Odontogenic tumors arise from tooth-forming tissues and can be divided into three categories: tumors of odontogenic epithelium without mesenchyme, tumors with both epithelium and mesenchyme, and tumors of mesenchyme alone. Ameloblastoma is the most common odontogenic tumor, representing 1% of jaw tumors. It typically presents as a multilocular radiolucency in the mandible and is classified as solid/multicystic, unicystic, or peripheral. Histologically it demonstrates islands of epithelial cells resembling dental lamina. Treatment involves wide local excision due to its persistence and recurrence.
ODONTOGENIC MYXOMA :
Benign mesenchymal lesion that mimics microscopically the dental pulp or follicular connective tissue
Derived from odontogenic ectomesenchymeClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effectedClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effectedClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effected
Radiographic feature :
Radiolucent and it appear as a well circumscribed or diffuse lesion
Often multilocular with honey comb pattern
Cortical plate expansion, root displacement or resorption may be seen Histopathology :
Tumor consist of acellular myxomatous connective tissue.
Benign fibroblast and myofibroblast with some amount of collagen are found in matrix
Bony island representing residual tubeculae
Capillaries are scattered through out the lesion
ODONTOGENIC MYXOMA :
Benign mesenchymal lesion that mimics microscopically the dental pulp or follicular connective tissue
Derived from odontogenic ectomesenchymeClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effectedClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effectedClinical feature:
Age : 10- 50 yrs with mean age of 30 yrs
No gender predilection
Both mandible and maxilla are equally effected
Radiographic feature :
Radiolucent and it appear as a well circumscribed or diffuse lesion
Often multilocular with honey comb pattern
Cortical plate expansion, root displacement or resorption may be seen Histopathology :
Tumor consist of acellular myxomatous connective tissue.
Benign fibroblast and myofibroblast with some amount of collagen are found in matrix
Bony island representing residual tubeculae
Capillaries are scattered through out the lesion
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
Central Giant Cell Granuloma :
WHO has defined it as an intraosseous lesion consisting of cellular and fibrous tissue that contains multiple foci of hemorrhage, aggregation of multinucleated giant cells and occasionally trabaculae of woven bone
Etiology JAFFE (1953): considered this lesion to be a local reparative reaction of bone, possibly to intramedullary hemorrhage or trauma, hence the term reparative giant cell granuloma was accepted.
Charles A Waldron & W G Shafer (1966) suggested trauma be an important etiological factor in the initiation of the CGCG of the jaws
Thoma K H (1986) suggested that the lesion may be due to capillary injury caused by defective wall due to some type of trauma
J V Soames and J C Southam (1997) suggested that it could be a reaction to some form of hemodynamic disturbance in bone marrow, perhaps associated with trauma and hemorrhage REGEZI AND SCIUBBA(1999) :
Suggested that
Response to previous traumatic or inflammatory episodes.
This lesion is charecterised by proliferation of fibroblasts and multinucleated giant cells, in a densely packed stromaThe CGCG is a benign process that occurs almost exclusively within the jaw bones
CLINICAL PRESENTATION
Found predominantly in children and young adult
It has a female predilection (2:1)
Most commonly affected site is the anterior portion of the jaws, with an increased frequency of occurrence in the mandible
Majority of the CGCG of jaws are painless, expansion of bone is detected on routine examination
Few cases may be associated with pain, paresthesia or perforation of a cortical bone plate, occasionally resulting in the ulceration of the mucosal surface by the underlying lesion
Radiographic featuresCentral giant cell lesions present as radiolucent defects. Which may be unilocular or multilocular.
