This document provides an overview of gingival enlargement, including its classification, causes, clinical presentation, histopathology, and management. It discusses inflammatory enlargement, drug-induced enlargement from anticonvulsants, immunosuppressants, and calcium channel blockers. Enlargement associated with systemic conditions like pregnancy and leukemia are also reviewed. The document describes neoplastic enlargement and provides classifications based on location and distribution. Scoring systems for grading enlargement and specific drug-induced varieties are outlined.
REFERENCES TAKEN FROM CARRANZA'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND LINDHE'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY. CONTAINS ENOUGH AND MORE DETAILS OF THIS TOPIC FOR BDS STUDENTS.HOPE THIS PRESENTATION WILL HELP U GAIN SOME KNOWLEDGE ABOUT PERIODONTAL PLASTIC AND ESTHETIC DENTISTRY.
REFERENCES TAKEN FROM CARRANZA'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND LINDHE'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY. CONTAINS ENOUGH AND MORE DETAILS OF THIS TOPIC FOR BDS STUDENTS.HOPE THIS PRESENTATION WILL HELP U GAIN SOME KNOWLEDGE ABOUT PERIODONTAL PLASTIC AND ESTHETIC DENTISTRY.
explained here is bone loos and patterns of bone loos in alveolar bone to various insults . Dr Harshavardhan pawal also gives emphasis on rate on bone loss and radius of action .
Certains medications have been associated with gingival enlargement.
the seminar gives a complete analysis of etilogy and pathogenesis involved in digo as well as sequlae of it
AGGRESSIVE PERIODONTITIS
PRESENTER
DR. REBICCA RANJIT
DEPT. OF PERIODONTOLOGY & ORAL IMPLANTOLOGY
Why is there localisation of disease to 1st molars and incisors in LAP?
Often subjects present with attachment loss that does not fit the specific diagnostic criteria (AP or chronic periodontitis).
Schenkein et al. 1995: cigarette smoking was shown to be a risk factor for patients with generalized forms of AgP.
Smokers with GAP had more affected teeth and greater mean levels of attachment loss than patients with GAP who did not smoke.
IgG2 serum levels as well as antibody levels against A.a. are significantly depressed in subjects with GAP who smoked.
Periodontitis is a complex infection initiated by bacteria –tissue destruction.
Host: the organism from which a parasite obtains its nourishment/ an individual who receives a graft
Modulation: the alteration of function or status of something in response to a stimulus or an altered physical or chemical environment
explained here is bone loos and patterns of bone loos in alveolar bone to various insults . Dr Harshavardhan pawal also gives emphasis on rate on bone loss and radius of action .
Certains medications have been associated with gingival enlargement.
the seminar gives a complete analysis of etilogy and pathogenesis involved in digo as well as sequlae of it
AGGRESSIVE PERIODONTITIS
PRESENTER
DR. REBICCA RANJIT
DEPT. OF PERIODONTOLOGY & ORAL IMPLANTOLOGY
Why is there localisation of disease to 1st molars and incisors in LAP?
Often subjects present with attachment loss that does not fit the specific diagnostic criteria (AP or chronic periodontitis).
Schenkein et al. 1995: cigarette smoking was shown to be a risk factor for patients with generalized forms of AgP.
Smokers with GAP had more affected teeth and greater mean levels of attachment loss than patients with GAP who did not smoke.
IgG2 serum levels as well as antibody levels against A.a. are significantly depressed in subjects with GAP who smoked.
Periodontitis is a complex infection initiated by bacteria –tissue destruction.
Host: the organism from which a parasite obtains its nourishment/ an individual who receives a graft
Modulation: the alteration of function or status of something in response to a stimulus or an altered physical or chemical environment
Periodontal instruments are designed for speciic purposes, such as
calculus removal, bioilm removal, and root planing. On irst investigation,
the variety of instruments available for similar purposes appears
confusing. With experience, however, clinicians select a relatively
small set that fulills all requirements.
Classification of Periodontal Instruments
Periodontal instruments are classiied according to the purposes they
serve, as follows:
1. Periodontal probes are used to locate, measure, and mark pockets,
as well as determine their course on individual tooth surfaces.
