Oral cancer can form in any part of the mouth or throat. Most oral cancers begin in the tongue and in the floor of the mouth. Anyone can get oral cancer, but the risk is higher if you are male, over age 40, use tobacco or alcohol or have a history of head or neck cancer. Frequent sun exposure is also a risk for lip cancer.
Oral cancer can form in any part of the mouth or throat. Most oral cancers begin in the tongue and in the floor of the mouth. Anyone can get oral cancer, but the risk is higher if you are male, over age 40, use tobacco or alcohol or have a history of head or neck cancer. Frequent sun exposure is also a risk for lip cancer.
oral cancer is the common melignancy in male and can leads to death of patient and social isolation among patient this ppt help in knowing the condition and refers by nurses for their knowledge and application in their clinical practice
Oral Cancer is an uncontrollable growth of cells which invades the vital structure. It can occur anywhere in the mouth. It occurs due to tobacco use, Areca nut, Alcohol, Poor nutrition, HPV virus, Genetic factors, Chronic trauma.
A red and white patches on lips or gum tongue or Buccal Mucosa having symptoms of pain, hoarseness of voices, loosening of teeth, Biopsy, Endoscopy, Imaging Technique are some way of examination.
Treated by Surgery , Radiation Therapy, Chemotherapy, Brachial Therapy.
Habit Cessation and Maintenance of oral hygiene prevents Cancer.
Call us regarding Oral cancer and its Treatment:-
Dr. Rajat Sachdeva
+919818894041,01142464041
drrajatsachdeva@gmail.com
Follow us here:-
• Google+ link: https://goo.gl/vqAmvr
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Learn more:-
• www.sachdevadentalcare.com
• www.dentalclinicindelhi.com
• www.dentalimplantindia.co.in
• www.dentalcoursesdelhi.com
• www.facialaestheticsdelhi.com
Oral cancer has been identified as Significant publec health threat. So its very important to know how to diagnose which is the first step in the treatment...
Hope you find it beneficial and rich .
oral cancer is the common melignancy in male and can leads to death of patient and social isolation among patient this ppt help in knowing the condition and refers by nurses for their knowledge and application in their clinical practice
Oral Cancer is an uncontrollable growth of cells which invades the vital structure. It can occur anywhere in the mouth. It occurs due to tobacco use, Areca nut, Alcohol, Poor nutrition, HPV virus, Genetic factors, Chronic trauma.
A red and white patches on lips or gum tongue or Buccal Mucosa having symptoms of pain, hoarseness of voices, loosening of teeth, Biopsy, Endoscopy, Imaging Technique are some way of examination.
Treated by Surgery , Radiation Therapy, Chemotherapy, Brachial Therapy.
Habit Cessation and Maintenance of oral hygiene prevents Cancer.
Call us regarding Oral cancer and its Treatment:-
Dr. Rajat Sachdeva
+919818894041,01142464041
drrajatsachdeva@gmail.com
Follow us here:-
• Google+ link: https://goo.gl/vqAmvr
• Facebook link: https://goo.gl/tui98A
• Youtube link: https://goo.gl/mk7jfm
• Linkedin link: https://goo.gl/PrPgpB
• Slideshare link : http://goo.gl/0HY6ep
• Twitter Page : https://goo.gl/tohkcI
• Instagram page : https://goo.gl/OOGVig
Learn more:-
• www.sachdevadentalcare.com
• www.dentalclinicindelhi.com
• www.dentalimplantindia.co.in
• www.dentalcoursesdelhi.com
• www.facialaestheticsdelhi.com
Oral cancer has been identified as Significant publec health threat. So its very important to know how to diagnose which is the first step in the treatment...
Hope you find it beneficial and rich .
Role of human papillomavirus and tumor suppressor genesishita1994
Oral cancer is synonymous to Squamous Cell Carcinoma (SCC) of oral mucosal origin that accounts for more than 90% of all malignant presentations at the aforementioned anatomical sites.