The defect is usually well delineated
The lesion may vary from a 5×5mm incidental radiographic findings to a destructive lesion greater than 10cm in size.
radiographic findings
A small unilocular lesion may be confused with periapical granuloma or cysts.
multilocular giant cell lesions cannot be radiographically distinguished from ameloblastomas or other multilocular lesions. Based on clinical and radiological features CGCG may be divided into two categories
- Non-aggressive lesion
- Aggressive lesion
The non aggressive lesion makes up most cases and exhibit few or no symptoms, they demonstrate slow growth and do not show cortical perforation or root resorption of teeth involved in the lesion. The aggressive lesions are characterized by pain, rapid growth, cortical perforation and root resorption and show marked tendency to recur when compared with non aggressive typeSoft spongy, brownish to reddish friable tissue of various size.
A specimen is usually coated with fresh or coagulated blood. Giant cell lesions of the jaws show a variety of features. Common to all is the presence of few to many multinucleated
Benign, locally aggressive tumor of odontogenic epithelium, Previously called adamantinoma, Second most common odontogenic tumor after odontoma, Mandible is most common site, Usually asymptomatic and can be found incidentally on routine dental examinations
Benig tumors of jaw/certified fixed orthodontic courses by Indian dental acad...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.
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
Central Giant Cell Granuloma :
WHO has defined it as an intraosseous lesion consisting of cellular and fibrous tissue that contains multiple foci of hemorrhage, aggregation of multinucleated giant cells and occasionally trabaculae of woven bone
Etiology JAFFE (1953): considered this lesion to be a local reparative reaction of bone, possibly to intramedullary hemorrhage or trauma, hence the term reparative giant cell granuloma was accepted.
Charles A Waldron & W G Shafer (1966) suggested trauma be an important etiological factor in the initiation of the CGCG of the jaws
Thoma K H (1986) suggested that the lesion may be due to capillary injury caused by defective wall due to some type of trauma
J V Soames and J C Southam (1997) suggested that it could be a reaction to some form of hemodynamic disturbance in bone marrow, perhaps associated with trauma and hemorrhage REGEZI AND SCIUBBA(1999) :
Suggested that
Response to previous traumatic or inflammatory episodes.
This lesion is charecterised by proliferation of fibroblasts and multinucleated giant cells, in a densely packed stromaThe CGCG is a benign process that occurs almost exclusively within the jaw bones
CLINICAL PRESENTATION
Found predominantly in children and young adult
It has a female predilection (2:1)
Most commonly affected site is the anterior portion of the jaws, with an increased frequency of occurrence in the mandible
Majority of the CGCG of jaws are painless, expansion of bone is detected on routine examination
Few cases may be associated with pain, paresthesia or perforation of a cortical bone plate, occasionally resulting in the ulceration of the mucosal surface by the underlying lesion
Radiographic featuresCentral giant cell lesions present as radiolucent defects. Which may be unilocular or multilocular.
The defect is usually well delineated
The lesion may vary from a 5×5mm incidental radiographic findings to a destructive lesion greater than 10cm in size.
radiographic findings
A small unilocular lesion may be confused with periapical granuloma or cysts.
multilocular giant cell lesions cannot be radiographically distinguished from ameloblastomas or other multilocular lesions. Based on clinical and radiological features CGCG may be divided into two categories
- Non-aggressive lesion
- Aggressive lesion
The non aggressive lesion makes up most cases and exhibit few or no symptoms, they demonstrate slow growth and do not show cortical perforation or root resorption of teeth involved in the lesion. The aggressive lesions are characterized by pain, rapid growth, cortical perforation and root resorption and show marked tendency to recur when compared with non aggressive typeSoft spongy, brownish to reddish friable tissue of various size.
A specimen is usually coated with fresh or coagulated blood. Giant cell lesions of the jaws show a variety of features. Common to all is the presence of few to many multinucleated
Benign, locally aggressive tumor of odontogenic epithelium, Previously called adamantinoma, Second most common odontogenic tumor after odontoma, Mandible is most common site, Usually asymptomatic and can be found incidentally on routine dental examinations
Benig tumors of jaw/certified fixed orthodontic courses by Indian dental acad...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.