2. Explorers are used to locate calculus deposits and caries.
3. Scaling, root-planing, and curettage instruments are used for
removal of bioilm and calciied deposits from the crown and
root of a tooth, removal of altered cementum from the subgingival
root surface, and debridement of the soft tissue lining the poc ket.
Scaling and curettage instruments are classiied as follows:
• Sickle scalers are heavy instruments used to remove supragingival
calculus.
• Curettes are ine instruments used for subgingival scaling,
root planing, and removal of the soft tissue lining the pocket.
• Hoe, chisel, and ile scalers are used to remove tenacious
subgingival calculus and altered cementumT. heir use is limited
compared with that of curettes.
• Implant instruments are plastic or titanium scalers and curettes
designed for use on implants and implant restorations.
• Ultrasonic and sonic instruments are used for scaling and
cleansing tooth surfaces and curetting the soft tissue wall of
the periodontal pocket.42,43,66
4. Periodontal endoscopes are used for deep visualization into
subgingival pockets and furcations, thereby alloinwg the detectio n
of deposits.
5. Cleansing and polishing instruments, such as rubber cups, brushes,
and dental tape, are used to clean and polish tooth surfaces.
Air-powder abrasive systems are also available for supragingival
and subgingival cleaning and polishing of tooth, root, and implant
surfaces.
The wearing and cutting qualities of some types of steel used in
periodontal instruments have been tested,88,89,157 but speciications
vary among manufacturers.157 Stainless steel is used most often in
instrument manufacture. High–carbon content steel instruments are
available and are considered by some clinicians to be superior. Newer
advanced proprietary manufacturing processes for heat treating and
cryogenically tempering stainless steel are producing blades that ar e
sharper and longer lasting than ever before. In addition, ohter processes
produce stainless steel instruments with titanium nitride or other
surface coatings that are not embedded or diffused into the base
material. Their cutting edges are sharp when new, but these coatings
wear down during normal use and cannot be resharpened. Each
group of instruments has characteristic features; individual therapist s
often develop variations with which they operate most effectivelyuuw
Periodontal instruments are designed for speciic purposes, such as
calculus removal, bioilm removal, and root planing. On irst investigation,
the variety of instruments available for similar purposes appears
confusing. With experience, however, clinicians select a relatively
small set that fulills all requirements.
Classification of Periodontal Instruments
Periodontal instruments are classiied according to the purposes they
serve, as follows:
1. Periodontal probes are used to locate, measure, and mark pockets,
as well as determine their course on individual tooth surfaces.
2. Explorers are used to locate calculus deposits and caries.
3. Scaling, root-planing, and curettage instruments are used for
removal of bioilm and calciied deposits from the crown and
root of a tooth, removal of altered cementum from the subgingival
root surface, and debridement of the soft tissue lining the poc ket.
Scaling and curettage instruments are classiied as follows:
• Sickle scalers are heavy instruments used to remove supragingival
calculus.
• Curettes are ine instruments used for subgingival scaling,
root planing, and removal of the soft tissue lining the pocket.
• Hoe, chisel, and ile scalers are used to remove tenacious
subgingival calculus and altered cementumT. heir use is limited
compared with that of curettes.
• Implant instruments are plastic or titanium scalers and curettes
designed for use on implants and implant restorations.
• Ultrasonic and sonic instruments are used for scaling and
cleansing tooth surfaces and curetting the soft tissue wall of
the periodontal pocket.42,43,66
4. Periodontal endoscopes are used for deep visualization into
subgingival pockets and furcations, thereby alloinwg the detectio n
of deposits.
5. Cleansing and polishing instruments, such as rubber cups, brushes,
and dental tape, are used to clean and polish tooth surfaces.
Air-powder abrasive systems are also available for supragingival
and subgingival cleaning and polishing of tooth, root, and implant
surfaces.
