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
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
Describe relationship between plaque and oral diseases
Describe role of plaque in development of caries
Define Dental Caries
Describe the aetiology and the role different factors play in ini4a4on and progression of the disease
Describe the role played by different microorganisms
Deep caries management /certified fixed orthodontic courses by Indian dental ...Indian dental academy
Welcome to Indian Dental Academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Indian dental academy has a unique training program & curriculum that provides students with exceptional clinical skills and enabling them to return to their office with high level confidence and start treating patients
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
Signs of Caries at SmalltalkHub (mooseday13/2)Yuriy Tymchuk
Presentation of SmalltalkHub data analysis with Moose. Event took place at second MooseDay of 2013 year (Lille). Epic SmalltalkHub visualisation can be found here: http://yuriy.tymchuk.me/Smalldromeda/
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
INCLUDES DEFINITION, CAUSATIVE AGENT, CURRENT CONCEPT OF DENTAL CARIES, KEY'S TRIANGLE, CLASSIFICATION OF DENTAL CARIES BASED ON ANATOMICAL SITE, SEVERITY AND RATE OF PROGRESSION, CLINICAL VARIANTS AND SEQUELAE OF DENTAL CARIES, MANAGEMENT AND TREATMENT OF DENTAL CARIES
Hume- “caries is essentially a progressive loss by acid dissolution of the apatite component of the enamel then the dentin or of the cementum then dentin.”
According to location:
Pit or Fissure caries
Smooth Surface caries
According to rapidity:
Acute
Chronic
Arrested
According to occurrence:
Primary (Virgin) caries
Secondary (Recurrent) caries
According to the site of occurrence:
Enamel caries
Cemental caries.
Acidogenic [ Miller’s Chemico-parasitic] theory.
Proteolytic theory.
Proteolysis- chelation theory.
details about the dental caries
Introduction
Definition
Etiology of dental caries
Clinical features of dental caries
Classification of caries
Theory of dental caries
Management of dental caries
#dentalcaries
THE HUMORAL THEORY
Vital Theory
Chemical theory
Parasitic theory
Miller Chemico Parasitic Theory
Proteolysis Chelation Theory
Sucrose Chelation Theory
types of dental caries
senile caries
backward caries
reversible caries
pit and fissure caries
root caries
Understanding and Treating Dental Caries in Young Children and Young AdultsDr Marielle Pariseau
Tooth decay is the end result of a transmissible bacterial infection that is preventable. This disease is called caries. Yet just placing fillings on teeth, which is what dentists have been doing all along, does not in the long haul stop this disease process.
The bacteria responsible for tooth decay generate acids from the fermentable carbohydrates we eat every day.
Dental caries is an infectious microbial disease of the tooth that results in localized destruction and dissolution of calcified tissues.
Dental caries is one of the most prevalent chronic diseases of people worldwide; individuals are susceptible to this disease throughout their lifetime.
a Topic from Chapter 9 of Proffitt's Orthodontics Edition 6, including the Mechanical Principles in Orthodontics.
In this Slide terminology of Biomechanics in Orthodontics is defined along with effects of wide & narrow bracket, with brief description of Moment & Couple used in Orthodontic Tooth Movement.
Notes made in my Final Year of Bachelor in Dental Surgery from Subject Oral & Maxillofacial Surgery. In this i have mentioned the 8 principles which are used in the treatment & prevention of odontogenic infection which are most common in dental practice. This documents is for professional dental undergraduates studying in their 4th year of BDS or DDS.
This Presentation tells 4th Stage of Comprehensive Orthodontic Treatment in Orthodontics, Retention, which is used to Prevent Relapse after Orthodontic Treatment.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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.
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.
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
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.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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!
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.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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2. WHAT IS DENTAL CARIES?
• Dental caries is a multifactorial,transmissible,infectious oral disease caused
primarily by complex interaction of cariogenic oral flora (biofilm) with fermentable
dietary carbohydrates on the tooth surface over time.
• However, not all persons with teeth, biofilm, & consuming carbohydrates will have
caries over time because of presence of several modifying risk & protective factors.
• It is product of disequilibrium b/w remineralization & demineralization
SARANG SURESH HOTCHANDANI 2
7. WHAT IS DENTAL CARIES? (CONT’D)
• Dental caries results from dynamic
process of demineralization &
remineralization.
• Critical pH
• Enamel; 5.5
• Dentine; 6.2
• This dynamic process is affected by
many factors;
• Number & type microbial flora
• Diet
• Oral hygiene
• Genetics
• Anatomy of tooth
• Use of fluorides
• Chemotherapeutic agents
• Salivary flow
• Buffering capacity
• Resistance of tooth
SARANG SURESH HOTCHANDANI 7
8. • Predominate pathologic environment Demineralization.
• Demineralization is characterized by localized dissolution
and destruction of calcified dental tissues resulting in
“Cavity” formation.
• Dentine demineralization exposes organic protein matrix, which
is denatured and degraded by host’s matrix metalloproteinases
(MMP) and bacterial proteases.
• Cavitation in tooth is Sign of underlying disease and it
is caused by imbalance between protective and
pathologic factors.
• Read Box 2.1 in Art & Science of Operative Dentistry.