The various cysts of the jaws, few key points for the diagnosis and the treatment options available for each.
Mentor: Dr Saikat Saha MDS, OMFS, SIliguri, West Bengal, India
Address: MAXFAC Center for Oral and Maxillofacial and Head & Neck Surgery, Siliguri
Email : maxfacmail@gmail.com
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
2. INTRODUCTION
Group of lesions arising from the tooth- producing
apparatus or its remnants
May originate from epithelial and/or
ectomesenchymal odontogenic tissues
1% of all jaw tumors
2
3. WHO HISTOLOGICAL TYPING OF ODONTOGENIC
TUMORS
1992 (MODIFIED)
Tumors of odontogenic epithelium without
odontogenic ecto-mesenchyme
Tumors of odontogenic epithelium with odontogenic
ecto-mesenchyme with or without dental hard tissue
formation (mixed)
Tumors of odontogenic ecto-mesenchyme with or
without odontogenic epithelium
3
5. TUMORS OF ODONTOGENIC EPITHELIUM WITH
ODONTOGENIC ECTO-MESENCHYME WITH OR
WITHOUT DENTAL HARD TISSUE FORMATION (MIXED)
• Ameloblastic fibro odontoma
• Adenomatoid odontogenic tumor (AOT)
• Ameloblastic fibroma
• Odontomes
Compound
Complex
5
6. TUMORS OF ODONTOGENIC ECTO-MESENCHYME WITH
OR WITHOUT ODONTOGENIC EPITHELIUM
Odontogenic fibroma
Odontogenic myxoma
Cementoblastoma
6
7. MALIGNANT ODONTOGENIC TUMORS
Odontogenic carcinoma
a. Malignant ameloblastoma
b. Primary intraosseous carcinoma
c. Malignant variant of other odontogenic epithelial tumors
d. Malignant changes in odontogenic cyst
Odontogenic sarcoma
a. Ameloblastic fibrosarcoma
b. Ameloblastic fibrodentinosarcoma
7
10. TUMORS OF ODONTOGENIC EPITHELIUM WITH ODONTOGENIC
ECTO-MESENCHYME WITH OR WITHOUT DENTAL HARD TISSUE
FORMATION
• Ameloblastic fibroma
• Ameloblastic fibrodentinoma (dentinoma)
• Ameloblastic fibro odontoma
• Odontomes
Compound type
Complex type
Odontoameloblastoma
Calcifying cystic odontogenic cyst
Dentinogenic ghost cell tumor
10
11. TUMORS OF MESENCHYME AND/ OR ODONTOGENIC ECTO-
MESENCHYME WITH OR WITHOUT ODONTOGENIC EPITHELIUM
Odontogenic fibroma
Odontogenic myxoma/ Myxofibroma
Cementoblastoma
11
12. BONE RELATED LESIONS
Other tumors – Melanotic neuroectodermal tumor of infancy
12
• Ossifying fibroma (Cemento Ossifying fibroma)
• Fibrous dysplasia
• Osseous dysplasia
• Cemento osseous dysplasia
Periapical cemental dysplasia
Focal cemento osseous dysplasia
Florid cemento osseous dysplasia
• Central Giant cell granuloma
• Cherubism
• Aneurysmal bone cyst
• Simple bone cyst
13. MALIGNANT TUMORS OF ODONTOGENIC ORIGIN
Odontogenic carcinoma
a. Malignant ameloblastoma
b. Ameloblastic carcinoma: Primary type (intraosseous)
c. Ameloblastic carcinoma: Secondary type (peripheral)
d. Primary intraosseous squmaous cell carcinoma
e. Primary intraosseous squmaous cell carcinoma derived
Keratocytsic odontogenic tumor
f. Primary intraosseous squmaous cell carcinoma derived from an
odontogenic cyst
g. Clear cell odontogenic carcinoma
h. Ghost cell odontogenic carcinoma
Odontogenic sarcomas
a. Ameloblastic fibrosarcoma (ameloblastic sarcoma)
b. Ameloblastic fibrodentinoma sarcoma & fibro odontosarcoma
13
14. 14
2017 WHO classification of
odontogenic tumors and cysts
Malignant odontogenic
tumors
Benign odontogenic
tumors
• Epithelial origin
• Mixed (Epi-mes)
origin
• Mesenchymal origin
22. DEFINITION
Ameloblastoma is a tumor that is “usually
unicentric, non-functional, intermittent
in growth, anatomically benign and
clinically persistent”.
