The document discusses several types of odontogenic tumors that can occur in the jaws. It focuses on describing ameloblastoma, adenomatoid tumor, and calcifying epithelial odontogenic tumor. Ameloblastoma is a benign but locally aggressive tumor arising from odontogenic epithelium. It commonly presents as a painless swelling in the mandible and radiographs show multilocular radiolucency. Histologically there are follicular or plexiform patterns. Adenomatoid tumor is a rare benign tumor associated with impacted teeth. Calcifying epithelial odontogenic tumor is a rare, locally aggressive tumor that can be mistaken for carcinoma, presenting with calcified masses visible on radiographs.
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
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.
Dentin dysplasia (DD) is a rare hereditary disturbance is inherited as an autosomal dominant trait.
unknown etiology that affects approximately 1 :100,000.
In 1972, Witkop classified it into type I and type II which affect both dentitions.DD Type I
Radicular dentin dysplasia
Characterized by:-
1.Both dentitions are affected.
2.Normal appearing crowns
3.No or only rudimentary root development (rootless teeth)
4.Incomplete or total obliteration of the pulp chamber.
5.Teeth may exhibit extreme mobility and exfoliate prematurely.DD type II
coronal dentin dysplasia
Characterized by:-
1.partial pulpal obliteration.
2.Thistle-tube-or flame-shaped coronal pulp chambers
3. Thread-like root canals
4. Usually the absence of periapical radiolucencies.
5. In this type of anomaly, teeth roots are of normal shape and contour.The enamel and the immediately subjacent dentin appear normal.
Deeper layers of dentin show an atypical tubular pattern with an amorphous, atubular area, and irregular organization.
Normal dentinal tubule formation appears to have been blocked so that new dentine forms around obstacles and takes on the characteristic appearances described as “lava flowing around boulders”The radiograph revealed features of dentine dysplasia type I with normal appearance of crown but no root development Autosomal Dominant Disorder:
Manifested in heterozygous states
At least one parent of index case is usually affected
Both males and females are affected.
Clinical feature can be modified by variation in penetrance and expressivity. Some individual inherit the mutant gene but are phenotpically normal. This is reffered to as “incomplete penetrance”.
In many condition the age of onset is delayed.
Inheritance Pattern:
Typical pattern is a heterozygous affected parent with a homozygous unaffected parent.
Every child has one chance in two of having the disease
Both sexes are affected equally..Autosomal Recessive Disorder
Largest category of Mendelian disorder
Usually does not affect the parent of the affected individual, but sibling may show the disease.
Complete penetrance is common.
Onset is frequently early in life.
Usually affect enzymatic proteins.
Pattern Of Inheritance:
Typical pattern is two heterozygous unaffected (carrier) parent.
The triat does not usually affect the parent, but siblings may show the disease
Siblings have one chance in four of being affected
Both sexes affected equally.
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.
Gingival cyst of newborn /orthodontic courses by Indian dental academy 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
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
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
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.
Dentin dysplasia (DD) is a rare hereditary disturbance is inherited as an autosomal dominant trait.
unknown etiology that affects approximately 1 :100,000.
In 1972, Witkop classified it into type I and type II which affect both dentitions.DD Type I
Radicular dentin dysplasia
Characterized by:-
1.Both dentitions are affected.
2.Normal appearing crowns
3.No or only rudimentary root development (rootless teeth)
4.Incomplete or total obliteration of the pulp chamber.
5.Teeth may exhibit extreme mobility and exfoliate prematurely.DD type II
coronal dentin dysplasia
Characterized by:-
1.partial pulpal obliteration.
2.Thistle-tube-or flame-shaped coronal pulp chambers
3. Thread-like root canals
4. Usually the absence of periapical radiolucencies.
5. In this type of anomaly, teeth roots are of normal shape and contour.The enamel and the immediately subjacent dentin appear normal.
Deeper layers of dentin show an atypical tubular pattern with an amorphous, atubular area, and irregular organization.