The wearing and cutting qualities of some types of steel used in
periodontal instruments have been tested,88,89,157 but speciications
vary among manufacturers.157 Stainless steel is used most often in
instrument manufacture. High–carbon content steel instruments are
available and are considered by some clinicians to be superior. Newer
advanced proprietary manufacturing processes for heat treating and
cryogenically tempering stainless steel are producing blades that ar e
sharper and longer lasting than ever before. In addition, ohter processes
produce stainless steel instruments with titanium nitride or other
surface coatings that are not embedded or diffused into the base
material. Their cutting edges are sharp when new, but these coatings
wear down during normal use and cannot be resharpened. Each
group of instruments has characteristic features; individual therapist s
often develop variations with which they operate most effectively
Oral submucous fibrosis (OSMF or OSF) is a chronic, complex, premalignant (1% transformation risk) condition of the oral cavity, characterized by juxta-epithelial inflammatory reaction and progressive fibrosis of the submucosal tissues (the lamina propria and deeper connective tissues). As the disease progresses, the jaws become rigid to the point that the person is unable to open the mouth.
The condition is remotely linked to oral cancers and is associated with areca nut or betel quid chewing, a habit similar to tobacco chewing, is practiced predominantly in Southeast Asia and India, dating back thousands of years.
*Increase in size of gingiva. Lead to false pockets.
*Difficulties associated with it are:
Difficulty in plaque control; Aesthetic concerns; Affect mastication
Interfere with speech
*TREATMENT:
Gingivectomy is the treatment of choice to remove false pockets.
In case of true pockets (osseous defects), gingivectomy with Flap surgery is done. First Gingivectomy is done. After that flap is raised and osseous surgery is performed (either osteotomy or regenerative depending upon the type of defect). Gingivectomy is done by scalpel or electro cautery/lasers (to minimize bleeding). Gingivectomy can be done only where at least 3mm of keratinized gingiva remains after completion of surgery. So it is contraindicated in patients with lack of sufficient keratinized gingiva
*REASONS OF RECURRENCE:
Responsible factors: Residual local irritation; and systemic or hereditary conditions causing noninflammatory gingival hyperplasia.
Recurrence of chronic inflammatory enlargements immediately after treatment indicates that all irritants have not been removed. Contributory local conditions like food impaction and overhanging margins of restorations are commonly overlooked.
If the enlargement recurs after healing is complete and normal contour is attained, inadequate plaque control by the patient is the most common cause.
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
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.
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
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
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
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.
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
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.
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.
3. Gingival enlargement
increase in the size of the gingiva
clinical descriptive term
Avoid pathological terms used in the past, such as
hypertrophic gingivitis and gingival hyperplasia.
•
5. Gingival enlargement has been classified based on etiologic factors and pathological changes, they are
Inflammatory enlargement
a. Acute
b .Chronic
Drug induced enlargement
•General information
•Anticonvulsants
•Immunosuppressant
•Calcium channel blockers
•Hereditary gingival fibromatosis
Enlargement associated with systemic diseases or conditions:
a. Conditioned enlargement:
•Pregnancy
•Puberty
•Vitamin C
•Plasma Cell Gingivitis
•Nonspecific Conditioned Enlargement (Pyogenic Granuloma)
b. Systemic diseases that cause gingival enlargement:
•Leukemia
•Granulomatous disease (e.g. Wegener’s Granulomatosis)
Neoplastic enlargement (gingival tumors)
•Benign
•False enlargement Malignant
6. BASED ON THE LOCATION AND DISTRIBUTION.
Localized: Limited to the gingiva adjacent to a single tooth or group of tooth.
Generalized: involving the gingiva throughout the mouth.
7. Marginal: confined to the marginal gingiva.
Papillary: confined to the interdental papilla.
8. Discrete: an isolated sessile or pendunculated tumor like
enlargement
Diffuse: involving the marginal and attached gingiva and papilla
9. SCORING OF GINGIVAL ENLARGEMENT:
BUCHNER AND HANSEN 1969
Grade 0: No signs of gingival enlargement
Grade I: Enlargement confined to interdental papilla .
Grade II: Enlargement involves papilla and marginal gingiva.
Grade III: Enlargement covers three quarters or more
of the crown
10.
11. INFLAMMATORY ENLARGEMENT:
CHRONIC INFLAMMATORY ENLARGEMENT:
Hirschfield et al:
Dental plaque-
poor oral hygiene,
Irritation by anatomic
abnormalities,
Improper restorative
and orthodontic
appliances.
