Detailed information about the dental calculus regarding its composition, classification, clinical appearance, stages of formation, theory of mineralization and many descriptive clinical images and illustrations.
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
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Detailed information about the dental calculus regarding its composition, classification, clinical appearance, stages of formation, theory of mineralization and many descriptive clinical images and illustrations.
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
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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
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APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
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.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. Contents
• Introduction
• Definition
• Etiology of dental caries
• Classification of dental caries
• Pathogenesis of caries
• Prevention
• Conclusion
• References
3. Introduction
Most common chronic disease of modern times.
Multifactorial in etiology with bacteria, susceptible tooth surfaces &
diet playing a major role.
The word caries means ‘rot’ or decay in latin.
4. Definition
“An irreversible, microbiologic disease of the calcified tissue of teeth,
characterised by demineralisation of the inorganic portion and
destruction of organic substance of the tooth, which often leads to
cavitation”
[Shafers]
Dental caries is an infectious microbiologic disease of teeth that
results in localised dissolution and destruction of the calcified tissues.
[Strudevant]
Localised post eruptive pathologic process of external origin involving
softening of the hard tissue and proceeding to the formation of a cavity
[WHO]
5. Theories of dental caries
Early theory- The legend of worm
Endogenous theory- Humoral
- Vital
Exogenous theory- Acidogenic Theory of Miller.
- Proteolytic Theory
-Proteolysis Chelation Theory
6. Miller’s Chemoparasitic Theory
Also known as acidogenic theory, proposed by W.D Miller.
Dental decay is a chemo parasitic process consisting of two stages
i. Decalcification of enamel and dentin (preliminary stage)
ii. Dissolution of softened residue(subsequent stage)
Acids resulting in primary decalcification is produced by the fermentation of
starches and sugar from retaining centres of teeth
ROLE OF CARBOHYDRATES
Cariogenicity of dietary carbohydrate varies with the frequency of ingestion,
physical form and chemical composition, route of administration and presence of
other food constituents.
Sticky, soft, solid refined carbohydrates are more caries producing.
Bacteria+ Sugars+ Teeth= Organic Acids= Caries.
7. ROLE OF MICRORGANISMS
Steptococcus salivarius, S. mitior, S. milleri, S. oralis, Peptostreptocoocus intermedius,
Lactobacillus acidophilus, Actinomyces viscous etc are some of the microorganisms
capable of inducing carious lesion.
Different organisms display certain selectively for the tooth surface they localize and
attack.
ROLE OF ACIDS
The exact mechanism of carbohydrate degeneration to form acids in the oral cavity bt
bacterial action is not known.
It probably occurs through enzymatic breakdown of the sugar and the acids formed are
chiefly lactic acid, although others such as butyric acid do form.
The localization of acids upon the tooth surface is fulfilled by dental plaque.
8. • ROLE OF DENTAL PLAQUE
Plaque is the soft, non-mineralised, bacterial deposit which forms on teeth and dental
prosthesis that are not adequately cleaned.
Even though enamel caries begins beneath the dental plaque, it does not necessarily
mean that a carious lesion will develop at that point.
However, when the plaque contain appreciable amount of highly acidogenic bacteria
such as S. mutans are exposed to readily fermentable dietary sucrose, they produce
sufficient concentrations of acids to demineralize the enamel
9. Proteolytic Theory
• It states that the organic component of the enamel is the first
broken down by proteolytic enzymes, opening up the pathway
for bacteria to attack the enamel by other processes such as by
acids or chelation.
• Even though the part played by proteolysis in the intiation of
dental caries is likely to be of no significance, its role in the
progression of the more advanced lesions cannot be ruled out.
10. Proteolysis Chelation Theory
• Schartz Et al proposed this in 1955.
• Chelation is a process in which there is complexing of the metal ions
to form complex substance via covalent bond formation resulting in
highly stable poorly dissociated and weakly ionised compound
• Metabolic products of the microorganisms have the ability to chelate
the calcium.