More than 300,000 new cases worldwide are being diagnosed with oral SCC (OSCC) annually.
Approximately, 30,000 (US) & 40,000(EUROPE).
Oral cancer is estimated by the WHO to be the 8th most common cancer worldwide.
In India & other Asian countries, oral & oropharyngeal carcinomas (OCs) comprise up to half of all malignancies, with this particularly high prevalence being attributed to the influence of carcinogens & region-specific epidemiological factors, especially tobacco & betel quid chewing.
Cancer is a disease in which some of the body’s cells grow uncontrollably and spread to other parts of the body.
Cancer can start almost anywhere in the human body.
It is made up of trillions of cells.
Normally, human cells grow and multiply (through a process called cell division) to form new cells as the body needs them.
When cells grow old or become damaged, they die and new cells take their place.
Sometimes this orderly process breaks down and abnormal or damaged cells grow and multiply when they should not.
These cells may form tumors, which are lumps of tissue.
Tumors can be cancerous (malignant) or not cancerous (benign).
Cancerous tumors spread into or over, nearby tissues and can travel to distant places in the body to form new tumors (a process called metastasis).
Cancerous tumors may also be called malignant tumors. Many cancers form solid tumors, but cancers of the blood, such as leukemias, generally do not.
Benign tumors do not spread into or over, nearby tissues.
When removed, benign tumors usually don’t grow back, whereas cancerous tumors sometimes do.
Benign tumors can sometimes be quite large, however. Some can cause serious symptoms or be life threatening, such as benign tumors in the brain.
Types of Genes that Cause Cancer
The genetic changes that contribute to cancer tend to affect three main types of genes—
proto-oncogenes
tumor suppressor genes
DNA repair genes.
These changes are sometimes called “drivers” of cancer.
Proto-oncogenes are involved in normal cell growth and division. However, when these genes are altered in certain ways or are more active than normal, they may become cancer-causing genes (oncogenes), allowing cells to grow and survive when they should not.
Tumor suppressor genes are also involved in controlling cell growth and division. Cells with certain alterations in tumor suppressor genes may divide in an uncontrolled manner.
DNA repair genes are involved in fixing damaged DNA.
Cells with mutations in these genes tend to develop additional mutations in other genes and changes in their chromosomes, such as duplications and deletions of chromosome parts. Together, these mutations may cause the cells to become cancerous.
TYPES OF CANCER
1) Carcinomas
A carcinoma begins in the skin or the tissue that covers the surface of internal organs and glands.
Carcinomas usually form solid tumors.
They are the most common type of cancer.
Examples of carcinomas include
Prostate Cancer,
Breast Cancer,
Lung Cancer,
Colorectal Cancer.
2) Sarcomas
A sarcoma begins in the tissues that support and connect the body.
A type of cancer that begins in bone or in the soft tissues of the body.
A sarcoma can develop in fat, muscles, nerves, tendons, joints, blood vessels, lymph vessels, cartilage, or bone.3) Leukemias
Leukemia is a cancer of the blood.
Leukemia begins when healthy blood cells change and grow uncontrollably.
The 4 main types of leukemia are :
4) Lymphomas
Lymphoma is a cancer that be
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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 simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
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.
2. Introduction:
– Oral cancer can be referred to as the cancer present in the oral
cavity in which 90% of these cancers are squamous cell
carcinoma.
– The most common sites of the oral cavity that are prone to
developing oral cancer include:
– The soft tissues of the oral cavity are covered by stratified
squamous epithelium.
– The oral epithelium plays an essential role in the protection of
the underlying tissues against:
– The epithelium is characterized by its continuous cell renewal and
replacement that is achieved through:
Lips
Labial and Buccal
Mucosa
Floor of the Mouth
Soft Palate Tongue
The loss of fluids
The penetration of potentially harmful
environmental agents such as enzymes,
microbial toxins & carcinogens from
foods and beverages
The division of cells present
in the deeper layers
The rapid desquamation of
surface cells
3. – This constant renewal acts as a protective mechanism as it:
– Cell death is a must for the compensation of cell proliferation in
which:
– DNA can be defined as a nucleic acid containing hereditary
information (genetic information) that gives the body cells
instructions for producing proteins necessary for important body
functions.