12. Clinical features
•appear bluish or deep red.
•ballooning of the interdental papilla and marginal gingiva-It may
be proximal or on the marginal or attached gingiva.
•life preserver shaped bulge around the involved tooth.
•Soft and friable and easy to bleed.
•.
14. Histopathology:
•Exudative and proliferative features.
•Contains inflammatory cells and fluid ,with vascular engorgement, new capillary
formation, and associated degenerative changes.
•Lesions with firm, resilent and pink have fibrotic component with an abundance of
fibroblasts and collagen fibers
15. Management:
•scaling and root planning is the first choice of treatment.
•If fibrotic component does not resolve -surgical removal is the only
treatment of choice.
•The most widely employed surgical approaches for the treatment of
gingival enlargements is
•Gingivectomy- by laser, electrocautery or conventional means
• Flap technique.
17. GINGIVAL ENLARGEMENT IN MOUTH BREATHERS:
Lite,Diamo et al 1955
Etiopathogenesis:
•The exact mechanism of enlargement in mouth breathers is not clear.
•It is thought to be due to alternate wetting and drying of the gingival surface.
•Its harmful effect is generally attributed to irritation from surface dehydration.
•However comparable changes could not be produced by air drying the gingiva
of experimental animals- Maier et al.
18. OCCURENCE
Patients present with mouth breathing habit that may be due to
•short upper lip,
•hyperactive labii superioris,
•proclined incisors,
• rhinitis.
19. Clinical features:
The gingiva appears red and edematous with diffuse
shiny surface.
enlargement in maxillary and mandibular anterior regions
and no involvement of posteriors.
In a typical bimaxillary protrusion case, the enlargement
will be limited to palatal aspect of maxillary anteriors and
labial aspect of mandibular anteriors.
21. Within 24 to 48 hrs, the lesion usually becomes fluctuant and
pointed with a surface orifice from which purulent exudates
may be expressed
•Due to bacteria carried deep into tissues when a foreign substance e.g. tooth brush, piece of apple core
or lobster shell fragment embedded into the gingiva.
In early stages, it appears as red
swelling with smooth, shiny
surface.
Limited to marginal gingiva or interdental
papilla.
25. DRUG INDUCED GINGIVAL ENLARGEMENT
(DIGO or DIGE):
Drugs associated with gingival overgrowth can be categorized broadly into major
groups according to their therapeutic actions, namely
•anticonvulsants,
•immunosuppressant
•calcium channel blocker
•Contraceptives
26. Clinical featureswithin 2-4 month of initiation of drug intake.
there is no pain.
as beadlike enlargement of the interdental papilla and eventually may involve marginal
gingiva.
the enlargement looks like mulberry shape,
firm, pink and resilient with minute lobulations
no bleeding on probing.
prominent in maxillary and mandibular anteriors.
absent in edentulous areas and will disappear in areas where teeth are extracted.
Moritti et al 1999
27. When infected secondarily, there is increase in the size of existing enlargement and
adds characteristic features of inflammatory enlargement.
31. Phenytoin induced gingival enlargement
initial enlargement of the
interdental papilla
present a granular or
pebbly surface, with the
enlarged papillae
extending facially and
lingually, obscuring the
adjacent tissue and tooth
surfaces.
resulting in the clinical
presence of pseudoclefts.
32. CYCLOSPORIN-INDUCED GINGIVAL
ENLARGEMENT:
•Cyclosporin A -Switzerland in 1970 as a metabolite of the
fungus species Tolypocludium.
potent immunosuppressive action, cyclosporine A prolongs
survival of allergenic transplants involving skin, heart, kidney,
liver, pancreas, bone marrow, small intestine and lung
33. Clinical Appearance:
Develops in first 6 months
Pebbly or papillary and is mostly restricted to the
keratinized gingiva, but it may grow in size with
time and cover the crowns of teeth causing
difficulties in mastication, speech, and profound
esthetic and psychological problem
more hyperemic and more prone to bleeding on
probing than Phenytoin
34. Calcium channel blockers
Dihydropyridines
•treatment of cardiovascular diseases such as
•hypertension,
•angina pectoris,
•coronary artery spasm and
• arrhythmia by reduced burden on the heart, decreased systemic
vascular resistance, smooth muscle vasodilatation and reduced heart
rate
35. Clinical Changes
Clinical changes appear 1-3 months after administration.
gingival overgrowth as a lobular or nodular enlargement on interdental
papilla located in the anterior interproximal regions.
