1) Premalignant lesions of the oral mucosa occur in 1.5-4.5% of the global population and account for 17-35% of new oral cancer cases, with an annual malignant transformation rate of 0.7-2.9%.
2) Common premalignant lesions include leukoplakia, erythroplakia, submucous fibrosis, and lichen planus. Leukoplakia may transform to cancer in 0.13-34% of cases depending on population.
3) Risk factors for oral premalignant lesions include smoking, smokeless tobacco, alcohol, HPV infection, and nutritional deficiencies. Early diagnosis and treatment can prevent malignant transformation
Includes most common tumors of oral cavity including scc,bcc, melanoma, ameloblastoma, odontoma, fibromas, pindborg tumors etc.
Presented by Dr. Binaya Subedi
Includes most common tumors of oral cavity including scc,bcc, melanoma, ameloblastoma, odontoma, fibromas, pindborg tumors etc.
Presented by Dr. Binaya Subedi
ORN is an inflammatory condition of bone that occurs after the bone has been exposed to therapeutic doses of radiation usually given for a malignancies.
Cancer of the oral cavity accounts for approximately 3% of all malignancies diagnosed annually in 270,000 patients world-wide. Oral cancer is the 12th most common cancer in women and the 6th in men. Many oral squamous cell carcinomas develop from potentially malignant disorders (PMDs). Lack of awareness about the signs and symptoms of oral PMDs in the general population and even healthcare providers is believed to be responsible for the diagnostic delay of these entities.
Oral cancer is one of the deadliest diseases affecting the human population, being one among the top ten causes of death occurring worldwide. Its high morbidity and mortality rate has not changed for the past 30 years, even after revolutions that are happening in its diagnosis and management. This alarming stage is a sequelae of its late diagnosis, with 80% of cases being diagnosed at late stages. A good number of screening techniques have been time tested for the predictive value in diagnosing oral cancer in an early premalignant stage. Although surgical biopsy is a gold standard for diagnosing, it needs professional services. Hence screening methods which are noninvasive and highly sensitive are accepted as an alternative of histopathology. Vital staining and vizilite are widely accepted methods among all the screening techniques and are widely used in a clinical setup.
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
ORN is an inflammatory condition of bone that occurs after the bone has been exposed to therapeutic doses of radiation usually given for a malignancies.
Cancer of the oral cavity accounts for approximately 3% of all malignancies diagnosed annually in 270,000 patients world-wide. Oral cancer is the 12th most common cancer in women and the 6th in men. Many oral squamous cell carcinomas develop from potentially malignant disorders (PMDs). Lack of awareness about the signs and symptoms of oral PMDs in the general population and even healthcare providers is believed to be responsible for the diagnostic delay of these entities.
Oral cancer is one of the deadliest diseases affecting the human population, being one among the top ten causes of death occurring worldwide. Its high morbidity and mortality rate has not changed for the past 30 years, even after revolutions that are happening in its diagnosis and management. This alarming stage is a sequelae of its late diagnosis, with 80% of cases being diagnosed at late stages. A good number of screening techniques have been time tested for the predictive value in diagnosing oral cancer in an early premalignant stage. Although surgical biopsy is a gold standard for diagnosing, it needs professional services. Hence screening methods which are noninvasive and highly sensitive are accepted as an alternative of histopathology. Vital staining and vizilite are widely accepted methods among all the screening techniques and are widely used in a clinical setup.
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
Premalignantlesions and conditions by Dr. Amit T. Suryawanshi, Oral Surgeon,...All Good Things
Hi. This is Dr. Amit T. Suryawanshi. Oral & Maxillofacial surgeon from Pune, India. I am here on slideshare.com to share some of my own presentations presented at various levels in the field of OMFS. Hope this would somehow be helpful to you making your presentations. All the best.
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 .
paediatric squamosal disease
uncompicated , underwent canal wall down mastoidectomy.
ct showing extensive disease with bone destruction , moderate conductive hearing loss in pre op period.
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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
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.
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!
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
3. Epidemiology
• Premalignant lesions occur in roughly between 1.5% and 4.5% of the
world's population
• Pre-malignant lesions account for 17% to 35% of all new cases of oral cavity
cancer
• Undergo malignant transformation between 0.7% and 2.9% annually.