11. Etiology of Dental Caries
• Presently, the chemoparasitic theory is most accepted, although not
as that proposed by miller.
• In addition to three primary factors : the host, microbial flora and
the substrate, a fourth factor the time is also considered as an
etiologic factor
• Caries requires a susceptible host, a cariogenic flora and a suitable
substrate that must be present for a sufficient length of time.
12.
13. Classification of Dental Caries
I. Based on Location
II. Based on speed of caries of progression
III. Based on if it is new or recurrent lesion.
IV. Based on extent of caries.
V. Based on pathway of caries spread
VI. Based on tooth surfaces involved
VII. Based on the treatment and restoration design(G.V BLACKS’s)
VIII. Based on whether caries is completely removed or not
IX. Based on the age of the patient
X. Based on tooth surfaces to be restored
XI. Based on WHO system
XII. Graham Mount’s classification.
14. Based on Location
PIT & FISSURE CARIES
This is found on the occlusal, buccal, and lingual
surfaces of posterior teeth as well as the lingual
surfaces of maxillary anteriors.
SMOOTH SURFACE CARIES
This is seen in all smooth surfaces of teeth
without pits, fissures and grooves.
16. Based on The Speed of Caries
Progression
ACUTE RAMPANT CARIES
This is rapidly invading caries, involving several teeth.
It appears soft and light coloured. If unattended,
acute caries can cause pulpal involvement.
CHRONIC CARIES
This is a slowly progressing long standing caries.
It appears hard in consistency and is dark in colour.
17. ARRESTED CARIES
Sometimes a chronic caries lesion can become arrested
due to change in the local environment such caries is called
This appears dark brown in colour and is hard in consistency.
Often seen on an approximal surface after the adjacent tooth
surface after the adjacent tooth has been extracted due to
elimination of the stagnantion area.
18. Based on Whether it is a New or
Recurrent Carious Lesion.
• INTIAL OR PRIMARY CARIES:
This is the first attack of caries on a tooth surface
• RECURRENT OR SECONDARY CARIES:
This is a caries seen under or around the margins of an existing restoration. It
occurs due to microleakage and other conditions favourable for caries to recur
after a restoration is placed .
19. Based on the Extend of Caries
INCIPIENT CARIES
It consist of demineralized enamel which has not
extended to the DEJ
Enamel surface is hard and intact.
Incipient caries can be remineralised by adopting
corrective measures early after diagnosis.
Hence also referred as reversible caries.
CAVITATED CARIES
Here the caries has spread beyond enamel into dentin. the
enamel surface is broken down and remineralisation is not
possible. Hence referred to as irreversible caries.
20. BASED ON THE PATH WAY
CARIES SPREAD WITH IN THE
TOOTH
A.FORWARD CARIES
• Whenever the caries cone in enamel is larger or the same size as that in
dentin it is referred to as forward caries.
B. BACKWARD CARIES
• Whenever the spread of caries along DEJ exceeds the caries cone in enamel,
the caries extends into enamel from the junction.
• Since the spread of caries here is in backward direction it is referred to as
backward caries
21. G.V Blacks Classification
• A.CLASS I CARIES
Caries occurring in pits fissures or defective grooves on the tooth surfaces. This
usually has three locations
Occlusal surfaces of molars and premolars.
Occlusal two-thirds of facial and lingual surfaces of molars.
Lingual surfaces of maxillary anteriors
22. • B.CLASS II CARIES
Caries found on the proximal surfaces of molars and premolars.
C. CLASS III CARIES
Caries occurring in the proximal surfaces of anterior teeth with out involving
the incisal angle.
23. D.CLASS IV CARIES
This is caries found the proximal surface of anterior teeth with involvement of
the incisal angle.
E.CLASS V CARIES
Caries seen at the gingival third of facial and lingual surface of anterior and
posterior teeth.
