This document provides an overview of red lesions that can occur in the oral cavity. It discusses normal variations in oral mucosa color and various factors that can affect color. Red lesions are classified and several common types are described in detail, including traumatic erythematous macules, purpuric macules, inflammatory fibrous hyperplasia, nicotine stomatitis, erythroplakia, carcinoma, and candidiasis. Diagnostic features, histopathology, differential diagnoses, and management are covered for key red lesions. The document aims to guide clinicians in identifying and diagnosing different oral red lesions.
Brief notes on the inflammation of Alveolar bone that surrounds a tooth that has recently been extracted. It occurs as a complication of tooth extraction.
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
The wasting diseases of teeth, namely attrition, abrasion and dental erosion have taken their toll in the population around the world due to the changing lifestyles, increase in the stress levels and many others factors that were persistent earlier but have suddenly increased drastically. This presentation brings to light the new factors that have attributed to this condition as well as discusses the previous ones.
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.
Brief notes on the inflammation of Alveolar bone that surrounds a tooth that has recently been extracted. It occurs as a complication of tooth extraction.
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
The wasting diseases of teeth, namely attrition, abrasion and dental erosion have taken their toll in the population around the world due to the changing lifestyles, increase in the stress levels and many others factors that were persistent earlier but have suddenly increased drastically. This presentation brings to light the new factors that have attributed to this condition as well as discusses the previous ones.
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.
Dentists play an important role in the diagnosis and management of desquamative gingivitis. The importance of being able to recognise and properly diagnose this condition is accentuated by the fact that a serious and life threatening disease may initially manifest as desquamative gingivitis.
H and E staining is most important part of the histopathological diagnosis, this presentation is to highlight some important basic concept of the Staining.
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
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
- 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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
5. Wide spectrum of pink colors varying from a
dark pink(reddish) to a very pale pink(almost
white)
1. Lining mucosa --- Reddish pink
2. Masticatory mucosa--Light pink
Protective layer of keratin
Dense sub epithelial connective tissue
6. Deep dusky red in color
contrast to light red
color of surrounding
tissue.
Painless red macular
bands may present
Richer blood supply
Individual normal
variation
12. Vascular dilations from
a. Inflammation (Erythema)
b. Congenital defects(e.g. hemangioma)
Extravasations of blood (e.g. trauma
hemostatic disease or both)
Atrophy or erosion of mucosa
Marked increase in hemoglobin
concentration of circulating blood
13. Inflammation
(Erythema)
Mechanical trauma
Thermal trauma
Chemical trauma
Infections
Ulcer with inflamed rim
Congenital defects(e.g.
hemangioma)
14. Erythematous macule
Erosion
The purpuric macule
Granulomatous stage of inflammatory
hyperplasia
15. Etiology --Produce by low grade, usually
chronic physical insult
Sharp margins of teeth & restorations
Ill-fitting prosthesis
Self inflected trauma
Habits
16. Clinical feature (c/f)
Erythematous macule are
on
Anterior & lateral border of
tongue
Cheek mucosa
Lip mucosa
Margins may or may not be
sharply defined
17. Mild tenderness
Digital pressure may
cause blanching
Regress quickly
after removal of
cause
20. Caused due to blunt trauma which is sufficient
force to cause the extravasations of blood.
Soon after the traumatic damage, lesion is red
afterwards converts into blue color.
Borders are poorly demarcated
Blanching on pressure does not usually occur
May also have secondary inflammatory
component.
22. The purpuric macule
due to oral
sexual practices.
Reddish
Elliptical
Purpuric macule
Occurring on palatal mucosa
near the junction of the hard & soft palate.
Disappear within 2 to 3 days
Judicial history with confidential setting revel
the true identity.
35. Caustic drugs or hot foods or beverages
Depends on duration & intensity of stimuli
Stimuli may produce coagulative necrosis
of superficial tissues that appears white
After scraping off that white layer it may
produce clinically appreciable red lesion
36. Ulceration & properly stripping off mucosa
Tender to painful
May blanch on pressure
Size & shape varies depend on stimuli.