Normal dentinal tubule formation appears to have been blocked so that new dentine forms around obstacles and takes on the characteristic appearances described as “lava flowing around boulders”The radiograph revealed features of dentine dysplasia type I with normal appearance of crown but no root development Autosomal Dominant Disorder:
Manifested in heterozygous states
At least one parent of index case is usually affected
Both males and females are affected.
Clinical feature can be modified by variation in penetrance and expressivity. Some individual inherit the mutant gene but are phenotpically normal. This is reffered to as “incomplete penetrance”.
In many condition the age of onset is delayed.
Inheritance Pattern:
Typical pattern is a heterozygous affected parent with a homozygous unaffected parent.
Every child has one chance in two of having the disease
Both sexes are affected equally..Autosomal Recessive Disorder
Largest category of Mendelian disorder
Usually does not affect the parent of the affected individual, but sibling may show the disease.
Complete penetrance is common.
Onset is frequently early in life.
Usually affect enzymatic proteins.
Pattern Of Inheritance:
Typical pattern is two heterozygous unaffected (carrier) parent.
The triat does not usually affect the parent, but siblings may show the disease
Siblings have one chance in four of being affected
Both sexes affected equally.
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.
Gingival cyst of newborn /orthodontic courses by Indian dental academy 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
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
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
Lesions/ Tumors/ Cysts doesn't follow the text books. Hence, every enthusiastic Pathologist should be updated with the current trends in the subject. Here is an attempt made from the most common text books of Oral pathology.
Odontogenic tumors are growths that develop in the jawbones or soft tissues of the mouth, arising from the tissues that form teeth. These tumors can be benign or malignant and vary widely in their presentation and behavior. Benign tumors include ameloblastoma, odontoma, and cementoblastoma, while malignant tumors include ameloblastic carcinoma and odontogenic sarcoma. Treatment typically involves surgical removal, and prognosis depends on the type and stage of the tumor.
Odontogenic tumors iii/certified fixed orthodontic courses by Indian dental a...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
An overview of various pathological processes affecting the Jaw Bones- Maxilla and Mandible including odontogenic cysts and tumours including their radiological findings!
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.
hypomineralization of systemic origin of one to four permanent first molars frequently associated with affected incisors and these molars are related to major clinical problems in severe cases
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
Odontogenic tumor
1. Odontogenic tumor
DR: Mazen Abood Bin Thabit. M.D, FRCPath
Assistant Prof Of General pathology
Senior lecturer of Oral pathology and oral
histology
2. Introduction
The most common
neoplasm of the jaws is
odontogenic and it is
unique to the jaws.
Copyright 2003, Elsevier Science (USA). All rights reserved.
4. Ameloblastoma
Is a benign locally aggressive
odontogenic tumor arises
from odontogenic epithelium
Enamel organ
The cause unknown
Copyright 2003, Elsevier Science (USA). All rights reserved.
5. Ameloblastoma
Clinical feature :
The most common
30-40 years
Male.
Rare in children .
80% in mandible
70% in posterior region ( Ramus )
2o% premolar 10% incisor .
Usually asymptomatic .
Slow grow expansion of the jaw
cortical bone produce shell bone
Copyright 2003, Elsevier Science (USA). All rights reserved.
7. Egg shell cracking .
Pain , paresthesia, mobility of
regional teeth .
Pathological fracture .
The overlying mucosa normal
Maxillary lesion may produces
pressure effect and nasal
obstruction
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8. Ameloblastoma
Radiography:
Uni or Multilocular radiolucent
areas
Soap bubbles
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9. Ameloblastoma
Radiography:
Soap bubbles appearance
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10. Ameloblastoma
Histopathology:
Usually there are many histological
Variants of ameloblastoma.
1. Follicular ameloblastoma.
Islands or trabeculae of epithelial cells
in a connective tissue stroma
Ameloblast-like cells" which have "
reversed polarity“
These pattern of growth resembling
the early stages of tooth development
Core of loosely arranged polyhedral
or angular cells resembling satellite
reticulum
1.
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11. Variants of ameloblastoma.
2. Plexiform ameloblastoma:
Arranged in a network or
anastomosing strands
3. acanthomatous amploblastoma.
central core of the neoplastic
epithelium shows squamous
metaplasia
Plexiform
acanthotic
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12. Variants of ameloblastoma.