-Robinson
22
23. HISTOGENESIS
Cell rests of the enamel organ
(remnants of dental lamina or HERS)
Epithelium of odontogenic cysts (esp. D C)
Disturbance of the developing enamel organ
Basal cells of oral mucosal epithelium
Heterotopic epithelium
23
33. Mixture of different patterns is
common
A lesion may exhibit one or more
histologic patterns
Lesions are sub-classified according
to the most predominant pattern
33
34. FOLLICULAR AMELOBLASTOMA
Islands of epithelial cells in a connective
tissue stroma
Epithelial islands have a core of loosely
arranged polygonal cells (resembling stellate
reticulum), surrounded by a peripheral layer
of tall, columnar ameloblast-like cells with
polarized nuclei
Cyst formation: microcysts to generally cystic
tumour (degeneration of stellate reticulum-like
cells).
34
45. GRANULAR CELL AMELOBLASTOMA
Relatively rare subtype
Resembles follicular type, but center of the
tumour islands form sheets of large
eosinophilic granular cells
Cytoplasmic granules consist of pleomorphic,
lysosome-like organelles
Aggressive variant with highest recurrence
rate
45
52. BASAL CELL AMELOBLASTOMA
Least common type
Occurs primarily in extra-osseous lesions
Nests of basaloid cells occupy the central
portions of the islands (no stellate reticulum-like
tissue)
52
56. PLEXIFORM AMELOBLASTOMA
Network of thin (inter-connecting)
strands of epithelium bordered by
columnar cells
Loose, vascular, sparsely cellular or
fibrous stroma may show areas of
cystic degeneration
56
70. Intraluminal / Plexiform unicystic
ameloblastoma:
Intraluminal plexiform proliferation, but no
infiltration of the cyst wall
(i.e., projects only into the lumen).
70
72. Mural ameloblastoma
Invasive islands of follicular or plexiform type of
ameloblastoma, sometimes continuous with cyst
lining, infiltrate the cyst wall.
72
80. RADIOGRAPHIC FEATURES
Rarely produces saucerization of underlying
bone
HISTOLOGIC FEATURES
Mostly acanthomatous > plexiform >
follicular type
80
84. Craniopharyngioma/Pituitary ameloblastoma
(copious ghost cell production, cystic morphology, and
the presence of osteoid or bone).
Adamantinoma of long bones
(lack the regular shape and reversed nuclear polarity of
ameloblastoma cells).
84
Extra-oral tumours resembling
Ameloblastoma
85. MALIGNANT AMELOBLASTOMA
An ameloblastoma that has given rise
to pulmonary or nodal metastases and
the metastases have retained the
microscopic appearances of the
primary growth
85
86. AMELOBLASTIC CARCINOMA
Ameloblastoma that has cytologic features
of malignancy in the primary lesion or in a
metastasis. Later, the metastases tend to
resemble less well-differentiated squamous
cell carcinoma
86
89. HISTOGENESIS
From stratum intermedium (cell resemble &
high alk phosphatase activity)
Reduced enamel epithelium?