40. Conventional smokers
Is seen primarily on the palate of pipe
smokers.
Also seen in bidi smoker
Does not having premalignant nature
It develops in response to heat rather than
tobacco.
41. Appears red in initial stage
In later keratotic
stage minor salivary
duct orifices
appear red
Men , 4-5 decade
44. Erythroplakia
• Commonly seen on buccal mucosa , floor of mouth,
tongue
Definition –
Persistent velvety red patch that can not be
identified as any other specific red lesion such as
inflammatory Erythema or those produce by blood
vessel anomalies or infection.
45. It appear red because
Absences of surface keratin layer
Connective tissue papillae, containing
enlarge capillaries, project close to the
surface.
46. C/F-
• Velvety red or
granular red macules.
• Varies greatly in size
• Borders may be
well defined
• Painless
• Drying of the mucosa will intensify the red colour
48. The lesion may have an irregular, red
granular surface interspersed with white
or yellow foci, which may be described as
granular erythroplakia.
There may be numerous, small irregular
foci of leukoplakia dispersed in the
erythroplakic patch, and this has been
called speckled leukoplakia.
49. Oral erythroplakia is soft to palpation and
does not become indurated or hard until an
invasive carcinoma develops.
50. Histopathologically
erythroplakia almost
always show dysplasia,
carcinoma in situ or
invasive squamous cell
carcinoma.
Epithelium is frequently
atrophic with lack of
keratin production.
The connective tissue
demonstrates chronic
inflammation.
51. If the lesion persist for more than 21 days
after all local trauma & infections foci have
been eliminated, biopsy is mandatory.
53. Malignant epithelial neoplasm exhibiting
Squamous differentiation as characterized
by formation of keratin & / or presence of
intercellular bridges
(pinborg JJ 1997)
54. Annually, nearly 30,000 new cases of oral
and oropharyngeal cancer are expected to
occur in men and women in the United
Sates.
The ratio of cases in men and women is
now about 2 to 1.
55. Tobacco,
Typically mixed with areca (betel) nut,
Slaked lime,
All forms of tobacco smoking
Reverse smoking
Alcohol
Poor nutritional status
HPV 16 & 18 has some role in the
development of OSCC.
Ultraviolet (UV) light
57. The first is loss of cell cycle control through
increased proliferation and reduced
apoptosis.
The second stage is increased tumor cell
motility, leading to invasion and
metastasis.
58. Carcinoma of the Lips:
Carcinomas of the lower lip are far more
common than upper lip lesions.
Pipe smoking, uv light exposure.
The growth rate is slower for lower lip
Favorable prognosis
Account for 25% to 30% of all oral cancers
59. Lesions arise on the vermilion surface
Appear as a chronic non healing ulcer
(Exophytic ,verrucous type may present)
Deep invasion -- later in the course of the
disease.
Metastasis to local submental or
Submandibular lymph nodes is uncommon
60.
61. One of the most common intraoral
malignancy.
Predilection for men (6-8th decade)
However, lesions may uncommonly be
found in the very young.
62. Exhibit a particularly aggressive behavior.
Lingual carcinoma is typically
asymptomatic.
As deep invasion occurs, pain or dysphagia
may be a prominent patient complaint.
63. Appear in one of four ways:
indurated, nonhealing ulcer,
a red lesion,
a white lesion,
a red-and-white lesion.
64. The neoplasm may occasionally have a
prominent exophytic, as well as
endophytic, growth pattern
65. The most common location of cancer of the
tongue is the posterior-lateral border.
Specific reason is due to chronic irritation
because of tooth
Approximately 1/4th of tongue cancers
occur in the posterior one third or base of
the tongue.
66. Metastases from tongue cancer are relatively
common.
The first nodes to become involved are the
submandibular lymph node.
Uncommonly, distant metastatic deposits may
be seen in the lung or the liver.
67. Second most common intraoral location of
squamous cell carcinomas.
Predominantly in older men,
68. Painless, nonhealing, indurated ulcer.
It may also appear as a white or red patch.