4. Basal cell ameloblastoma.
Trabecular pattern of growth with
little evidence of palisading at the
periphery. They have been mistakes
with basal cell carcinoma
5. Granular cell ameloblastoma.
6. Desmoplastic ameloblastoma:
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13. 7. Flexiform unicystic ameloblastoma:
Children between 10-19 years
Typically in the mandible .
80% ,the cyst enclose the crown
of impacted .
severely displaced mandibular 3rd
molar
Unilocular radio-lucency
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14. Variants of ameloblastoma.
8. Peripheral ameloblastoma.
These tumors are extraosseous and
therefore occupy the lamina propria
underneath the surface epithelium
but outside of the bone.
Histologically, these lesions have the
same features as the intraosseous
forms of the tumor
Patients respond well to local surgical
excision.
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15. Ameloblastoma.
Ameloblastoma is locally
aggressive tumor and may
extened to the bone or
surrounding soft tissue
Treatment:
Enaculation with thorough bone
curettage .
Radical surgical approch
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16. Adenomatoid tumor
Uncommon benign tumor,
originated from reduced
enamel epithelium of post
secretory phase of enamel
development
3-7% of all odontogenic tumors
REE
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17. Adenomatoid tumor
Clinical feature :
Associated with an impacted.
Asymptomatic
Late adolescent or young
adulthood .
Female .
65% in the maxilla
75% associated with impacted
teeth
Small slow growing mass on the
anterior maxilla, rarely premolar
Cause an elevation of the upper
lip.
Pain and tooth placement.
Radiolucent area surrounding impacted tooth
Rarely extra-osseous (Gingival)
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18. Adenomatoid tumor
Radiography:
AOTs typically appear as
pericoronal radiolucencies, which
may have radiopaque material
(“snowflake” calcifications) within
the lucency
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20. Adenomatoid tumor
Histopathology:
Sheets or islands of epithelial cells
arrange around microcyst ( Ducts or
ductules ) .
Surrounded by thin vascularized stroma .
The ductules bordered by ameloblast like
cells .
The lumen filled by homogenous
eosinophilic material .
Small foci of calcification .
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21. Calcifying epithelial odontogenic tumor
Benign , locally aggressive
tumor originated from the rest
of dental lamina and/or REE .
" Bindborg" tumor.
Rare tumor ( Less than 1%)
,could be mistaken with poorly
differentiated squamous cell
carcinoma
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22. Calcifying epithelial odontogenic tumor
Clinically :
Affect adult ,40 years.
More common in the mandible
Molar and premolar region
crown of the unerupted teeth.
Either central or peripheral
Intraosseous lesion mainly
produce slowly growing painless
mass at the mandible.
Nasal obstruction, epistaxis are
some time present in the
maxillary lesion.
Peripheral ( Extraosseous) is
most commonly present in the
anterior part of the mouth .
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23. Calcifying epithelial odontogenic tumor
Radiograph:
The lesion appears as
radiolucent area with poorly
defined margin with fine flecks
of radio-opacities (due to
calcification).
Impacted tooth and flicks of
calcification
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24. Calcifying epithelial odontogenic tumor
Histopathology:
Sheets or strands of epithelial
cells
Cells are polyhedral exhibit
pleomorphism, including
multinucleated giant .
Stroma lacks of inflammatory
infiltrate
Pools of homogenous
eosinophilic material seen within
and between the epithelial
sheets with spherical
calcification
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25. Treatment:
Conservative local resection
is the treatment of choice as
these lesions are typically
less aggressive than the
ameloblastoma.
With this treatment the
recurrence rate is
approximately 15 % and the
overall prognosis is good
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26. Squamous odontogenic tumor
Rare tumour, believed to
be arise from neoplastic
transformation of rest of
malassiz
Rest of malassiz
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27. Squamous odontogenic tumor
Clinical feature:
Affect the patient 2nd -7th decade
( Mean age 40).
Occur in mandible and maxilla in
equal frequency.
Typically involve the alveolar
process anterior to the molars of
either jaws. Close to the roots of
erupted tooth.