89
90. CLINICAL FEATURES
Occurs over a wide range from 3-92
years; (average = 40 years)
Mandible > maxilla; molar region
Painless, slow-growing swelling
May be associated with unerupted or
impacted tooth (third molars)
90
92. RADIOGRAPHIC FEATURES
May exhibit considerable variation
• Diffuse or well-circumscribed radiolucent area
(may be with an impacted tooth)
• Mixed radiolucent / radio-opaque picture with
many small irregular bony trabeculae traversing
the radiolucent area
• Multilocular or ‘honeycomb’ pattern
• Scattered flecks of calcification in the RL areas-
‘driven –snow’ appearance
• Peripheral CEOT- saucerization of underlying
92
94. HISTOLOGIC FEATURES
Islands, sheets or strands of pleomorphic, slightly
eosinophilic epithelial cells in a connective tissue
stroma
Distinct cell membranes and intercellular bridges
of epithelial cells
Nuclei vary in number, size and shape
Mitosis is rare
Presence of a homogeneous eosinophilic
amyloid-like substance, which may calcify to form
concentrically lamellated ‘Liesegang rings’
94
96. TUMOR CELLS WITH LARGE CENTRALLY LOCATED
HYPERCHROMATIC NUCLEI
96
97. TUMOR CELLS WITH VARIABILITY IN NUCLEAR SIZE, SHAPE AND
STAINING
97
98. 98
Amyloid- homogenous eosinophilic substance
Thought to be
• Filamentous degeneration of keratin
filaments conversion into amyloid
• Tissue degeneration
• Type IV collagen
• Basal lamina
• Enamel matrix
101. CALCIFICATION OF AMYLOID-LIKE DEPOSITS
101
• Presence or absence of calcification in
CEOT has prognostic implications
• Lack of calcification indicates less tumor
differentiation and hence favors more
chance of recurrence
102. CONCENTRIC LAYERS OF CALCIFICATION WITHIN AMYLOID-LIKE
MATERIAL LIESEGANG RINGS
102
104. CLEAR CELL VARIANT OF CEOT
Cells have clear vacuolated cytoplasm with
round or oval nuclei, or nuclei flattened
against the cell membrane
Clear cells comprise the bulk of the tumour,
or are seen in a few scattered foci
Clear cells are mucicarmine-negative
104
109. ADENOMATOID ODONTOGENIC
TUMOUR
(AOT)
(Adenoameloblastoma,
Ameloblastic adenomatoid tumour)
Characterised by formation of duct-like structures by
epithelial component of the lesion
Uncommon; completely benign; may be hamartomas
1992 WHO classification it was under epi-mes tumor
2005 WHO classification & 2017 its under epithelial
without ectomesenchyme origin
109
111. CLINICAL FEATURES
Slow growing, painless swelling;
< 3cm in size
May be associated with an
unerupted tooth (cuspid)
111
112. 112
2/3rd of cases occur in 2nd decade
2/3rd of cases occur in females
2/3rd of cases occur in ant maxilla
2/3rd of cases associated with
unerupted canine
2/3rd tumor
113. RADIOGRAPHIC FEATURES
Rounded radiolucency with well-
defined outline with faint radio-opaque
foci
(‘snow-flake’ calcifications) in 60% of
cases.