• Premalignant Conditions of the Oral Cavity edited by Peter A. Brennan, Tom Aldridge, Raghav C. Dwivedi
4. WHO Definition
Pre-cancerous lesions
A precancerous lesion is a
morphologically altered tissue in
which oral cancer is more likely to
occur than in apparently normal
counterpart.
Leukoplakia
Erythroplakia
Submucous fibrosis
Lichen planus
5. Histology of oral mucosa
• Contains a complex
variety of tissues from the
hardest enamel to delicate
salivary gland
parenchyma.
6. Histology
• Oral surface of the lips, cheeks,
floor of the mouth and ventral
tongue are covered by a stratified
non-keratinised epithelium.
• Deep to the epithelium lies the
lamina propria where minor salivary
glands are located.
• Masticatory mucosa requires a
harder-wearing surface hence the
need for keratinised epithelium,
gingivae and palate
https://www.google.com/url?sa=i&url=https%3A%2F%2Fwww.youtube.com%2Fwatch%3Fv
%3DGIAhrwnk79Y&psig=AOvVaw0bhWQLwV5Ew2AqT04y7WHR&ust=1668714251040000
&source=images&cd=vfe&ved=0CBEQjhxqFwoTCNC6p5C7s_sCFQAAAAAdAAAAABAE
7. The molecular basis of carcinogenesis
• Mutation / genetic variation
• Genetic instability
• Oncogenes and proto-oncogenes-
positively regulates a cell cycle
• Tumour suppressor genes are
negative regulators of the cell cycle
• Evasion of apoptosis
Actinic keratosis,lower lip
8.
9. Gene Mutations
The Cancer Genome Atlas Network. Comprehensive genomic characterization of head
and neck squamous cell carcinomas. Nature. 2015;517:576–82.
12. Field Cancerization in Oral Epithelium
• Slaughter proposed in 1953 the
field cancerization process in
oral stratified squamous
epithelium, showing that
clinically normal tissue
surrounding oral squamous cell
carcinoma already harboured
histopathological changes.
• The field cancerization in oral
mucosa can be as large as 7
cm
17. High and low risk factors
Premalignant Conditions of the Oral Cavity
edited by Peter A. Brennan, Tom Aldridge, Raghav C. Dwivedi
18. Smoking
• Tobacco products may also cause
methylation of tumour suppressor
genes,
• Induction of oxidative stress, and
inflammatory reactions.
• Oral cancer cells in smokers
contain more hypomethylated and
hypermethylated genes than non-
smokers, indicating a change in the
normal methylation pattern.
19. Betel Quid
• Betel quid has two basic
carcinogenic actions in the oral
mucosa.
• First is the cytotoxic and mutagenic
effect of its components
(arecoline,alkaloids and
polyphenols) on epithelial cells.
• Second is associated with induced
fibrosis, which reduces the oxygen
supply to the epithelial cells.
Premalignant Conditions of the Oral Cavity
edited by Peter A. Brennan, Tom Aldridge, Raghav C. Dwivedi
20. Alcohol
• In chronic alcohol consumption, the CYP2E1
enzyme is utilized and results in
acetaldehyde formation in peroxisomes.
• Acetaldehydes are very toxic and affect DNA
synthesis and repair.
• Acetaldehyde can bind and form Products
with proteins, lipids, and DNA, which impairs
their functions
• Increased oxidative stress, release of
inflammatory cytokines,
• Impairment of retinoid metabolism, and
inhibition of DNA methylation.
21. HPV
• E6 and E7 HPV proteins function as the
dominant onco-proteins of high-risk
HPVs, and they inactivate the tumour
suppressor proteins p53 and pRB,
• TP53 is the “guardian of the genome”,
and its malfunction in most cancers is
the result of DNA mutation. In HPV-
associated cancers, the E6 onco-protein
degrades the wild-type p53 protein and
leads to chromosomal instability
22.
23. Oral leukoplakia
• World Health Organization (WHO) first
defined oral leukoplakia as
• “a white patch or plaque that cannot be
characterized clinically or pathologically
as any other disease”.