Limits the invasion and colonization of microorganisms
adherent to the mucosal surfaces
Eliminates malfunctioning and diseased cells
The production of
cells in the deeper
layers
Balanced by cell
desquamation
from the surface
Results in the
maintenance of
the oral mucosa
integrity
4. – Genes are considered to be the basic physical and functional units
of heredity in which all living organisms rely on them for holding
information necessary for maintaining and building their body
cells
Definition of Oral Cancer:
– An imbalance between cell proliferation and apoptosis which is
the programmed cell death results in the development of cancer
in susceptible patients.
– Thus, cancer can be referred to as the uncontrollable growth of
the tissue in these patients.
Transcription involves copying a gene’s DNA sequence when the gene is
active
Contain sequence of nucleotides that are responsible for determining
what the gene does and when the gene is active (expressed)
Make up chromosomes
Are portions of DNA
Genes
5. Incidence:
– Oral cancer accounts for about:
– The causes of these differences include:
Age, sex & race:
– An increase in age is associated with an increase in the risk of
intraoral cancer as with so many carcinomas suggesting that
any carcinogen have to act over a prolonged period of time.
Overall male to female
ratio
3:1
•White men are associated with the higher risk of
developing intraoral cancer than do any other group
After 65 Years of Age
•Males tend to have a much higher incidence of intraoral
cancer than females
At All Age Levels
40% in
India,
Srilanka
, Sudan
1-2% In the
United
Kingdom
5% In
the
United
States
Different population
habits such as the
tobacco or snuff
chewing habit which is
considered to be
widely spread (40%)
Inadequate education
for the prevention of
oral cancer
The quality of medical
records in different
countries
6. Oral cancer: A Genetic Disease
– Cancer forms when genes within a normal cell are damaged and
mutated.
– Mutations occur in certain key genes which can be grouped into
three classes:
Proto-Oncogenes:
•These are growth promoting genes
•They are normal genes that aid in the regulation of cell
differentiation and growth
•Their normal function is to give instructions to cells about when
to grow and divide
Tumor Suppressor Genes {Anti-Oncogenes}:
•These are growth inhibition genes
•They play a major role in the protection of cells from being one
step on the path to cancer
•Their normal function is to maintain cells in a non-dividing state
DNA Repair Genes:
•Their normal function is to repair damage to DNA
Key Genes
Proto-Oncogenes
Tumor Suppressor
Genes {Anti-
Oncogenes}
DNA Repair
Genes
7. – Mutations may result in the transformation of a proto-oncogene
into activated oncogene by the action of:
– The activation of oncogenes results in the stimulation of the
production of new genetic material in excessive amounts.
– Oncogenes are genes that play a vital role in the onset and
development of cancer.
– How key genes become defective?
It is considered difficult to address the answer of this
question
Chemical
Carcinogens
Irradiation Viruses
The cell can progress to cancer
This causes a loss or reduction in the gene's function
It becomes inactive
When a tumor suppressor gene {anti-oncogene} is mutated
8. Oral cancer is considered to be a multifactorial disease in
which:
Theory of Carcinogenesis:
– The theory of carcinogenesis suggests that cancer develops in
two-stage processes.