Associated with local factors
Edentulous areas have not been seen however, it can affect the mucus around
the implant.
36.
37. Dose
multidrug
anticonvulsants,
bacterial plaque,
host genetics
dropped levels of serum
folic acid.
Dosage -50% Girgis et al
found correlation .
Age-younger patient
dose,
bacterial plaque,
age,
Multidrug treatment,
gender
graft.
less in patients over 40 years
due to the growth hormone
and high metabolism of
fibroblast in childhood and
adolescence.
Taylor cyclosporine with
nifedipine caused a 6-fold.
HLA 37
Plaque
Dose
Age
Gender
genetic
polymorphism,
cytochrome P450
40. Debate is ongoing regarding whether
drug-induced gingival overgrowth is
due to hyperplasia of the gingival
epithelium or of submucosal
connective tissue, and/or both/
Genetic?
41. phenytoin first reported in 1939 by Kimball.
1939 Faurbye and in 1959, Strean & Leoni -alkalinity of phenytoin might be the cause of the
gingival side effect.
1948, Brandon hypothesized -direct action on the gingival tissues.
1975, Angelopoulos argued that phenytoin induced degranulation of mast cells which resulted in
the generation of a substance that increased collagen formation.
Larmas, in 1976-proliferating effect primarily on the basal cell layer of the oral epithelium thus
increasing the epithelium-connective tissue interface area, which was confirmed by Hassel et al.
1977, Vogel speculated -end-organ folic acid deficiency, which could lead the gingival tissues
susceptible to inflammation by causing degenerative changes in the gingival sulcular epithelium,
the main physical barrier against local irritants.
42. CsA-induced gingival hyperplasia was first reported by Seymour et al. in
1983.
Despite the cellular and molecular basis of the development of CsA-
induced gingival hyperplasia, the exact mechanism underlying this
condition is still unclear.
A recent study suggested that the imbalance between cell proliferation
and apoptosis may contribute to the pathogenesis of the hypercellularity
observed in CsA-induced gingival hyperplasia.
43. Calcium channel blocker
•Nifedipine-induced gingival enlargement was
first reported by Lederman in 1984 .
•first case of amlodipine-associated
gingival overgrowth was reported by Ellis
in 1993.
47. •Platelet derived growth
factor B
•mitogen and chemo attractant for
fibroblast proliferation and
synthesis of glycosoaminoglycans,
fibronectin, and collagen..
Jung et al 2008
48. he best hypothesis so far is that calcium
antagonists inhibit the influx of calcium ions which is
needed for the degradation and synthesis of collagen.
The accumulated collagen and extracellular matrix not
degraded owing to inhibition of calcium influx by calcium
antagonists is suggested to cause gingival hyperplasia.
49. Side effects
.
Nephrotoxicity
Neurotoxicity
Hypertension
Hypertrichosis
Metabolite OL_17
megaloblastic anemia
Accelerate gingival
wound healing and
increase the tensile
strength of abdominal
wounds.
Metabolite: 5 -
parahydroxyphenyl- 5
-phenylhydantoin and
accounts for 50-75%
of the daily dose.
Nifedipine+diabetes
Type II =periodontal
destruction.
tachycardia and facial
redness can be seen in
patients taking these
drugs.
50. Histological characteristics -phenytoin
•thick stratified squamous epithelium with long
thin rete pegs, often acanthotic
•lamina propria is characterized by
proliferation of fibroblasts and increased
collagen formation, accompanied by an
increase in non-collagenous proteins
51. Histopathology- Cyclosporine
•Seen changes in Connective tissue and secularization
as well as focal inflammatory cells particularly plasma
cells.
•Pisantly argued that gingival enlargement is simply
due to the epithelial acanthosis and accumulation of
extracellular matrix and the connective tissue does not
change in size.