Painless swelling or as loosening
of teeth
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28. Squamous odontogenic tumor
Appear as non-specific
radiolucent lesions. They may
be well-circumscribed or ill-
defined. They often appear
triangular in shape and lateral
to the tooth root.
Some time mimic sever bone
loss from periodontitis.
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29. Squamous odontogenic tumors
Histologically, they appear as
islands of bland-appearing
well differentiated squamous
epithelium in a mature
fibrous connective tissue
stroma.
The peripheral cells flattening
do not show the
characteristic polarization
seen in the ameloblastoma
Treatment:
Conservative local excision or curettage
appears to be effective treatment and there
have only be a few recurrences reported
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30. Ameloblastic fibroma
Rare biphasic tumor,
because the epithelial
and mesendymal
components are part of
the neoplastic process.
Resembles dental
papillae
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31. Clinical feature:
Young adult and children.
70% in mandible
frequently located at mandibular
molar area, often over an
unerupted tooth
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32. Radiography:
Generally, these lesions
appear as either a unilocular
or multilocular radiolucency.
They tend to be well-defined
and may have a sclerotic
border.
Approximately, 50 % are
associated with an unerupted
toot
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33. Odontogenic fibroma
Histopathology :
Microscopically characterize
by thin strand and cords of
odontogenic epithelium that
resemble dental lamina at the
cap and bell stages of early
odontogenesis.
The background compose of
loose but cellular fibromyxoid
connective tissue wildly
separated by fibroblast,
which resemble the immature
dental papillae.
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34. Ameloblastic fibro-odontomas
In these pathological entity
cells in one or more foci
continue the differentiation
process and produce enamel,
dentin and cementum in the
form of compound or
complex
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35. Ameloblastic fibro-odontomas
Most common in the 5-12 year age
More common in the
premolar/molar regions of both
jaws.
Radiographic Features: Usually
appears as a well-defined
unilocular or rarely multilocular
radiolucency with variable
amounts of calcified material
which is radiopaque. Therefore, it
may appear as a
mixed, radiolucent-radiopaque
lesion.
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36. Ameloblastic fibro-odontoma
Histopathology :
Identical to the ameloblastic
fibroma. The calcified portion
consists of foci of enamel and
dentin matrix formation in
close relationship to the
epithelial structures.
The ameloblastic fibro-odontoma is usually
treated by conservative curettage .
Prognosis is excellent and recurrence is unusual
Dentin
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37. Odontogenic fibroma
Benign neoplasm derived from
connective tissue of
odontogenic origin containing
widely scattered islands and
strands of embryonic
odontogenic epithelium and
calcification.
Two types:
1. Central ( Intraosseous) WHO type
odontogenic fibroma .
2. Peripheral odontogenic fibroma .
Peripheral odontomas
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38. Odontogenic fibroma
Uncommon
Patient age ranged from 9-80
years old with a mean of 40
years.
More common in Female
60 % in the maxilla ,anterior
to the first molar.
In the mandible, 50 % occur
in the posterior jaw.
Small lesion usually
asymptomatic.
The larger associated with
localized bony expansion or
with the loosening of
adjacent teeth
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39. Odontogenic fibroma.
Histopathology:
The WHO type odontogenic
fibroma appears as a fairly
cellular fibrous connective tissue
with collagen fibers arranged in
interlacing bundles.
Odontogenic epithelium in the
form of long strands or isolated
nests is present throughout the
lesion.
Calcifications composed of
cementoid and/or dentinoid may
be present.
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40. Odontogenic myxoma
Locally aggressive intraosseous
lesion derived from dental
mesenchymal tissue,
resembling microscopically the
dental pulp or follicular
connective tissue.
Dental papilla
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41. Odontogenic myxoma
Clinical feature :
Young people without sex
predilection.
More common in the mandible
Mandibular lesion found in molar
and premolar areas often
extended into ramus.
Maxillary lesion erode into sinus
Most lesion are show growing
painless, fusiform swelling that
some time displace teeth
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42. Odontogenic myxoma
Histopathology:
The tumor is composed of
loosely arranged stellate,
spindle-shaped and round
cells in an abundant, loose
myxoid stroma with few
collagen bundles.