SARANG SURESH HOTCHANDANI 8
10. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 10
11. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 11
12. ROLE OF DENTAL PLAQUE OR BIOFILM IN
CARIES PROCESS.
• Soft, tenacious film accumulating on
the surface of teeth.
• Composition (bio), Structure (film)
• Composition
• Bacteria
• Bacterial by products
• Extracellular matrix
• Water
• It is not food debris or haphazard
collection of microbes.
• Formation of Plaque;
• Formation of acquired pellicle over
perikymata ridges of enamel in 30min-
2hr
• Attachment of plaque bacteria to pellicle
• Cocci 12-24 hrs.
• Filamentous 1-3 days
• Growth of microbes
Surface of non-cavited enamel lesion have “Punched out appearance in Electron MicroscopeSARANG SURESH HOTCHANDANI 12
13. ROLE OF DENTAL PLAQUE OR BIOFILM IN
CARIES PROCESS.
• Plaque anaerobically metabolize
carbohydrates.
• Plaque pH independent of Quantity
carbohydrates but it Depends on Frequency
of carbohydrate intake
• In active caries lesion, mineral loss is
not continuous but alternating period of
demineralization & remineralization.
• Different areas of oral cavity or even
different teeth and different surfaces of
same teeth contains the different
community of microbes in the dental
plaque of that area not the same.
SARANG SURESH HOTCHANDANI 13
14. MICROBES OF DENTAL PLAQUE
• Normal non-carious teeth
• Streptococcus sanguis
• Streptococcus mitis
• Enamel caries
• Streptococcus mutans
• Dentine caries
• S. Mutans
• Lactobacilli
• Root caries (filamentous & spiral)
• Actinomyces
• S. Mutans = Initiation of
Caries
• Lactobacilli = Progression
of Caries
• High sugar intake
increases the
concentration of mutans
streptococci & lactobacilli
while restriction of sugar
intake decrease them.
SARANG SURESH HOTCHANDANI 14
15. ROLE OF DENTAL PLAQUE OR BIOFILM IN
CARIES PROCESS.
• Biofilm is controlled by
professional tooth
cleanings.
• Pellicle form within 2
hours.
• pellicle is formed by
precipitation of saliva.
• Functions of Pellicle
• Protect the enamel
• Reduce friction b/w
teeth
• Provide matrix for
remineralization.
SARANG SURESH HOTCHANDANI 15
16. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 16
17. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 17
18. ROLE OF TEETH IN DENTAL CARIES.
• The tooth is ideal surface for attachment of
plaque because it lacks the shedding
mechanism like other areas of body.
• Enamel in primary teeth is
• less mineralized,
• optically more active, have
• greater porosity &
• less resistant to caries.
• Dentine is more vulnerable to caries than
enamel because of structural differences and
greater number of impurities in its crystal.
• Sites of tooth where caries
frequently occur;
• Pits & fissure
• Smooth enamel surface
• Gingival to proximal contacts
• Gingival 3rd of facial &
lingual/palatal surfaces
• Root surface
• Subgingival areas
SARANG SURESH HOTCHANDANI 18
19. PIT & FISSURES (FIG; 2-12, 2-15 TO 2-19)
• Most common surface for development
of caries.
• Dominated by; S. sanguis other
streptococci.
• Initial lesion develop on lateral walls of
fissure.
• They have small site of origin on
occlusal surface with wide base.
• Shape of pit & fissure lesion is inverted
V.
SARANG SURESH HOTCHANDANI 19
20. SMOOTH ENAMEL SURFACE
• Proximal enamel surface gingival
to the contact area are 2nd most
common susceptible area to
caries.
• These surfaces are free from
effects of mastication, tongue
movement & salivary flow.
• Smooth surface lesion is V-
shaped with wide origin &
narrow base.
• Apex of V directed towards
pulp. (figure 2-21 in art &
science)
SARANG SURESH HOTCHANDANI 20
21. ROOT SURFACE CARIES
• Mostly occur in gingival
recession.
• More common in old age persons
because;
• Decreased salivary flow
• Poor oral hygiene
• Lack of motivation
• Lowered digital dexterity
• Gingival recession
• Root caries is more damaging than
other surface caries because;
• It has rapid progression because it
starts directly from dentine and dentine
is less resistant than enamel.
• It is often asymptomatic
• It is closer to pulp.
• More difficult to restore.
• U shaped in cross sectionSARANG SURESH HOTCHANDANI 21
22. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 22
23. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 23
24. ROLE OF ORAL HYGIENE IN CARIES
• Careful mechanical cleaning of teeth disrupts the biofilm and leaves clean enamel
surface.
• Cleaning process does not destroy the oral bacteria but merely removes them from tooth
surface to prevent growth of biofilm.
• Some obligate anaerobes may be killed by exposure to oxygen during tooth cleaning.
• Biofilm species are not destroyed but they are continue to be present but most of them
are unable to initiate colonization on clean tooth surface.
SARANG SURESH HOTCHANDANI 24
25. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 25
26. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 26
27. SALIVA; NATURAL ANTI-CARIES AGENT.
• Decreased salivary production or
salivary flow will lead to Rampant caries
& xerostomia
• Salivary is decreased in following
condition;
• Medications
• Illness
• Radiation to head & neck
• Salivary glands become fibrotic
• Autoimmune disease
• Protective mechanisms of
saliva which maintain normal
flora of oral cavity and tooth
surface integrity include;
• Bacterial clearance
• Direct antibacterial activity
• Remineralization.
