This document discusses clinical and microscopic changes that occur in gingivitis. It notes that gingivitis is characterized by inflammation of the gingiva caused by plaque bacteria. Key signs include redness, bleeding, changes in consistency from firm to soggy. Microscopically, there is thinning of sulcular epithelium and dilation of blood vessels. The document also outlines factors that can affect gingival features like color, contour, size, surface texture and position in health and disease.
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
Dental Plaque
Soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable & fixed restorations”
Bowen , 1976
Bacterial aggregations on the teeth or other solid oral structures
Lindhe, 2003
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
Dental Plaque
Soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable & fixed restorations”
Bowen , 1976
Bacterial aggregations on the teeth or other solid oral structures
Lindhe, 2003
INTRODUCTION
DEFINITION
TYPES OF TRAUMA FROM OCCLUSION
GLICKMAN CONCEPT
WAERHAUG CONCEPT
STAGES OF TISSUE RESPONSE TO INJURY
CLINICAL AND RADIOGRAPHIC FEATURES OF TFO
CLINICAL DIAGNOSIS OF TFO
TFO AND IMPLANTS
TREATMENT OF TFO
CONCLUSION
REFRENCES
INTRODUCTION
DEFINITION
TYPES OF TRAUMA FROM OCCLUSION
GLICKMAN CONCEPT
WAERHAUG CONCEPT
STAGES OF TISSUE RESPONSE TO INJURY
CLINICAL AND RADIOGRAPHIC FEATURES OF TFO
CLINICAL DIAGNOSIS OF TFO
TFO AND IMPLANTS
TREATMENT OF TFO
CONCLUSION
REFRENCES
The presentation three main topics :
- The clinical features of gingivitis.
- Extension of inflammation from the gingiva in the supporting perodontal tissue.
- Chronic periodontitis
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
All about gingivitis
*definition
*classification
*Signs and Symptoms: Increased GCF, Gingival Bleeding, Color change, Consistency, Surface texture (STIPPLING), Position of Gingiva, Gingival Contour, Size.
Treatment consisits of scaling and root planing. The more inflamed a gingival unit appears clinically, the better the chances of therapeutic measures resulting in a return to normal gingival health
explaining about Periodontal disease
The term periodontal disease is used in a general sense to encompass all diseases of the periodontium.
The most common disease is initiated by plaque accumulation in the gingivodental area and is basically inflammatory in character, termed marginal periodontitis or more accurately chronic destructive periodontitis.
The periodontal tissues can also be involved by other nosologic entities and many of these fall into degenerative or neoplastic categories. They are considered as periodontal manifestations of systemic diseases
CHRONIC DESTRUCTIVE PERIODONTITIS
Periodontitis
Marginal periodontitis
Slowly progressing
Rapidly progressing
Refractory
Juvenile form of periodontitis
Generalized form
Localized form
Necrotizing Ulcerative Periodontitis
Trauma from occlusion*
Periodontal atrophy*
Presenile atrophy
Disuse atrophy
MARGINAL PERIODONTITIS
Clinical features: chronic inflammation of the gingiva, pocket formation, and bone loss. Tooth mobility and pathologic migration appear in advanced cases.
Etiology: dental plaque
Types: slowly progressing periodontitis, rapidly progressing periodontitis, refractory periodontitis
Presenile atrophy
reduction in the height of periodontium that is uniform throughout the mouth and without apparent cause
Disuse atrophy
Results when the functional stimulation for the maintenance of the periodontal tissues is markedly diminished or absent.
characterized by thinning of periodontal ligament, thinning and reduction in the number of periodontal fibers and disruption of fiber bundle arrangement, thickened cementum, reduction in height of alveolar bone, and osteoporosis
A periodontal pocket is a pathologically deepened sulcus: it is one of the important clinical features of periodontal disease.
SYMPTOMS:
Localized pain or a sensation of pressure after eating, which gradually diminishes
A foul taste in localized areas.
A tendency to suck material from the interproximal spaces.
Radiating pain “deep in the bone”
A “gnawing” feeling or feeling of itchiness in the gums.
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
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
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.
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!
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.