– These two stage processes include an initiation stage followed
by a promotion stage:
• It involves being exposed to a specific
carcinogenic agent
Initiation
Stage
• It occurs by either being continuously
exposed to this specific carcinogenic
agent or to non-specific irritants
Promotion
Stage
There is no detection of a single specific cause for oral
cancer
Many factors tend to be likely included in the etiology of
oral cancer as these vary in several groups
9. Etiological factors:
– Several factors are involved in the human cancer:
– Carcinogenesis usually involves combination of these intrinsic &
extrinsic factors >>> complimentary effects
– The main intrinsic & extrinsic factors that may cause oral cancer
are:
carcinogens
(tobacco
smoke, alcohol,
chemicals ...)
abnormalities
in the genetic
material
cancer
direct local
extrinsic effect
• tobacco
• sunlight
• iron deficiency (makes the host more
susceptible to carcinogen's effect)
• alcohol
tobacco alcohol
diet &
nutritional
deficiency
radiation & UV
rays
infectious
agents
dental factors immunosuppresion occupation
precancerous
lesions
10. tobacco
chronic
irritation
damage
of oral
mucosal
cells
1-Tobacco:
– It is the primary & most important risk factor for developing oral
cancer
– 75% of oral cancers are referred to the use of smoked & smokeless
tobacco
– This rate increases with:
Smoking tobacco: (cigarettes, pipe, cigar …)
4000 chemical
agents + > 60
carcinogens (CO,
tar, arsenic, Pb...)
the amount smoked/ chewed
usage duration
cigar
cigarette
pipe
11. Cigar & pipe smokers are at higher risk for having oral cancer
than cigarette smokers
Reverse smoking:
Heat & smoke
from cigar,
cigarettes &
pipe
irritate the
mucous
membranes of
the mouth
• 6x more prone to have oral cancer
cigar smokers (who inhale deeply)
• static contact of the pipe stem with the lower lip
>>> high risk for lip cancer
pipe smokers
holding the lighted end of the
cigarette inside the mouth
common in women
wide spread in indea, South
America & other countries
12. Smokeless tobacco:
Snuff tobacco:
Snuff is a finely ground or powdered tobacco
It may be inhaled:
Dry
Moist (snuff-dipping)
reverse
smoking
high
concentrations
of carcinogens
hitting the
palatal surface
in a focal area
palatal
carcinoma
placing a pinch of snuff between
the gum & the cheek or the upper
lip for a prolonged period
hyperkeratotic lesions of the gingiva & buccal mucosa
increased risk for carcinoma
13. Betel quid (pan):
24 hr a
Pan is usually chewed after meal >> aids in the digestion &
produce slight euphoric effect
It is kept in the mouth for a long time (24 hrs/day)
Note: chewing tobacco + snuff >>> irritation from direct
contact with the mucous membranes
2- Alcohol:
– It is the 2nd
risk factor for developing oral cancer
Consists of betel nut + lime wrapped in
betel leaf
Tobacco & other spices are added
according to custom & individual taste
Leukoplakia (where pan is held in the
mouth)
Malignant transformation (development
of papilliferous & ulcerated masses)
Most of oral
cancer patients
drink and
smoke at the
same time
it is difficult to
have alcohol
alone as a
carcinogenic
factor
Alcohol is
regarded as a
promoter
14. – The effect of alcohol occurs through:
– Histological studies reveal atrophy of oral mucosa
– Notes:
the effect of alcohol & tobacco is multiplicative
The risk depends on:
3- Diet & Nutrition
Iron deficiency:
Iron is important to the normal functioning od epithelial
cells
time
dose
its ability to irritate & dry the mucosa (make it more exposed to
carcinogens in tobacco)
its ability to act as a solvent for carcinogens (specially
tobacco)
contaminants & additives with carcinogenic potential
found in it
acting intrinsically through systemic mechanism ( liver damage or
cirrhosis >>> impaired metabolism & nutritional deficiencies >>>
damage the ability of oral mucosa to maintain its barrier function)
15. Plummer- Vinson syndrome
Vitamin A deficiency:
iron deficiency
atrophic or
immature mucosa