SARANG SURESH HOTCHANDANI 27
29. ROLE OF SALIVA IN CARIES
• Lubricates oral tissues
• Bathes teeth & biofilm
• Flushes micro-organisms
which are not adherent to oral cavity.
• Flushing effect is most effective during
mastication or oral stimulation due to large
volume of saliva.
• Slowest on labial aspects of Max. incisors &
buccal aspects of mandibular molars.
• Adult produce 1 – 1.5 liters of saliva
per day.
• Very little saliva is produced during
sleep.
• Saliva possess direct antibacterial
activity from its components, but normal
oral flora has developed resistance to
most of these antibacterial mechanisms.
SARANG SURESH HOTCHANDANI 29
30. ROLE OF SALIVA IN CARIES.
• Antibacterial proteins in saliva play important
role in defense of soft tissues while they have
little effect on caries.
• Similar levels of antibacterial proteins are
found in caries active and caries free persons.
• So, it is clear that caries susceptibility does
not depend on composition of saliva in
healthy persons.
• While caries susceptibility depends on
quantity of saliva.
SARANG SURESH HOTCHANDANI 30
32. ROLE OF SALIVA IN CARIES
• Saliva also possess buffering
capacity.
• Buffering capacity of saliva depends
on;
• Concentration of bicarbonate ions
(Primary)
• Volume of saliva
• Buffering capacity is measured by
titration techniques.
• Molecules of saliva which increase the pH of
biofilm;
• Urea
• Sialin
• Hydrolysis of these compounds produce ammonia
which increase the pH of biofilm.
• Saliva help in remineralization of teeth.
• Saliva contains Statherian, a proline rich peptide
that stabilizes the calcium and phosphate and
prevents excessive deposition of these ions on
teeth.
SARANG SURESH HOTCHANDANI 32
33. ROLE OF SALIVA IN CARIES
• Flow rate & buffering capacity are most important protective
mechanisms of saliva.
• Normal stimulated flow rate = 1.0 ml/minute
• Stimulated flow rate below 0.7 ml/minute is a high risk for caries
• Areas which are inaccessible to salivary flow or flushing are;
• Interproximal areas
• Fissures
• Cavity
SARANG SURESH HOTCHANDANI 33
35. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 35
36. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 36
37. DIET & CARIES
• High frequency exposure is most important factor in development of caries.
• Frequent ingestion increases growth of highly acidogenic bacteria.
• When ingestion of carbohydrates is restricted, biofilm is made but it does not lead to caries
because acid is not produced.
• Dietary Sucrose is important in development of caries.
• Acidic food also lead to caries because the ultimate metabolic product of cariogenic
diet is acid which cause demineralization.
• So we should advise the patient to avoid frequent use of sweet and acidic products, not
just sucrose.
SARANG SURESH HOTCHANDANI 37
38. DIET & CARIES.
• Principles of dietary advice for caries prevention.
• The pH drops for 30 for approx. 30 minutes.
• However if the salivary flow is low pH drop may be longer.
• Long pH depression occur in those areas of oral cavity where salivary flow is restricted as mentioned in
previous slide.
• Frequency of sugar intake is more important than quantity of sucrose.
• Stickiness of food is important factor in its cariogenecity.
• During retention time, carbohydrates are hydrolyzed to simple sugar providing more substrate to bacteria.
• Example; chocolate, caramel, potato chips.
• Caries preventive effect is small with sugar restriction as compared to fluoride use.
• Means fluoride use better reduces prevalence of caries as compared to sugar restriction.
SARANG SURESH HOTCHANDANI 38
39. • So, Snack in
MODERATION, limited
to 3 OR 4 SNACKS A DAY.
SARANG SURESH HOTCHANDANI 39
42. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 42
43. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 43
44. ROLE OF TIME IN DENTAL CARIES.
• Caries is chronic disease.
• Substrate/ dietary sugars require sufficient time for
demineralization.
• Same, time is required for remineralization process.
• Because caries does not develop in overnight but take time.
SARANG SURESH HOTCHANDANI 44
45. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 45
46. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
FluorideSARANG SURESH HOTCHANDANI 46
47. ROLE OF FLUORIDE IN DENTAL CARIES.
• A lack of fluoride constitutes caries risk.
• Fluoride administration is more effective in reducing caries than lowering use of
carbohydrates.
• Post-eruptive use of fluoride is more effective against caries than pre-eruptive
use of fluoride.
• Fluoride protects enamel more effectively when it is present in ambient solution
during acid challenge than when it is incorporated into the enamel crystals.
SARANG SURESH HOTCHANDANI 47
48. ROLE OF FLUORIDE IN DENTAL CARIES.
• Fluoride inhibits remineralization by;
• Reprecipitation of dissolved calcium & phosphate and prevent
them from being leached out of enamel.
• Fluoride hamper penetration of acid into enamel.
• By narrowing the pores in enamel surface which help in
diffusion of acids.
• Fluoride facilitate remineralization.
SARANG SURESH HOTCHANDANI 48
49. ROLE OF FLUORIDE IN DENTAL CARIES.
• Retention of fluoride is site specific.