Myxoma
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43. Odontogenic myxoma
Radiography:
Typically appears as multi
locular radiolucent area with
well defined scalloped margin
or soap bubble.
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44. Odontogenic myxoma
Treatment :
Small odontogenic myxomas are
treated by curettage, while
larger lesions may require
surgical resection.
Odontogenic myxomas are not
encapsulated and tend to
infiltrate adjacent tissues.
Recurrence rates of up to 25 %
are reported.
Overall, the prognosis is good for
most odontogenic myxomas.
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45. Cementoblastoma
Benign neoplasm of the
cementoblastic origin
compose of cementum like
tissue growing in continuity
with apical cemental layer of
molar and premolar that
produce expansion of cortical
bone and pain.
Cementoblastoma
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46. Cementoblastoma
Clinical feature:
2nd and 3rd decade.
Comentoblastoma forms an
irregular or rounded mass
attached to the apical ⅓ of the
roots.
They are slow growing and the jaw
is not usually expanded
Pain is diagnostic feature , usually
of low grade intermittent pain and
become more intense when the
area is palpated.
The tooth is vital
More often seen in mandible than
the maxilla .
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47. Cementoblastoma
Radiography:
Typically appears as radio
opaque rounded mass with
thin radiolucent margin.
Attached to the root.
Resorption of the related root
is common.
Cementoblastoma
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48. Cementoblastoma
Histopathology:
Conglomerate of cementum
which often contain reversal
line and cells are enclosed in
lacunae.
Peripheral zone has unmine
ralized tissue while the
center more mineralized .
Intervening soft tissue is
loose very cellular and
vascularized, contain
multinucleated cementoclast
and cementoblast.
Reversal lines
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49. Odontomas
Odontomas are developmental
malformation ( hamartoma) of
dental tissue, it is not neoplasim
Compound
1. Compound: Composed of Complex
multiple small tooth-like
structures.
2. Complex: composed of a
conglomerate mass of enamel
and dentin, which bears no
anatomic resemblance to a
tooth
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50. Odontomas
Clinical feature :
70% of odontogenic tumor .
More common in the maxilla.
The compound type is more
often in the anterior maxilla .
complex type occurs more
often in the posterior regions
of either jaw.
Most odontomas are small
and do not exceed the size of
a normal tooth in the region.
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51. Odontomas
Large lesion cause expansion
of the jaw.
Most odontomas are
asymptomatic.
Odontomas may block the
eruption of a permanent
tooth .
Erupted odontomas
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52. Odontomas
Compound Complex
The compound type shows apparent tooth shapes while
the complex type appears as uniform opaque mass with
no apparent tooth shapes present
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53. Odontomas
Histopathology:
The compound odontoma is
composed of enamel, dentin
and cementum arrange in
recognizable tooth forms;
some enamel matrix may be
retained in immature and
hypomineralized specimens. Compound
The complex odontoma is
composed of enamel, dentin
and cementum but these
tissues are arranged in a
random manner that bears no
morphological resemblance
to a tooth.
Complex
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54. Malignant Ameloblastoma and Ameloblastic Carcinoma
Less than 1 % of the
ameloblastomas show malignant
behavior with the development of
metastases.
Malignant ameloblastoma is a
tumor that shows histologic
features of the typical (benign)
ameloblastoma in both the
primary and secondary deposits. Carcinoma
Ameloblastic carcinoma is a
tumor that shows cytologic
features of malignancy in the
primary tumor, in recurrence and
any metastases
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55. Ameloblastic fibrosarcoma
Malignant counterpart of
the ameloblastic fibroma
in which the mesenchymal
portion shows features of
malignancy.
The ameloblastic
fibrosarcoma may arise as
malignant transformation
of an ameloblastic fibroma
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56. Ameloblastic fibrosarcoma
Histopathology:
The epithelial component
histologically benign.
The mesenchymal portion is
highly cellular. The cells are
hyperchromatic and quite
pleomorphic. Mitoses are
usually prominent
Mitosis
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