52. Histopathological Changes-nifedipine:
•In the study conducted by Barak, the gingival epithelium
proliferation was more responsible for gingival enlargement
than connective tissue proliferation.
•An increase was reported in production of acid
mucopolysaccharides and the number of cytoplasmic secretory
granules.
53. Other drugs
Gingival overgrowth has been associated with the use of
erythromycin -Valsecchi et al in 1992: Lombardi et al in 1989
54. CONTRACEPTIVES
Gingival enlargement associated with contraceptives was
first reported in 1967 by Lynn.
Despite case reports, contraceptives are not known as
inducers of gingival enlargement.
After a few months of administration, the cumulative
dose will be 6-15 times greater than the expected and the
effects will disappear by stopping the administration.
Norethindrone Mestranol
56. Key strategies in gingival
enlargement.
•Plaque control
•medical management
•periodontal surgical procedures
•multidisciplinary dental care
57. Nifedipine with Isradipine ( 20 mg BD).(westbrook in 2001)
ACE Inhibitors like Captopril (12.5 to 50mgBD), Enalapril
(2.5to20 mg OD) to control hypertension
Phenytoin with Phenobarbital(60 mg TDS), Primidone (
100mg TDS) Carbamezepine (200-400mg TDS) Valproic acid
(200-500mg TDS)
Cyclosporin A with Tacrolimus (0.15 to 0.20/kg/d) Rapamycin
Drugs substitute:
58. Gingivectomy
Excision of gingiva. Simple & quick technique
Advantages
Permits an adequate contouring of the tissue Controls hemorrhage
Disadvantages Unpleasant odour Irreparable damage to bone Use
limited to superficial procedures Heat generated can cause tissue damage
& loss of periodontal support.
59. Co2 lasers used for excision of gingiva
Advantages Excellent soft tissue ablation
Haemostatic characteristic
Disadvantages Healing is delayed
Requires precautionary measures
Application to root surface or alveolar bone
causes carbonization & major thermal
damage.
Electrocautery
60. IDIOPATHIC GINGIVAL
ENLARGEMENT:
•Also referred to as congenital familial fibromatosis,
gingivomatosis, idiopathic fibromatosis, elephantiasis and
hereditary gingival hyperplasia.
•It presents as unusual fibrotic gingival enlargement of
localized or generalized extent.
•It may present as a specific entity or as a part of syndrome.
•Autosomal recessive and autosomal dominance.
61. •Diagnosis can be made by a positive family history of gingival
enlargement.
•It usually begins with the eruption of the primary or permanent
dentition.
•A frequent finding could be presence of firm bulky
enlargement of gingiva restricted to maxillary and mandibular
second and third molar areas only.
•The enlarged mass may be pink or reddish and may be firm/
nodular, pebbly on palpation.
•Involve attached gingiva, marginal gingiva and interdental
papilla
•It affects the marginal gingival, attached gingival and
interdental
62. •Alveolar bone is rarely affected, but presence of pseudo-
pockets and difficulty in maintaining oral hygiene may lead
to some periodontal problems.
•Extensive overgrowths can lead to esthetic and functional
concerns to the patient.
•Seen in tuberous sclerosis –inherited disorder characterized
by triad of epilepsy, mental deficiency and cutaneous
Angiofibromas-stirrups et al 1972 :Thomas et al 1992
63. CONDITIONED GINGIVAL ENLARGEMENT
Hormonal:
•Generalized gingival hyperplasia, during pregnancy and puberty,
is influenced by hormonal changes that pretentious the response to
local irritants.
•The interproximal gingiva shows more prominent enlargement
than the facial and/or lingual surfaces .
•The enlarged gingiva usually is soft and friable, bright red or
magenta, with a smooth, shiny surface.
64. •Bleeding may occur extemporaneously or on mild
stimulation.
The enlargement may reduce spontaneously after the delivery,
but complete elimination may require the removal of all local
irritants and additional surgical intervention of any fibrotic
remnants.