24. F.CLASS VI CARIES
Caries found on the incisal edges of anterior teeth and cusp tips of posterior
teeth
25. Based on whether the caries is
completely removed or not during
treatment
RESIDUAL CARIES
• Caries that remains in the prepared cavity even after the restoration is
completed.
• This may be left behind either by accident, neglect or intention.
• Residual caries left behind due to operator's negligence is not acceptable
especially if it is at the DEJ or in enamel.
• But sometimes, during indirect pulp capping procedures, a small amount of
soft caries close to pulp may be intentionally retained to prevent pulp
exposure.
26. Based on the Age of Patient
A. NURSING BOTTLE CARIES
During early infancy, bottle fed babies develop rapidly spreading caries
usually on maxillary anteriors.
27. B. ADOLESCENT CARIES
Acute caries seen in the teenage population due to dietary habits.
C. SENILE CARIES
Caries occurring in the elderly population, characterized by involvement of root
surfaces due to gingival recession coupled with other factors like reduced
salivation & poor oral hygiene.
28. Based on Tooth Surfaces to be
Restored
• O- OCCLUSAL SURFACE
• M- MESIAL SURFACE
• D- DISTAL SURFACE
• F-FACIAL SURFACE
• B- BUCCAL SURFACE
• L-LINGUAL SURFACE
• MOD-MESIO-OCCLUSO-DISTAL
29. WHO System
In this classification the shape & depth of the caries lesion can be scored on a
four point scale.
• D1: Clinically detectable enamel lesion with intact surfaces (non cavitated).
• D2: Clinically detectable cavities limited to enamel.
• D3: Clinically detectable cavities in dentin.
• D4: Lesion extending into pulp
30. Graham Mound Classification
• This is a recent classification based on site, size and complexity of the caries.
Cavity size Size 1
Minimal
Size 2
moderate
Size3
enlarged
Size 4
extensive
Site 1
Pit & fissure
1.1 1.2 1.3 1.4
Site 2
Proximal
surface
2.1 2.2 2.3 2.4
Site 3
Cervical
region
3.1 3.2 3.3 3.4
32. Prevention
1.BY IMPROVING ORAL HYGIENE
• Plaque free tooth surfaces do not decay
• Oral hygiene procedures
-Toothbrushing
-Flossing
-Professional prophylaxis
• Daily personal oral hygiene recommended for good hygiene and for control of
gingival diseases
33. INTERDENTAL CLEANING AIDS
• Approximal surfaces and malaligned teeth
• For these areas additional cleaning required
• (1)dental floss or tape
• (2)wooden sticks
• (3)interdental brushes
• (4)single tufted brushes
34. DENTRIFICES
• Usually available as paste form
• Can be used in conjunction with toothbrushing
• Aid in cleaning and polishing . tooth surfaces
• Not necessary to effectively remove dental plaque
• Some dentifrices contain abrasives that help remove stain and polishing
agents that restore tooth luster.
DISCLOSING AGENTS
They are solutions, tablets or wafers containing a red vegetable dye like
erythrosin
Stains bacterial plaque on tooth surfaces
35. DIET MODIFICATION
ANTICARIOGENIC FOODS
*MILK contain lactose.... Least cariogenic
*CHEESE casein phosphatase give anticariogenic property
*Fibrous foods
*TEA green, oolong and black tea
*Artificial sweeteners(xylitol)
#Prevent S.Mutans from binding to sucrose
#Increase concentration of amino acids ammonia neutralizing plaque acids
And
#Bacteriostatic, as they are nonfermentable
#Increase salivary flow, enhance remineralization
36. SALIVARY STIMULANTS
• saliva has important role in caries prevention
• xerostomia patients increased caries risk is seen
• gums, paraffin waxes, or salivary substitutes can be prescribed as adjuncts
FLUORIDE APPLICATION
fluoride therapy is the delivery of fluoride to the teeth topically or
systemically in order to prevent tooth decay
37. Conclusion
• Dental caries remains a commonly encountered clinical problem in routine
dental practice
• So identifying and eliminating the causative factors for caries must be the
primary focus