May widely infiltrate the soft tissues of the floor
of the mouth,
Decreased mobility of the tongue.
Metastasis to Submandibular lymph nodes is
common
71. It is slow growing
Usually well differentiated,
Rarely metastasizes,
Has a favorable prognosis
72.
73. Palatal squamous cell carcinomas
generally present as asymptomatic red
or white plaques or as ulcerated and
keratotic masses
74. 1. Well differentiated:
It consists of sheets and nests of cells of
squamous epithelium.
Cells are large and show distinct cell
membrane but intercellular bridges or
tonofibrils are not seen.
Pleomorphic nuclei and becomes
hyperchromatic.
75. Mitotic figures are seen but not numerous.
Individual cell keratinization and
formation of numerous keratin pearl.
Group of cells invades underlying
connective tissue.
76.
77. Shape of cells and their arrangement may
be altered.
The growth rate of individual cells is more
rapid and this is reflected in the greater
numbers of mitotic figures.
Keratin pearl formation may or may not be
seen.
78.
79.
80. More pleomorphic cells.
Loss of keratinization and keratin pearl.
Loss of individual cell differentiation.
Increase mitotic figures.
83. Coxsackie virus A4 -cause a majority of cases
of Herpangina,
Types A1 to A10, A16 to A22
Herpangina may be seen more than once in
the same patient.
Herpangina frequently occurs in epidemics
The majority of cases affect young children
adolescents.
84. Clinical Manifestations.
After a 2- to 10-day incubation period,
The infection begins with generalized
symptoms of fever, chills, and anorexia.
85. The fever and other symptoms are
generally milder than those experienced
with primary HSV infection.
The patient complains of sore throat,
dysphagia, and occasionally sore mouth.
86. Lesions start as punctate macules, which
quickly evolve into papules and vesicles
involving the posterior pharynx, tonsils,
faucial pillars, and soft palate.
Lesions are found less frequently on the
buccal mucosa, tongue, and hard palate.
87. Within 24 to 48 hours, the vesicles rupture,
forming small 1 to 2 mm ulcers.
The disease is usually mild and heals
without treatment in 1 week.
88. Definition Infectious mononucleosis is an acute,
self-limited infectious disease that primarily affects
children.
Etiology
Epstein–Barr virus transmitted through saliva
transfer,
Cytomegalovirus (CMV)
CMV is the major cause of non-Epstein-Barr virus
infectious mononucleosis in the general
population.
89. The oral manifestations are early and
common, and consist of
palatal petechiae,
uvular edema,
tonsillar exudate,
gingivitis,
rarely ulcers
90. Generalized
lymphadenopathy,
hepatosplenomegaly,
maculopapular skin rash,
sore throat are common.
Prodromal symptoms such as anorexia,
malaise, headache, fatigue, and later fever
occur before the clinical manifestations.
93. It is the infection with yeast like fungus Candida albicans
Earlier termed moniliasis
Types
ACUTE CHRONIC
Psuedomembranous Hyperplastic
Atrophic Mucocutaneous
Atrophic
Candidiasis
94. clinical type Appearance
Erythematous Red
Atrophic Red
Hyperplastic White, red raised
Mixed Red/ white keratotic / white necrotic
Mucocutaneous Lip/ angles
Psuedomembranous White lesion
99. Due to denture cuts off the underlying
mucosa from the protective action of
saliva.
The erythema is sharply limited to the area
of mucosa occluded by a well-fitting upper
denture or even an orthodontic plate.
101. It is red colored unraised area usually
present on buccal mucosa.
It is usually capillary type,
Also occur as port wine stain on skin.
102. History of long duration
It is non tender
Even no inflammatory component
Absence of recurrent traumatic episode
103. References-
Text book of oral and maxillofacial
pathology- Neville
Differential diagnosis of oral lesions by-
Wood and Goaz, Fifth Edition
Shafer’s textbook of oral pathology 6th
edition .
Textbook of oral medicine Burkait 10th
edition .