• Mostly found on maxillary labial surfaces of incisors & buccal surfaces of lower
mandibular molars after rinsing with fluoride solution.
• Fluoride from tablets remain highly concentrated at the site of tablet dissolution.
• There is very little or no transport of fluoride b/w the right & left sides of mouth or
maxillary & mandibular arches.
• Coz of this localized caries lesion in the mouth may be related to insufficient spread of
fluoride when person used fluoride paste.
SARANG SURESH HOTCHANDANI 49
53. SOCIAL & DEMOGRAPHIC FACTORS
• In western world, dental caries is more prevalent in;
• Lower socioeconomic
• Less affluent areas
• Some ethnic minorities
• Root caries is more prevalent in older persons of low socio economic status.
SARANG SURESH HOTCHANDANI 53
54. RATE OF CARIES LESION PROGRESSION
• Now a days, caries lesion progress more slowly than they did several decades ago, due to
increased use of fluoride.
• Rate of caries progression is not same for each site or each tooth.
• Not all initial fissure lesion will develop to involve the dentine but number of them may
become arrested.
• The progression rate of caries is independent of the DMFS of individuals.
SARANG SURESH HOTCHANDANI 54
55. RATE OF CARIES LESION PROGRESSION
(CONT’D)
• Rate of caries progression on proximal surface is low than pit & fissure lesion.
• Distal surfaces of 1st molars are.
• Caries lesion on smooth surfaces progress more slowly than on proximal surfaces or pits
and fissures.
• If there is not cavity and caries has not reached dentine, preventive measure can be used
to stop the caries process.
SARANG SURESH HOTCHANDANI 55
56. PULP-DENTINE COMPLEX RESPONSES TO
CARIES
• 3 levels of dentinal reaction to caries occur.
• Reaction to long term, low-level acid demineralization
associated with slowly advancing lesion.
• Reaction to a moderate-intensity attack
• Reaction to sever, rapidly advancing caries characterized
by very high acid levels.
SARANG SURESH HOTCHANDANI 56
58. DETECTION & DIAGNOSIS OF CARIES
• Caries Detection; it is an objective method of
determining whether or not clinical signs of
caries are present at one point in time through;
• Clinical examination,caries diagnostic aids,etc.
• Caries Diagnosis; it is assessment of dynamics
and determinants of caries process.
SARANG SURESH HOTCHANDANI 58
61. VISUAL EXAMINATION OF DENTAL CARIES
• The first clinical sign of caries: a chalky and matte
whitish surface.
• this white spot is a porous surface that can easily be
stained into brown or black discoloration by
chromogens from foods; thus, a caries lesion
can be seen either as a white or as a
brown/black spot lesion.
• MOST COMMON METHOD OF CARIES EXAMINATION.
SARANG SURESH HOTCHANDANI 61
62. PREREQUISITES FOR VISUAL
EXAMINATION OF DENTAL CARIES
• CLEAN TOOTH;
• Plaque must be removed from teeth
• DRY TOOTH;
• Teeth should be dried with air – water
syringe before examination.
• A white spot lesion is porous surface, in
which pores are filled with saliva when
teeth are wet.
• MAGNIFICATION & LIGHTENING
• For good visual examination appropriate
magnification & lightening are necessary.
• Drying the tooth surface during
examination has diagnostic as well as
prognostic value;
• Diagnostic Value of Dr ying;
• If white spot lesion is visible on wet tooth; it
indicate that demineralization is
extended into dentine.
• No chances of reversal, lesion only can be
arrested
• If white spot lesion is visible after drying of
tooth; it indicate that demineralization is
in enamel and is NOT extended into
dentine.
• Better chances of reversal of lesion
SARANG SURESH HOTCHANDANI
62
64. • The cavitation of tooth surface produces a synergetic
acceleration of the growth of cariogenic biofilm and
expansion of demineralization and cavity.
• When enamel caries reached DEJ, rapid lateral expansion
occurs.
SARANG SURESH HOTCHANDANI 64
65. CLINICAL SITES FOR CARIES INITIATION
• Characteristics of caries lesion depends upon the nature of the surface on which it
develops;
• Developmental pits and fissures (most susceptible)
• Smooth enamel surface
• Root surface
• Each of the above surface have different surface topography, environment, biofilm
population, treatment, prevention etc.
SARANG SURESH HOTCHANDANI 65
66. PROGRESSION OF CARIES LESIONS
• The time for progression from non-cavited caries to cavitation on smooth surface is
18 months ±6months
• Peak rate of incidence of new lesion occur 3 year after eruption of the tooth.
• Poor oral hygiene and frequent sucrose intake produces white spot in 3 days.
• Radiation induced xerostomia can lead to caries in 3 months from the onset of
radiation.
• Caries rate is slow in healthy as compared to compromised individuals
• Caries progression is delayed by fluoride use.
SARANG SURESH HOTCHANDANI 66
67. ENAMEL CARIES
• Non cavited enamel caries lesion;
• White spot, chalky white, opaque area revealed
after desiccation.
• Loss of translucency in them is due to
subsurface porosity caused by
demineralization.
• Softened chalky enamel that can be chipped
away with explorer is sign of active caries.