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
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
2. Inflammation of gingiva is termed as gingivitis.
The main cause of gingivitis is plaque induced
microorganisms.
These microorganisms release certain products such
as collagenase, hyaluronidase, protease, chondroitin
sulfatase etc. which can cause damage to the
epithelial and connective tissue constituents.
The intercellular spaces between the junctional
epithelial cells are destroyed and may permit the
bacterial products or bacteria themselves to gain
access into the connective tissue.
Absence of treatment of gingivitis can lead progress
of gingivitis into periodontitis.
3. STAGE VASCULAR
CHANGES
MICROSCOPIC
CHANGES
CLINICAL
CHANGES
1. Initial lesion
(2-4 days)
Classical vaculities
subjacent to junctional
epithelium
Presence of
leukocytes(PMNs),
Loss of perivascular
collagen, changes in the
coronal most portion of
junctional epithelium.
Exudation of fluid from
the gingival sulcus.
Subclinical gingivitis
2. Early lesion
(4-7days)
Vascular proliferation Rete peg formation in
junctional epithelium,
presence of lymphocytes,
Loss of collagen,
fibroblasts show
cytoplasmic alterations
Erythematous, gingival
bleeding on probing
3. Established lesion
(14-21 days)
Same as early lesion, with
blood stasis
Proliferation, apical
migration & lateral
extension of junctional
epithelium, Atrophic areas,
plasma cells are
predominant, furthur loss
of collagen, increased
enzyme levels such as acid
& alkaline phosphatase,
beta glucuronidase etc.
Changes seen in
consistency & surface
texture.
Bluish he around the
reddened gingiva.
4. Advanced lesion Same as early &
established lesion
Persistence of features
seen in established lesion,
Ectension of inflammation
into deeper structures,
presence of all types of
inflammatory cells
Formation of periodontal
pocket and its aa
4. Depending on course and duration
Depending on distribution
Depending on the course and duration:
1) Acute gingivitis is of sudden onset and short duration;
and can be painful.
2) Subacute gingivitis is a less severe phase of acute
infection.
3) Recurrent gingivitis reappears either after treatment
or disappears spontaneously.
4) Chronic gingivitis is show in onset, of long duration,
usually painless and the most commonly occuring
gingival condition.
5. Depending on distribution
Localized gingivitis: It is the condition is
involving a single tooth or group of tooth.
Generalized gingivitis: It is the condition
involving entire mouth.
According to distribution: gingivitis could be
marginal, papillary, or diffuse.
Marginal gingivitis: In this the inflammation is
limited to the marginal gingiva.
Papillary gingivitis: In this the inflammation is
limited to interdental papilla.
Diffuse gingivitis: In this the inflammation involves
attached gingiva.
6. GINGIVAL FEATURES IN HEALTH FACTORS RESPINSIBLE IN DISEASE FACTORS RESPNSIBLE DISEASE CONDITION
1. Color Coral pink Vascular supply
Thickness &
degree of
keratinization of
epithelium
Presence of
pigment
containing cells
Color changes
may be :
Marginal
Diffuse
Diffuse or patch
like
Varying shades of
reddish blue,
deep blue
Color changes
Shiny slate gray
Dull whitish gray
Chronic Gingivitis
Chronic Gingivitis
Acute gingivitis
ANUG/HIV
Gingivitis
Herpetic
gingivostomatitis
• Vascular
proliferation
• Reduction of
keratinization
owning to
epithelium
compression by
inflamed tissue.
• Venus stasis
• Tissue necrosis.
2. Contour Marginal gingiva:
Scalloped & Knife
edged
Interdental papilla:
Anterior: pyramidal
shaped
Posterior: Tent shaped
• Shape of the tooth
and thus alignment
in the arch.
• Location and size of
proximal contact.
• Dimensions of facial
and lingual gingival
embrasures
• Marginal gingiva
becomes rolled or
rounded,
interdental papilla
becomes blunt and
flat.
• Punched out and
crater like
depression at the
crest of interdental
papilla extending to
marginal gingiva.