65. VITAMIN C DEFICIENCY:
•Deficiency of vitamin C is defined as a serum ascorbic acid level
< 2 μg/mL
•Diabetes, stress and smoking are the commonly labeled factors
leading to mild vitamin C deficiency.
•Causes hemorrhage, collagen degeneration and
edema
•The gingiva, of vitamin C deficiency associated enlargement, is
bluish red, soft and friable with a smooth, shiny surface.
•Involve marginal.
•Bleeding may occur spontaneously or on slight irritation.
•Surface necrosis with pseudomembrane formation is also
frequently seen.
66. PLASMA CELL GINGIVITIS:
•The etiology difficult to establish,
•Appears due to hypersensitivity reaction with affluent
plasma cells seen histologically.
•Usual allergens known to be associated with this lesion
could be, e.g., toothpaste, food product particularly
cinnamon, chewing gum or unknown origin
•Associated with
cheliosis and
Glossitis,
Rapid progressive periodontitis
67. •It might bleed on provocation.
•Patients usually complain about burning
sensation on eating hot and spicy food.
• Appearance is reddish in color, involves almost
complete attached gingiva, slight granular
surface appearance is typical.
69. GINGIVAL ENLARGEMENT ASSOCIATED WITH
SYSTEMIC DISEASE:
LEUKEMIA:
•Generalized gingival enlargement associated with leukemia is due to
the massive infiltration of leukemic cells in the gingival connective
tissue.
•Clinically it may mimic inflammatory origin.
Apart from gingival enlargement
other associated features could be
oral ulceration, spontaneous
gingival bleeding,
petechiae,
mucosal pallor,
herpetic infections and candidiasis.
70. •Rarely, numbness in chin and/or tooth pain.
serious condition associated with gingival enlargement
-acute myeloid leukemia.
It can be associated with signs and symptoms of bone
marrow failure, such as ecchymoses, night sweats,
recent infections and lethargy.
An expeditious diagnosis can be made by a simple full
blood count.
71. CLINICAL FEATURES
•enlargement may be diffuse or marginal
•localized or generalized
•may appear as a diffuse enlargement of the
gingival mucosa
•oversized extension of the marginal gingiva, or
a discrete tumor like interproximal mass
72. WEGENER’S GRANULOMATOSIS:
Rare disease affecting respiratory tract and kidney
•Strawberry gingivitis, formed by reddish-purple
exophytic gingival swelling with petechiae
hemorrhages,
•The oral lesions -help in timely diagnosis of this
potentially fatal condition, because they persist for a
long time before multi-organ involvement occurs.
73. •At least two of the following conditions should be fulfilled to
diagnose the condition as Wegener’s Granulomatosis:
(1) Ulcerative lesions of oral mucosa or nasal bleeding or
inflammation;
(2) Nodules, fixed infiltrates or cavities in chest radiograph;
(3) Abnormal urinary sediment; and
(4) Granulomatous inflammation on biopsy
74. •Seen in renal failure patients.
•use of immunosuppressive drugs has
produced prolonged remissions in more than
90% of cases –Kornblut 1980
etiology
75. CLINICAL FEATURES
•reddish purple and bleeds easily on stimulation
•considered an immunologically mediated tissue injury –Cotran
1989
76. BENIGN TUMORS OF THE GINGIVA
:
EPULIS :
•It is a generic term used clinically to designate all discrete tumors
and tumor like masses of the gingiva.
•Most lesions referred to as epulis are inflammatory rather than
neoplastic.
77. FIBROMA
•arise from the gingival connective tissue or from the
periodontal ligament.
•They are slow-growing, spherical tumors that tend to be firm
and nodular but may be soft and vascular.
•Fibromas are usually pendunculated.
HISTOPATHOLGY
Well formed collagen bundles with scattering of fibrocytes
78. PERIPHERAL GIANT CELL GRANULOMA:
•arise interdentally or from the gingival margin.
•Occur most frequently on the labial surface, and may
he sessile or pendunculated.
•Varies from smooth, regularly outlined masses to
irregularly shaped, multilobulated protuberances with
surface indentations.
•Painless.
79. CENTRAL GIANT CELL GRANULOMA:
• These lesions arise within the jaws and produce central
cavitation.