• Non cavited enamel lesion on radiograph
appear as faint radiolucency that is limited to
superficial enamel
• If, the radiolucency is clear, then the caries
have been advanced and histologic changes of
caries in dentine will be present.
• Non cavited enamel lesion can be re-
mineralized.
• Because they retain the original crystalline
framework of enamel rods which are etched
from the acid of bacteria.
• These etched crystallites serve as nucleating
agent for remineralization where calcium and
phosphate from saliva bind resulting re-
mineralization.
SARANG SURESH HOTCHANDANI
67
69. • Fluoride enhances this precipitation of ions from saliva and increase resistance to
caries attack by incorporating Fluorapatite.
• Active or arrested caries on radiograph look similar in appearance that’s why we can
diagnose the caries on the basis of radiograph only.
• The change in color of arrested caries is because of trapped organic debris and
metallic ions within enamel.
• Arrested caries lesion is more resistant than the normal unaffected enamel
SARANG SURESH HOTCHANDANI 69
71. DENTINE CARIES
• Progression of caries in dentine is different from that of enamel because of structural
differences of dentine.
• Dentinal caries is V shaped in cross section because DEJ allows rapid lateral spread when
caries from enamel reaches at DEJ before going to dentine.
• Wide BASE at DEJ and apex towards PULP.
• Caries progress more in dentine than enamel because dentine contain less mineral
content resulting decrease in resistance to acid attach/ demineralization.
• Pain in caries occurs due to stimulation of pulp by the movement of fluid through dentinal
tubules that have been opened to the oral environment.
SARANG SURESH HOTCHANDANI
71
72. CLINICAL VISUAL CARIES SCORING
SYSTEM
ICDAS (International Caries Detection and Assessment System) is a two-stage, two-digit coding system
comprised of a code for the restoration and sealant status of the tooth surface, followed by a code for the caries
severity.
SARANG SURESH HOTCHANDANI 72
First digit (restoration and sealant codes) Second digit (caries severity codes)
0 = No sealant or restoration 0 = sound tooth surface
1 = partial sealant 1 = First visual change (opacity or discoloration) in enamel
hardly visible on the wet surface but distinctly visible after air
Drying
2 = full sealant 2 = Distinct visual change (opacity or discoloration) in enamel,
visible without air drying
3 = Tooth-colored restoration 3 = Enamel breakdown, no dentin visible
4 = Amalgam restoration 4 = Dentin shadow (not Cavitated into dentin)
5 = Stainless steel crown 5 = Distinct cavity with visible dentin
6 = Porcelain, gold, PFM crown or veneer 6 = Extensive distinct cavity with visible dentin
7 = Defective restoration
8 = Temporary restoration
73. CORRELATION OF THE ICDAS CARIES SEVERITY CODES WITH
THE HISTOLOGIC DEPTH OF THE LESIONS INTO THE TOOTH
TISSUE ON THE OCCLUSAL SURFACE
Caries Severity Code Histologic Depth
0 No Enamel Demineralization
1 Enamel demineralization limited to outer half of enamel
layer
2 Demineralization involving enamel & outer 3rd of dentine
3 – 4 Demineralization involving the middle 3rd of dentine
5 – 6 Demineralization involving the pulpal 3rd of dentine
SARANG SURESH HOTCHANDANI 73
74. INTERNATIONAL CARIES CLASSIFICATION SYSTEM
SARANG SURESH HOTCHANDANI
740 (green)–sound tooth surface; 1 (yellow)–distinct, visual noncavitated change
in enamel; 2 (orange)–localized enamel breakdown; 3 (red)—distinct cavity
with visible dentin.
75. VISUAL EXAMINATION OF
PIT & FISSURE CARIES LESIONS
• Shadowing or grayish discoloration of the adjacent translucent
enamel along the pits and fissures may indicate possible
undermining of enamel by hidden caries.
• Opaque, matte texture of enamel adjacent to the stained pits and
fissures may indicate the presence of active caries underneath
them.
Illustration of the visual detection of lesions on the walls of stained
pits/fissures.(a) A stained fissure (red circle) under visual
examination.(b ) Looking perpendicularly through the translucent
adjacent healthy enamel along the fissure (white arrows),lesions on
the walls of the fissure are seen as discoloration extending (ie,
underneath the translucent enamel) beyond the confines of the
fissure with a “bottle-brush” appearance (red arrows).
SARANG SURESH HOTCHANDANI
75
76. THE EXPLORER TIP CAN EASILY DAMAGE
WHITE SPOT LESIONS
SARANG SURESH HOTCHANDANI 76
77. VISUAL EXAMINATION OF CARIES LESION
ON PROXIMAL SURFACES
• Extensive active proximal lesions of posterior teeth can be revealed by shadowing or grayish
discoloration of the undermined occlusal enamel ridge.
• when there is contact between proximal surfaces, the radiograph is the most accurate method for
detecting demineralization of proximal caries lesions.
• For detection of proximal lesions in anterior teeth, the fiber-optic trans illumination technique is
particularly appropriate and convenient.
• a fine light, coned down to a 0.5-mm diameter, is transmitted through a contact area.
• A lesion appears as a dark shadow.
• use of an orthodontic separator has been advocated in some cases to allow the dentist to see
more clearly and to gently feel for a break in the enamel surface.