• Exaggerated
scalloping
apostrophe shaped
indentations
extending from and
into the gingival
margins for varying
distance on the
facial surface.
• Life saver like
enlargement of
marginal gingiva.
Chronic gingivitis.
ANUG
Stillman’s cleft
McCall’s festoons
Inflammatory changes
• As a result of
trauma from
occlusion
• Enlargement of
interdental papilla
with no
enlargement of
marginal gingiva
7. GINGIVAL FEATURES IN HEALTH FACTORS RESPINSIBLE IN DISEASE FACTORS RESPNSIBLE DISEASE CONDITION
3. Consistency Firm & resilient • Collagenous nature
of lamina propria
and its contiguity
with the
mucoperiosteum of
alveolar bone
• Cellular and fluid
content of the
tissue.
• Soggy puffiness that
pits on pressure.
• Marked softness and
friability.
• Firm leathery.
• Defuse puffiness
and softening.
• Sloughing.
• Vesicle formation.
Chronic gingivitis
Exudative
Fibrotic
Actuate gingivitis
• Infiltration by fluids
and cells.
• Degeneration of CT
and epi.
• Fibrosis.
• Necrosis
4. Size Normal Some total of bulk of
cellular and
intercellular elements
and there vascular
supply.
Increased Gingival enlargement Increase in fibers and
decrease in cells and
vice versa.
5. Surface texture Stippling present • Due to the
attachment of
gingival fibers to
underline bone.
• Microscopically
papillary layer of
connective tissue
projects into the
elevations.
Loss of stippling
Smooth and shiny
Firm and nodular
Peeling of surface
Leathery texture
Minutely nodular
surface
Gingivitis
Exudative chronic
gingivitis
Fibrotic chronic
gingivitis
Chronic
desquamative
gingivitis
Hyperkeratosis
Non inflammatory
gingival hyperplasia
Due to destruction of
gingival fibers as a
result of inflammation
6. Position 1mm above the
cementoenamel
junction
• Position of tooth in
arch
• Root bone angle
• Mesiodistal
curvature of tooth
surface
• Apically placed
• Coronally replaced
• Gingival recession
• Pseudopockets
• Tooth brush trauma.
• Gingival
inflammation
• High frenum
attachment
• Tooth malposition
• Friction from soft
tissue
7. Bleeding on probing Intact sulcular
epithelium and normal
capillaries
Present
Chronic recurrent,
spontaneous bleeding
or slight bleeding
• Chronic gingivitis
• ANUG
• Systemic disease
Dilation and
engorgement of
capillaries and thinning
or ulceration of
sulcular epithelium.
8. GINGIVAL BLEEDING ON PROBING:
Significance of gingival bleeding on probing:
i. It is one of the earliest visual signs of inflammation.
ii. It can appear earlier then colour changes or any other
visual signs of inflammation.
iii. It also provides an additional advantage, by being a more
objective sign that requires less subjective estimation
by the examiner.
iv. Gingival bleeding on probing also helps us to determine
whether the lesions is in an active or inactive state. In
inactive lesion, there will be little or on bleeding on
probing, whereas active lesions bleed more readily on
probing.
v. The severity and ease with bleeding can be provoked-
indicates the integrity of the inflammation.
9. Etiological factors responsible for gingival
bleeding on probing:
Etiological factors can be divided into:
• Acute Factors
• Chronic Factors
Local
Factors
• Hematological Disease
• Excessive use of drugs
Systemic
Factors
10. LOCAL FACTORS:
Acute Factors: These factors cause acute bleeding.
causes are:
1. Toothbrush trauma.
2. Impaction of sharp pieces of hard food.
3. Gingival burns from hot foods or chemicals.
4. In conditions such as acute necrotizing ulcerative
gingivitis(ANUG).
Chronic Factors: These factors cause chronic
bleeding.
causes are:
1. Chronic inflammation due to the presence of
plaque and calculus.
2. Mechanical trauma, e.g. from tooth brushing,
tooth picks or food impaction.
3. Biting into solids foods such as apple.
11. SYSTEMIC FACTORS:
Hematological disease such as vitamin K
deficiency, platelet disorders such as
thrombocytopenia purpura, other coagulation
defects such as hemophilia, leukemia and
others.