Displacement of adjacent teeth / roots;
resorption is rare
113
114. 114
2 variants :
1. Follicular variant – tumour contains a tooth
2. Extra follicular variant – no tooth in the
tumour; seen between roots of teeth
116. HISTOLOGIC FEATURES
Well-defined capsule
Spindle-shaped or cuboidal epithelial
cells in sheets, whorls, strands; may
form rosettes
Columnar or cuboidal cells arranged in
ductal pattern, with ductal lumina
containing eosinophilic coagulum
116
117. HISTOLOGIC FEATURES
Loose, scanty, sparsely cellular connective
tissue stroma
Fragments of amorphous or crystalline
calcification (possibly amyloid) seen among
sheets of epithelial cells
Small foci of calcification scattered throughout
the tumour (attempted formation of enamel or
dentine or cementum)
117
128. Complete differentiation of epithelial
and mesenchymal cells
→ functional ameloblasts and odontoblasts
→ enamel and dentin formation
Improper morpho-differentiation of
odontogenic cells
→ haphazard deposition of enamel and dentin
128
133. CLINICAL FEATURES
Any age
any site
maxilla : mandible: : 2:1
right side > left
compound > complex
compound – anterior maxilla
complex – posterior jaws
133
134. Small
Asymptomatic, but may result in unerupted /
impacted teeth, retained deciduous teeth
134
135. RADIOGRAPHIC FEATURES
Irregular mass of calcified material / variable
number of tooth like structures surrounded by
a narrow radiolucent band with a smooth
periphery
Between the roots of teeth
Associated with unerupted /impacted tooth
135
138. HISTOPATHOLOGICAL FEATURES
Normal appearing dental tissues
(that may or may not resemble
normal teeth) in a fibrous connective
tissue
Presence of ‘ghost’ cells
138
150. Neoplasms composed of proliferating
odontogenic epithelium embedded in a
cellular ectomesenchymal tissue that
resembles the dental papilla, with varying
degrees of inductive change and dental
hard tissue formation.
(WHO definition, 1992)
150
151. Simultaneous proliferation of both
epithelial and mesenchymal tissue
without formation of enamel or
dentin
151
152. CLINICAL FEATURES
posterior region of mandible
14.6 yrs
♂
mostly asymptomatic; sometimes
associated with pain, tenderness or
mild swelling
152
169. INDUCTION OF THIN LAYER OF
ATUBULAR DENTIN IN THE STROMA BY
THE AMELOBLAST-LIKE CELLS
169
170. PRIMORDIAL ODONTOGENIC TUMOR
1st described by Mosqueda-Taylor et al
Benign odontogenic tumor developing during
primordial stages of tooth developemnt
Classified under mixed odontogenic tumors- dental
papilla surrounded by delicate ameloblastic
epithelium
Only around 14 cases reported until now
Occurs in young age- 2nd decade of life
170
171. PRIMORDIAL ODONTOGENIC TUMOR
Slight male predilection
Mandible the most common site; unerupted tooth
Asymptomatic swelling presenting with expansion
of cortical bone
171
172. X- ray:
large well defined radiolucency
involving an completely unerupted tooth – 3rd
molar
Root resorption seen
Buccal and lingual cortical plate expansion
Gross findings
Encapsulated solid nodule, pale, slippery
172
175. Histopathology
Variably cellular to loose fibrous tissue with
areas mimicking dental papilla surrounded
by epithelial cells – cuboidal to columnar
No hard tissue formation
Calcifications may be seen in myxoid CT
stroma
175
177. Treatment
Enucleation and extraction of involved tooth
Conservative surgical excision
Prognois – good
Recurrences- rare
177
178. DENTINOGENIC GHOST
CELL TUMOR
COC was first described by Gorlin and his colleagues in 1962,
Controversy as to whether COC is a cyst or a tumor
Two organizing principles of classification of
Monistic concept: postulates that all COCs are neoplastic in
nature, even though the majority are cystic in architecture and
appear to be non-neoplastic
Dualistic concept favored by most researchers proposes that
COCs contain two different entities- cyst & Tumor
Cyst- “Calcifying Cystic Odontogenic Tumors” (CCOT)
Neoplasm-“Dentinogenic Ghost Cell Tumor” (DGCT)
178
179. DGCT term 1st proposed by Praetorius et al. in 1981 for
the neoplastic variety of COC, i.e., the Type 2 of COC
DGCT has also been termed as odontogenic ghost cell
tumor by Colmenero et al.