SARANG SURESH HOTCHANDANI
77
78. VISUAL EXAMINATION OF CARIES LESIONS
ON BUCCAL, LINGUAL & ROOT SURFACE
• Active caries lesions in smooth, free enamel surfaces are
typically located close to the gingival margin and have
chalky matte, whitish/ yellowish surfaces.
• A caries lesion on a root surface is seen as a clearly
demarcated, light brown, dark brown, or black discolored
area on the root surface or at the cemento-enamel junction.
SARANG SURESH HOTCHANDANI
78
81. • Bitewing radiograph is essential for proximal caries.
• However,it cannot distinguish b/w cavited or non cavited lesions.
• Radiographic evaluation of occlusal surfaces has been found to be of minimal diagnostic value
for detecting enamel caries and superficial dentinal caries because of the large amounts of
surrounding sound enamel.
SARANG SURESH HOTCHANDANI
81
• E1—less than halfway
through proximal
enamel;
• E2—more than halfway
through proximal
enamel, not penetrating
past the Dentino enamel
junction;
• D1—slightly past the
DEJ;
• D2—less that halfway
through dentin toward
the pulp;
• D3—halfway or more
through dentin.
83. ASSESSING CARIES ACTIVITY
Characteristics of active and arrested lesions in enamel and roots
SARANG SURESH HOTCHANDANI 83
CONDITION TOOTH TISSUE ACTIVE ARRESTED
Appearance ENAMEL Lesion is chalky (lacks luster) when air
dried and is whitish or yellowish
Lesion has shiny surface when air
dried and may be whitish,
brownish, or blackish.
ROOT Clearly demarcated and may be
discolored yellowish/light brown Note:
Color change is not a reliable indicator
SAME AS ACTIVE LESION
TEXTURE ENAMEL Feels rough with explorer Feels hard and more smooth with
explorer
ROOT Lesion has soft or leathery base on
gentle probing using blunt or CPITN
probe
Lesion has hard and shiny base
using blunt or CPITN probe.
TRANSLUCENCY ENAMEL Opaque Semi transparent
ROOT Not available Not available
LOCATION ENAMEL Plaque stagnation areas Location is plaque free
ROOT Anywhere Anywhere
84. ASSESSING CARIES ACTIVITY
Characteristics of active and arrested lesions in enamel and roots
SARANG SURESH HOTCHANDANI 84
CONDITION TOOTH TISSUE ACTIVE ARRESTED
CAVITATION ENAMEL From localized surface defect (micro
cavity) in enamel only to distinct cavity
with soft or leathery base on gentle
Probing.
From localized surface defect
(micro cavity) in enamel only to
distinct cavity with hard base on
probing with gentle pressure;
surface of cavity may be shiny
ROOT Cavitated if there is loss of surface
integrity or if the depth is ≥ 0.5 mm
measured using the ball of the CPITN
probe;
Noncavitated if no loss of surface
integrity or if the depth is < 0.5 mm
SAME AS ACTIVE LESION
85. SARANG SURESH HOTCHANDANI
85
Active Caries Lesion Arrested Caries Lesion Matte, white, active cervical caries lesion
Cavited, Active Cervical Caries Lesions
86. ASSESSING CARIES RISK
• CARIES RISK; it is probability of an
individual developing caries lesion.
• Common Causes of DRY MOUTH
• Medications;
• antidepressants, antipsychotics,
tranquilizers, antihypertensives, and
diuretics
• Sjögren syndrome;
• affects the salivary and lacrimal glands,
leading to a dry mouth and dry eyes;
• rheumatoid arthritis may indicate the
presence of this disorder
• Eating disorders,
• induce hypo salivation;
• this, combined with a poor diet,
can lead to extensive caries
• Radiation therapy in the region of the
salivary glands for a head and neck
malignancy, which often induces
xerostomia
SARANG SURESH HOTCHANDANI
86
88. AMERICAN DENTAL ASSOCIATION (ADA)
RECOMMENDED GUIDE TO IDENTIFYING AN
OVERALL CARIES RISK STATUS
SARANG SURESH HOTCHANDANI 88
CARIES RISK
CATEGORY
YOUNGER THAN 6YEARS 6YEARS OR OLDER
Low Risk No white spot or Cavitated primary or
secondary caries lesions during the last 3
years and no factors that may increase
caries risk.
No white spot or Cavitated primary or
secondary caries lesions during the last 3
years and no factors that may increase
caries risk.
Moderate Risk No white spot or Cavitated primary or
secondary caries lesions during the last 3
years but presence of at least one factor
that may increase caries risk
One or two white spots or Cavitated primary
or secondary caries lesions in the last 3
years
OR
No white spot or Cavitated primary or
secondary caries lesions in the last 3 years
but presence of at least one factor that may
increase caries risk
89. AMERICAN DENTAL ASSOCIATION (ADA)
RECOMMENDED GUIDE TO IDENTIFYING AN
OVERALL CARIES RISK STATUS
SARANG SURESH HOTCHANDANI 89
CARIES RISK
CATEGORY
YOUNGER THAN 6YEARS 6YEARS OR OLDER
High Caries Risk • Any white spot or Cavitated primary or
secondary caries lesions during the
last 3 years.