Bleeding could also be as a result of excessive
administration of drugs such as salicylates and
anticoagulants such as dicumarol and heparin
12. Microscopic changes associated with gingival
bleeding on probing:
1. In the epithelium: Thinning and micro
ulcerations of the sulcular epithelium is seen.
2. In the connective tissue: Dilation and
engorgement of the capillaries takes place.
13. COLOR CHANGES IN THE GINGIVA:
Color of the gingiva is an important clinical sign of
gingival diseases.
Normally, gingiva appears to be coral pink.
The factors that are responsible for this are tissue
vascularity, degree of keratinization and thickness of
the epithelium.
Generally, color of the gingiva may change to red, to
bluish red to pale pink.
Systemically absorbed heavy metals may also cause
gingival pigmentation, e.g. bismuth, arsenic, mercury,
lead and silver.
Abnormal melanin pigmentation of the gingiva may be
observed in conditions like Addison’s disease, peutz-
jeghers syndrome.
14. CHANGES IN CONSISTENCY OF GINGIVA:
Normal gingiva exhibits a firm and resilient
consistency.
Factors that are responsible are cellular and
fluid content and collagenous nature of lamina
propria.
In disease conditions, it can be soggy and
edematous or firm; and leathery consistency.
15. CHANGES IN SIZE OF GINGIVA:
Normal size depends on the sum of the bulk
cellular and intercellular elements, and their
vascular supply.
In disease, the size is increased, which can be
termed as gingival enlargement.
Factors responsible for
this are increase in bulk
of cellular and
intracellular elements.
16. SURFACE TEXTURE:
Under normal conditions, gingiva appears to be
stippled(orange peel appearance)
This is due to attachment of gingival fibers to
the underlying bone.
Stippling is absent in disease
conditions. Hence, the
gingiva may appear
smooth and shiny.
17. CHANGES IN POSITION OF GINGIVA:
Normally, the gingiva is attached to the tooth
at the cementoenamel junction.
In disease, the position can be shifted either
coronally (pseudo-pocket) or apical to the
cementoenamel junction (gingival recession).
GINGIVAL RECESSION:
Defination:- Gingival recession is defined as
the exposure of the root surface by an apical
shift in the position of the gingiva.
18. Types:-
In gingival recession, there are two types:
Visible, which is clinically observable.
Hidden, which is covered by gingiva and can
only be measured with probe.
Gingival recession may also be localized and
generalized.
19. Classification of Gingival Recession:
Two classification systems are available:-
1) According to Sullivan & Atkins: Shallow-
narrow, shallow-wide and deep-wide.
2) According to PD Miller’s: Class-I ,Class-II,
Class III, Class IV.
20. Etiology of gingival recession:
Plaque-induced gingival inflammation is the
primary etiological factor responsible for
gingival recession
Other common cause is faulty tooth-brushing.
Other secondary factors on gingival recession
are broadly categorized as-
i. Anatomic factors
ii. Habits
iii. Iatrogenic factors
iv. Physiologic factors
21. Clinical significance of gingival recession:
1) The exposed root surface may be extremely
sensitive.
2) Hyperemia of the pulp may result due to
gingival recession.
3) Interproximal recession creates oral hygiene
problems thereby resulting in plaque
accumulation.
4) Finally, it is aesthetically unacceptable.
22. Changes in gingival contour:
Normally, marginal gingiva is scalloped and knife
edges, whereas interdental papilla in the anterior
region is pyramidal and posteriorly tent-shaped.
The factors that maintain normal contour are,
shape of the teeth and its alignment in the arch,
location and size of the proximal contact and
dimensions of the facial and lingual gingival
embrasures.
In diseased conditions, the marginal gingiva may
become rounded or rolled, whereas interdental
papilla can become blunt and flat.
23. Stillman’s clefts are apostrophe shaped
indentations extending from and into the
gingival margin varying distance on the facial
surface.
Mccall’s festoon isa life preserver shaped
enlargement of gingiva, most commonly seen
on the facial surface of canine and premolar
area.