasal obstruction, obliterated sinus, deviated nasal septum
Alveolar ridges enlarge symmetricallyAlveolar ridges enlarge symmetrically
If dentulous – spacing between teethIf dentulous – spacing between teeth
If edentulous – dentures no longer fitIf edentulous – dentures no longer fit
Extractions maybe difficult due to hypercementosisExtractions maybe difficult due to hypercementosis
Extensive hemorrhage due to increased vascularityExtensive hemorrhage due to increased vascularity
Osteomyelitis in sclerotic phaseOsteomyelitis in sclerotic phase
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125. Paget’s Disease…Paget’s Disease…
Radiographic FeaturesRadiographic Features
Decreased radio-density of bone; skull show large circumscribedDecreased radio-density of bone; skull show large circumscribed
areas of radiolucency – osteoporosis circumscriptaareas of radiolucency – osteoporosis circumscripta
Alteration in tabecular pattern – cotton wool appearanceAlteration in tabecular pattern – cotton wool appearance
Teeth show hypercementosisTeeth show hypercementosis
Bone scintigraphy – entire mandible show marked uptake fromBone scintigraphy – entire mandible show marked uptake from
condyle to condyle - Lincoln’s sign or black beardcondyle to condyle - Lincoln’s sign or black beard
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126. Paget’s Disease…Paget’s Disease…
Histopathological FeaturesHistopathological Features
Uncontrolled alternating resorption andUncontrolled alternating resorption and
deposition of bonedeposition of bone
Basophilic reversal lines indicating junctionBasophilic reversal lines indicating junction
between alternating resorptive and formativebetween alternating resorptive and formative
phases of bone – mosaic or jigsaw patternphases of bone – mosaic or jigsaw pattern
Numerous osteoblast and osteoclast in lacunaeNumerous osteoblast and osteoclast in lacunae
rim bone trabeculaerim bone trabeculae
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128. Paget’s Disease…Paget’s Disease…
Laboratory DiagnosisLaboratory Diagnosis
Serum calcium and phosphorous levels are normalSerum calcium and phosphorous levels are normal
Serum alkaline phosphatase levels are elevatedSerum alkaline phosphatase levels are elevated
Bone resorption markersBone resorption markers
Urinary hydroxyprolineUrinary hydroxyproline
N-telopeptides assayN-telopeptides assay
Pyridinoline cross-link assayPyridinoline cross-link assay
TreatmentTreatment
Analgesics for bone painAnalgesics for bone pain
Calcitonin and bisphonatesCalcitonin and bisphonates
Dentures to be remade periodically to accommodate increase inDentures to be remade periodically to accommodate increase inwww.indiandentalacademy.com
129. Paget’s Disease…Paget’s Disease…
PrognosisPrognosis
< 1% show malignant transformation< 1% show malignant transformation
Osteosarcoma of pelvis and lower extremities;Osteosarcoma of pelvis and lower extremities;
jaw ostesarcomas are rarejaw ostesarcomas are rare
Associated with poor prognosisAssociated with poor prognosis
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131. References(cont..)References(cont..)
Ham’s histology ; 9Ham’s histology ; 9thth
edition; David H. Cormackedition; David H. Cormack
Textbook of human histology;Inderbir singhTextbook of human histology;Inderbir singh
Color atlas of histology;2Color atlas of histology;2ndnd
edition;M.B.L.Craigmyleedition;M.B.L.Craigmyle
Langman’s medical embryology;7Langman’s medical embryology;7thth
edition;T.W.Sadleredition;T.W.Sadler
Wheater’s functional histology;B. young,J.W.HeathWheater’s functional histology;B. young,J.W.Heath
Bone remodeling and its disorders;2Bone remodeling and its disorders;2ndnd
edition;Gregoryedition;Gregory
R. MundyR. Mundy
www. eMedicine .comwww. eMedicine .com
www.cytochemistry.netwww.cytochemistry.net
www.bonehistologylab.comwww.bonehistologylab.com
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