more susceptible
to chemical
carcinogens
impaired cell
mediated
immunity
o Also known as Paterson Kelly syndrome
o It is a severe form of iron-deficiency
o Manifested by:
Painful red tongue
Epithelial atrophy
Dysphagia
o Associated with high frequency of oral
squamous cell carcinoma
vitaminA
maintain intact epithelial
tissues as a physical barrier
to infection
protective role in oral
precancer & cancer
16. antioxidants
• vitamin C
• vitamin E
• Beta-caroten
Vitamin C & vitamin E deficiencies:
Antioxidants protects cell against oxidation damage that can
lead to cancer
Note:
4- Radiation & UV rays
Radiotherapy:
high intake of
antioxidants
decreased risk
of oral cancer
o Beta-carotene is a yellow carotenoid
pigment
o It gives a reddish color to plants (such as
carrots & tomatoes)
o It is usually used as a vitamin supplement
because liver can't convert it into vitamin A
decreases the
immune reactivity
produces
abormalities in
the chromosomal
material
17. Radiotherapy to the head & neck region:
The effect is dose-dependent
Sun (Ultraviolet) rays
UV light is a carcinogenic agent
A person with:
increase the risk for the
later development of new
primary oral malignancy
(carcinoma or sarcoma)
routine
dental
radiograph
small
amount of
radiation
not
associated
with oral
mucosa
chronic
sunlight
exposure
compromis
ed
immunity
increased risk
of developing
cancer of the
lower lip
18. Outdoor workers (farmers, fishermen…) >>> more liable to
develop lip and skin cancer
Confined predominantly to fair skinned people
It is rare in dark skinned people
5- Infectious agents
Viral (HPV-HSV-HIV-EBV)
Oncogenic viruses >> play a major role in variety of cancers
However, no virus has definitively been proven to cause oral
cancer
o Actinic cheilosis:
Diffuse premalignant alteration of the lower lip
dark skin
increased
melanin
pegmintation
protection
against UV
light
viral agents
control the host's ability
to regulate normal
growth & proliferation of
the infected cell
facilitate the
malignant
trasnformation
19. Bacterial (syphilis) tongue lesion (3ry stage):
Tongue carcinomas >>> due to the effect of arsenical
compounds used to treat syphilis
• causes burkitt's lymphoma
Epstein- Barr Virus (EBV)
• increased incidence of Kaposi's sarcoma
HIV
• wide spread in normal epithelium >> it's difficult to cause
oral cancer but they may act with other factors (alcohol,
smoking...)
• HBV 16,18,31,33 subtypes >> detected in oral carcinoma
Human Papilloma Virus (HPV)
• confirmed to cause uterine cervix cancer
• suggested to cause oral caner
Herpes Simplex Virus (HSV)
in the teriary
stage of the
disease
associated
with tongue
carcinoma
(on top of
syphylitic
leukoplakia)
syphilis
20. mechanical
trauma
from
• ill fitting denture
• broken fillings
• sharp edges of teeth
patients having
renal
transplantation
take
immunosuppressive
therapy
newly created
malignant cells
can't be
recognized &
destroyed at an
early stage
increased risk of
oral cancer
Fungal (chronic candidiasis)
Usually associated with speckled leukoplakia (more likely to
undergo malignant transformation)
Fungus >>> suggested to cause this transformation
6- Dental factors
Oral cancer is most common in neglected mouth
Chronic irritation >>> promoter rather than initiator of oral
cancer
7- Immunosuppression
AIDs patients >>> increased risk of oral cancer
the hyphae
interfere
with the cell
metabolism
dysplastic
change
Incriminated in
the etiology of
oral cancer
21. 8- Occupation
References:
1- Ram H, Sarkar J, Kumar H, Konwar R, Bhatt M, Mohammad S. Oral
Cancer: Risk Factors and Molecular Pathogenesis. Journal of
Maxillofacial and Oral Surgery. 2011;10(2):132-137.
2- Kumar M, Nanavati R, Modi T, Dobariya C. Oral cancer: Etiology
and risk factors: A review. Journal of Cancer Research and
Therapeutics. 2016;12(2):458.
increased risk
of having oral
carcinomas
specially those
exposed to raw
cotton & wool
textile workers
increased risk of
having oral
carcinomas
workers in the
printing trades