• Presence of multiple factors that may
increase caries risk
• Low socioeconomic status, especially in
children too young for their risk to be
based on caries history
• Suboptimal fluoride exposure
• Xerostomia
• Three or more white spots or Cavitated
primary or secondary caries lesions in
the last 3 years.
• Presence of multiple factors that may
increase caries risk
• Suboptimal fluoride exposure
• Xerostomia.
90. SPECIFIC CARIES RISK FACTORS THAT MAY
GUIDE THE OVERALL CARIES RISK STATUS
SARANG SURESH HOTCHANDANI 90
92. ALGORITHM FOR CARIES MANAGEMENT IN
FISSURED SURFACES OF PERMANENT TEETH.
SARANG SURESH HOTCHANDANI 92
93. ALGORITHM FOR MANAGEMENT OF INITIAL
CARIES LESIONS IN NON-PROXIMAL CORONAL
SMOOTH SURFACES OF PERMANENT TEETH.
SARANG SURESH HOTCHANDANI 93
94. ALGORITHM FOR DIAGNOSIS AND MANAGEMENT OF CARIES
LESIONS IN ROOT SURFACES OF PERMANENT TEETH.
SARANG SURESH HOTCHANDANI
94
95. GENERAL GUIDELINES FOR CARIES
MANAGEMENT FOR A HIGH CARIES- RISK
PATIENT, BASED ON PTPM
SARANG SURESH HOTCHANDANI 95
96. GENERAL GUIDELINES FOR CARIES
MANAGEMENT FOR A HIGH CARIES- RISK
PATIENT, BASED ON PTPM
SARANG SURESH HOTCHANDANI 96
97. GENERAL GUIDELINES FOR CARIES
MANAGEMENT FOR A MODERATE-
CARIES-RISK PATIENT,
SARANG SURESH HOTCHANDANI 97
Step 1: Plaque
control
• Provide
prophylactic
treatment
followed by
fluoride
application
• See patient
regularly to
reinforce
oral hygiene
Step 2:
Treatment of
existing caries
lesions
• Treat
noncavitated
lesions as
needed
• Restore
cavitated
lesions and seal
surrounding
pits and fissures
as needed
Step 3:
Protection of
surfaces at
risk
• Seal all
deep pits
and fissures
• Apply
fluoride
varnish to
exposed
roots
Step 4: Maintenance care for prevention
• Review oral hygiene and dietary habits and advise
patient to:
• Reduce the number of between-meal sweet snacks
• Substitute snacks rich in protein
• Advise patient to brush twice daily with over-thecounter
fluoride toothpaste
• Advise patient to floss once daily
• Provide home treatment and/or other adjunctive
therapy:
• Use over-the-counter fluoride rinse daily
• Chew or suck xylitol-containing gum or candies three
times daily
• Recall patient every 3 to 6 months to:
• Reevaluate current caries risk
• Receive fluoride varnish treatment of all teeth
• Obtain bitewing radiographs every 12 to 18 months to
check for cavities
98. GENERAL GUIDELINES FOR CARIES
MANAGEMENT FOR A LOW CARIES- RISK PATIENT
SARANG SURESH HOTCHANDANI 98
Step 1: Plaque control
Step 2: Maintenance care for
prevention
• Review oral hygiene habits
• Advise patient to brush twice
daily with over-the-counter
fluoride toothpaste
• Recall patient every 12 to 24
months to reevaluate current
caries risk
• Obtain bitewing radiographs
every 24 months to check for cari
100. BASIC PREVENTIVE STEPS FOR
MODERATE/HIGH-RISK PATIENTS
SARANG SURESH HOTCHANDANI 100
Patient Motivation
• Emphasis on
Behavioral Change
Diet Counselling
• Reduce carbohydrate
intake & frequency
Toothbrushing
• Twice daily with
fluoride toothpaste
Flossing
• Daily, Few Times a
week
Sugar Free Gum
• Two pieces for ≥ 5
minutes three times a
day (after each meal
preferred)
Sealant
101. ADJUNCT TOPICAL THERAPIES FOR
MODERATE/HIGH-RISK PATIENTS
SARANG SURESH HOTCHANDANI 101
HOME
FLUORIDE
OPTIONS
• Prescription fluoride
(5,000 ppm) toothpaste
• Apply via tray daily for
patients with radiation-
induced hypo salivation
• Fluoride Rinse
• Twice daily/daily/weekly
depending on need
102. ADJUNCT TOPICAL THERAPIES FOR
MODERATE/HIGH-RISK PATIENTS
SARANG SURESH HOTCHANDANI 102
• Fluoride gel/foams
• 1.23% APF or neutral 2% NaF
• 4 minutes, two to four times per year
• For root caries, four times over 2 to 4
weeks
• Fluoride varnishes
• Apply to lesions and other surfaces at
risk two to four times per year
depending on risk
IN OFFICE FLUORIDE OPTIONS
104. SOME POINTS
• If interdental spaces are closed = advice dental floss
• If interdental spaces are open = advice interproximal brush
• Want to prevent caries only = floss once daily
• want to prevent caries & gingivitis = floss twice daily
• Stannous fluoride = inhibit plaque formation
• Triclosan = disrupt cell wall of plaque bacteria
SARANG SURESH HOTCHANDANI 104
105. HOME USE FLUORIDE GEL - 1.1 % NAF.
• recommended for high-risk adults and children 6 years and
older
• applied once daily over the tooth surfaces using a finger,
toothbrush, or individually fitted trays, preferably
immediately before bed.