•They occasionally create a deformity of the jaw that makes
the gingiva appear enlarged.
80.
81. The peripheral odontogenic fibroma (PODF) is
definedas a relatively rare tumor that occurs exclusively in the
soft tissues covering tooth-bearing areas of the jaws.
It is considered to represent the soft tissue counterpart of the central
odontogenic fibroma that occurs in bone.
Confusion existsregarding this gingival entity because it has been
referred to bya number of different names, has a debatable
histogenesis, andis often mistaken for the relatively common reactive
lesion, the peripheral ossifying fibroma
83. MALIGNANT TUMORS OF THE GINGIVA:
CARCINOMA:
•Oral cancer accounts for less than 3% of all malignant
tumors in the body but is the sixth most common cancer
in males and the twelfth in females." The gingiva is not a
frequent site of oral malignancy (6% of oral cancer).
•Squamous cell carcinoma is the most common
malignant tumor of the gingiva.
It may be exophytic,
presenting as an irregular
outgrowth, or ulcerative,
which appear as flat, erosive
lesions
84. MALIGNANT MELANOMA:
•rare oral tumor that tends to occur in the hard palate and maxillary
gingiva of older persons.
•
•darkly pigmented and is often preceded by the occurrence of
localized pigmentation .
•flat or nodular and is characterized by rapid growth and early
metastasis
85. SARCOMA:
•Fibrosarcoma, lymphosarcoma, and reticulum cell
sarcoma of the gingiva are rare .
•Kaposi's sarcoma often occurs in the oral cavity of
patients with acquired immunodeficiency syndrome
particularly in the palate and the gingiva.
86. METASTASIS:
•not common
•Such metastasis has been reported with various tumors,
including adenocarcinoma of the colon, lung
carcinoma, primary hepatocellular carcinoma.
•Ulcerations that do not respond
• to therapy in the usual manner,
•as well as all gingival tumors
• and tumor like lesions
•must be biopsied and submitted for microscopic
diagnosis.
87. FALSE ENLARGEMENT:
•not true enlargements of the gingival tissues but may appear
as such as a result of in- creases in size of the underlying
osseous or dental tissues.
• The overlying gingiva presents with no abnormal clinical
features except the massive increase in size of the area.
88. UNDERLYING OSSEOUS LESIONS:
•occurs most commonly in tori and exostosis, but it can also
occur in Paget's disease, fibrous dysplasia, cherubism, central
giant cell granuloma, ameloblastoma, osteoma, and osteosarcoma
.
Gingival tissue can appear normal or may have unrelated
inflammatory changes
89.
90. UNDERLYING DENTAL TISSUES:
•During the various stages of eruption, particularly of the
primary dentition, the labial gingiva may show a bulbous
marginal distortion caused by superimposition of the bulk of
the gingiva on the normal prominence of the enamel in the
gingival half of the crown-developmental enlargement
•Physiologic and ordinarily present no problems.
91. GENETIC DISORDERS ASSOCIATED WITH GINGIVAL
ENLARGEMENT:
They can be divided into 4 primary categories based on their etiology,
clinical features and histology.
•Idiopathic Gingival Enlargement
•Lysosomal Storage Disorders,
•Vascular Disorders
•Dental abnormalities
•syndromes typically associated with gingival enlargements:
Apert’s syndrome, Cross–McKusick–Breen syndrome also
known as "Cross syndrome, Melkersson-Rosenthal Syndrome,
Sturge weber syndrome
92. CONCLUSION:
•Inspite of etiology, gingival enlargements can often be diagnosed
by a careful history (e.g., drug influenced or hormonal influenced
gingival enlargement), by location (e.g., mouth-breathing
enlargement around anterior teeth) or by the clinical presentation
(e.g., strawberry gingivitis).
•Presence of local irritants (plaque= and calculus) could be
primary or associated cause of gingival enlargements. Hence,
plaque control is an essential aspect of management in all the
patients.
•An excisional/incisional biopsy and/or hematologic/histologic
examination may be needed occasionally to correctly diagnose the
uncommon cases of gingival enlargement.
•The clinician should have an open mind and consider all
possibilities before coming to the final diagnosis of condition at
hand.
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