DGCT is an extremely rare odontogenic tumor
Central and a peripheral type
179
Histogenesis- cell rests of Serre or the surface epithelium but
unclear
β-catenin plays an important role in the tumorigenesis of DGCT
by an improper differentiation process coordinated by Wnt
signaling pathway
180. Age- 50yrs (17-72yrs)
Slight male predilection
Maxilla = Mandible
Canine to 1st molar region affected
Asymptomatic – few pain & discomfort
Tooth bearing area or edentulous jaw
180
181. X rays shows
Unilocular & multilocular
Radiolucency with scattered radio-opaque calcifications
Occlusal radiographs show a bicortical expansion
Root resorption or an impacted tooth in relation to the tumor
mass is also noted in some cases
181
183. Histopathology
Islands of odontogenic epithelium
Tall columnar ameloblast-like cells with hyperchromatic nuclei
Large areas of eosinophilic globules suggestive of dentinoid
Ghost cells showing keratinization and calcification
183
Dentin like
Calcification in
ghost cells
Giant cell
184. Treatment
Enucleation or surgical resection- enbloc, segmental
Locally aggressive lesion
Recurrence rate is high (71%)
Malignant transformation has been reported
184
186. Small focal excessive mass of enamel
(ectopic nodule) on the surface of a
tooth root
186
187. At furcation of roots or near the CEJ
Maxillary molars > mandibular molars
Asymptomatic
Higher incidence in Mongoloid and
Eskimo populations
187
188. ETIOPATHOGENESIS
localised bulging of the odontoblastic layer
↓
prolonged contact between HERS and the
developing dentin
↓
inductive influence
↓
formation of enamel
188
191. May consist purely of
enamel; may also contain
underlying dentin and
pulp tissue
191
192. Potential complications:
Weak periodontal attachment; attachment
by hemidesmosomes
Area of stagnation that favours plaque
retention and improper cleansing
Enamel pearl may sometimes contain vital
pulp tissue
192
201. THREE BASIC CONCEPTS REGARDING
THE TUMOUR :
Lesion around the crown of an unerupted
tooth resembling a dentigerous cyst
Lesion of fibrous connective tissue with
scattered islands of odontogenic epithelium
Fibroblastic neoplasm containing varying
amounts of odontogenic epithelium and
calcified material resembling dysplastic
dentin / cementum
201
202. CLINICAL FEATURES
Age: 1st – 8th decades (mean age: 40 years)
Female >males
Mandible > maxilla
Maxilla – (lesions located anterior to I molar)
Mandible – (lesions located posterior to I molar)
Asymptomatic
May be associated with an unerupted tooth
202
203. RADIOGRAPHIC FEATURES
Smaller lesions:
well-defined unilocular radiolucencies
larger lesions → multilocular
Lesions are seen in the peri-radicular
area; may cause root resorption
203
206. SIMPLE COF:
Tumour mass composed of mature collagen
fibres with stellate fibroblasts in a whorled
pattern
Small islands / nests of inactive odontogenic
epithelium
206
213. CLINICAL FEATURES
2nd and 3rd decade of life;
(rare before age of 10 years or after 50)
Males = Females
Mandible > Maxilla
Usually asymptomatic
Rare lesions expand the bone and may
cause destruction of cortex
213
214. RADIOGRAPHIC FEATURES
Unilocular / multilocular radiolucent lesion
May have a mottled appearance
May cause displacement / resorption of teeth
The radiolucent area may contain thin wispy
trabeculae of residual bone arranged at right
angles to one another
‘Tennis-racket’ / ‘step-ladder’ appearance
214
218. HISTOLOGICAL FEATURES
Loosely arranged spindle-shaped and
stellate cells with long fibrillar processes
Myxoid intercellular substance with few
collagen fibrils
The ground substance contains two acid
mucopolysachharides
(↑ hyaluronic acid; ↓ chondroitin sulfate)
218
222. Tumour cells exhibit high alkaline
phosphatase and lactate dehydrogenase
activity
Ultrastructural studies show two types of
cells
Pale cells (represent secretory cells; synthesis of
mucopolysaccharide)
Dark cells (contain crystallised collagen fibrils)
222