• The gel should be left in contact with the teeth surfaces for 5
minutes, after which the individual should spit and not rinse.
SARANG SURESH HOTCHANDANI 105
106. Acidic topical fluoride solutions, such as APF
solutions and other acidified fluoride
preparations, degrade glass-ionomer materials,
porcelain crowns, and veneers and should be
avoided in these patients
SARANG SURESH HOTCHANDANI 106
107. DIETARY MANAGEMENT FOR CARIES
PREVENTION
• Eat a diet that is low in sucrose and retentive fermentable carbohydrates.
• Reduce the frequency of eating or drinking fermentable carbohydrates.
• Combine cooked and processed foods with non acidogenic foods.
• Do not eat cariogenic snacks.
• Include foods of firm or hard texture.
• Choose fats in diet wisely to reduce risk of chronic disease while still benefiting from fat
coating on tooth surfaces, which reduces the adherence of plaque.
• Chew sugarless gum (preferably with xylitol) for 15 to 20 minutes after eating to increase
salivary benefits.
• Combine and sequence foods to encourage chewing and saliva production.
• Only eat sweets with non cariogenic sweeteners
SARANG SURESH HOTCHANDANI
107
108. PIT & FISSURE SEALANTS
Resin based
Composites
Glass Ionomer
Cement
Release fluoride
Light cured
GIC in varnish
form
Used on where
moisture control is
difficult just like
partially erupted
molar
SARANG SURESH HOTCHANDANI 108
111. LESION ARREST
(REMINERALIZATION THERAPY)
SARANG SURESH HOTCHANDANI 111
Improved Oral
hygiene and
application of
topical fluorides
every 3 months
until caries activity
is under control
The choice of treatment for active noncavitated lesions on proximal
coronal surfaces depends on the CARIES RISK STATUS OF THE
PATIENT as well as the DEPTH OF THE LESION.
112. OCCLUSAL &
PROXIMAL
SEALANT
• Done in ICDAS Score 1 & 2
• Perform Acid Etching for
Resin Composite Sealant.
• Perform Conditioning for
GIC Sealant.
• Sealants are more effective
during the period of tooth
eruption, but can be applied
on older persons.
SARANG SURESH HOTCHANDANI 112
113. ADVANTAGES OF SEALANTS
• No irreversible intervention necessary.
• Active dentine or enamel lesion do not progress
further.
• Possible developments of new lesions in other sites
of fissure is prevented.
SARANG SURESH HOTCHANDANI 113
114. LESION
INFILTRATION• It is a new technique & alternative to sealant.
• Used for treating lesions extending into inner enamel or outer 3rd of dentine. –
ICDAS 1 & 2.
• It occludes lesion pores with low – viscosity light
curing resins in order to create diffusion barrier
& arrest caries progression.
SARANG SURESH HOTCHANDANI 114
115. STEPS IN LESION INFILTRATION
SARANG SURESH HOTCHANDANI 115
Etch
• HCL
Dry
• Ethanol & Air
Drying
Apply the
INFILTRATE for 3
minutes & Light
Cure
2nd Coat of
Infiltrate for 1
minute only &
Light Cure it.
117. INDICATIONS OF RESTORATIVE
TREATMENT
• The Cavitated tooth is sensitive to hot, cold, sweetness, etc.
• Occlusal and proximal lesions extend deep into dentin (and cannot be
reached by the toothbrush).
• The pulp is endangered.
• Previous attempts to arrest the lesion have failed, and there is evidence
that the lesion is progressing (such evidence usually requires an
observation period of months or years).
• The patient’s ability to provide effective home care is impaired.
• Drifting is likely to occur through loss of proximal contact.
• The tooth has an unaesthetic appearance
SARANG SURESH HOTCHANDANI
117
118. PREVENTIVE RESIN RESTORATION &
PREVENTIVE AMALGAM RESTORATION
• In this, Restoration of the carious surface occur
accompanied with sealing of surrounding pits
and fissures with sealant.
• Advantages
• Conserve surrounding sound tooth structure.
• Protects margins of restoration
• Prevent secondary caries
SARANG SURESH HOTCHANDANI 118
119. INTERIM THERAPEUTIC RESTORATION
(ITR)
It involves removal of caries using hand
instrument or low-speed rotary instruments,
with caution not to expose the pulp, followed by
restoration of the tooth with an adhesive
restorative material, such as conventional or
resin-modified glass ionomer cement.
SARANG SURESH HOTCHANDANI 119
120. INDICATIONS OF ITR
• When Caries control is necessary before placement of definitive
restoration.
• Multiple caries lesions.
• Children experiencing early childhood caries.
• Rampant caries
• High caries risk patients
• Uncooperative patients
• During stepwise excavation technique.
SARANG SURESH HOTCHANDANI 120
121. ADVANTAGES OF ITR
• Reduce level of cariogenic bacteria in the oral
cavity.
• Make tooth surfaces more cleansable prior to
placing definitive restoration.
SARANG SURESH HOTCHANDANI 121