• The term leukoplakia be used in a
descriptive clinical sense only with no
histologic association.
27. Malignant transformation of leukoplakia
• Malignant transformation of oral leukoplakia
varies from 0.13% to 34% in different
populations and geographic areas.
• Dysplastic lesions are about 15 times more
likely to undergo a malignant transformation
than non-dysplastic ones
Warnakulasuriya S, Ariyawardana A. Malignant transformation of oral leukoplakia: a systematic
review of observational studies. J Oral Pathol Med. 2016;45:155–66.
28. Diagnosis of leukoplakia
Elimination of
possible
causes
Biopsy Adjunctive
techniques
Wait for 2-4
weeks
Single deep
biopsy from
edge
Brush biopsy
Toluidine blue
29.
30. Treatment
Preventive Conservative Surgical
Cessation of tobacco ,
alcohol,
Public education
Good oral hygiene,
Balanced diet
vitamin A and retinoids,
systemic
beta carotene,
lycopene, ketorolac
Complete excision
LASER ablation
Life time follow up
31. Erythroplakia and Erythroleucoplakia
• Bouquot in 1994 updated the definition for erythroplakia as “a chronic
red mucosal macule which cannot be given another specific diagnostic
name and cannot be attributed to traumatic, vascular, or inflammatory
causes.
• Erythroplakia should not display histopathologic features of any other
recognizable condition and is a diagnosis of exclusion.
36. Management principle
• Reducing risk/exposure factors.
• Visual examination by trained health care workers
• Biopsy/complete removal of the suspicious lesion.
• Follow-up by continuous monitoring may be lifetime.
• Chemo-prevention : Retinoids, COX inhibitors, green tea polyphenols,
p-53-targeted agents like ONYX-015, thiazolidinediones ,EFGR
inhibitors, blue-green microalgae spirulina, vitamin E, etc. – limited
success
37. Oral Lichen Planus and the Lichenoid
Group of Diseases
• Chronic auto-immunologic and inflammatory muco-cutaneous disorder
that may involve the skin, nails, hair, and mucosa, including the oral
cavity, genital, ocular, otic, esophageal, and, less commonly, bladder,
nasal, laryngeal, and anal mucosa.
• Affect approximately 0.5–2% of the general population.
• Antigenic challenges in the skin and mucosa in a genetically
predisposed patient may represent the initial event to the development
of the disease
• OLP is typically characterized by episodes of remission and
recurrence.
39. Microscopic features
Epithelium demonstrate areas of hyperkeratosis and atrophy.
Elongated epithelial projections (saw-tooth ridges).
Superficial band-like inflammatory infiltrate predominantly composed of T
lymphocytes and the liquefactive destruction of the epithelial basal layer.
Mucositis and the presence of degenerated keratinocytes (Civatte
bodies).
A narrow, eosinophilic, and PAS-positive zone in the basal membrane.
43. Management
Lavanya, Nagarajan &
Palani, Jayanthi & Rao,
Umadevi &
Ranganathan, Kannan.
(2011). Oral lichen
planus: An update on
pathogenesis and
treatment. Journal of oral
and maxillofacial
pathology : JOMFP. 15.
127-32. 10.4103/0973-
029X.84474.
44. Oral Submucous Fibrosis
• Chronic, insidious, progressive
oral mucosal disease affecting
the oral cavity, pharynx, and
upper digestive tract, causing
stiffness of the oral mucosa,
restricted mouth opening, and
impaired ability to eat, speak,
or care for oral hygiene.
46. Distribution in Indian population
• Oral submucous fibrosis: A
contemporary narrative review with a
proposed inter-professional approach
for an early diagnosis and clinical
managementJanuary 2020Journal of
otolaryngology - head & neck surgery =
Le Journal d'oto-rhino-laryngologie et
de chirurgie cervico-faciale
47. Pathogenesis
Rai A, Siddiqui M, Parveen
S, Parveen S, Rasheed A,
Ali S. Molecular
Pathogenesis of Oral
Submucous Fibrosis: A
Critical Appraisal. Biomed
Pharmacol J 2019;12(4).