This document provides an overview of diseases of the pulp. It discusses pulpitis, which is inflammation of the pulp that can be reversible or irreversible depending on the severity. Reversible pulpitis involves mild inflammation that can return to normal, while irreversible pulpitis is persistent and may lead to necrosis without treatment. Other topics covered include causes of pulp inflammation, classifications of pulpitis, features of acute and chronic pulpitis, necrosis, and management approaches for different pulp conditions. The document aims to inform pediatric dentists about diseases that can affect the pulp.
Bone loss and patterns of bone destructionvidushiKhanna1
- introduction
- bone resorption
- factors causing bone destruction in periodontal disease
-- destruction by extension of gingival inflammation
--- histopathology
--- pathways of spread of inflammation
--- radius of action
--- periods of destruction
---- mechanism of destruction
-- bone destruction caused by TFO
-- bone destruction caused by systemic disorders
- factors determining bone morphology in periodontal disease
-- normal variation of alveolar bone
-- exostosis
-- butressing bone formation
-- food impaction
-- agressive periodontitis
- patterns of bone destruction
-- horizontal bone loss
-- vertical or angular defects
-- osseous craters
-- bulbous bone contours
-- reversed architecture
-- ledges
- furcation involvement
-- classification
-conclusion
Tooth resorption is the progressive loss of dentine and cementum by the action of osteoclasts. This is a physiological process in the exfoliation of the primary dentition, caused by osteoclast differentiation due to pressure exerted by the erupting permanent tooth
A detailed description about endo perio interrelationship, including introduction, development and etiology, historical aspects, definition, classification, diagnosis, differential diagnosis, management, special consideration in management,controversies prognosis, conclusion.
This lecture present to you the very basics of dental management of asthmatic patient in dental clinics. I kept it short and comprehensive as I can, for more info please refer to the reference mentioned in the lecture
Bone loss and patterns of bone destructionvidushiKhanna1
- introduction
- bone resorption
- factors causing bone destruction in periodontal disease
-- destruction by extension of gingival inflammation
--- histopathology
--- pathways of spread of inflammation
--- radius of action
--- periods of destruction
---- mechanism of destruction
-- bone destruction caused by TFO
-- bone destruction caused by systemic disorders
- factors determining bone morphology in periodontal disease
-- normal variation of alveolar bone
-- exostosis
-- butressing bone formation
-- food impaction
-- agressive periodontitis
- patterns of bone destruction
-- horizontal bone loss
-- vertical or angular defects
-- osseous craters
-- bulbous bone contours
-- reversed architecture
-- ledges
- furcation involvement
-- classification
-conclusion
Tooth resorption is the progressive loss of dentine and cementum by the action of osteoclasts. This is a physiological process in the exfoliation of the primary dentition, caused by osteoclast differentiation due to pressure exerted by the erupting permanent tooth
A detailed description about endo perio interrelationship, including introduction, development and etiology, historical aspects, definition, classification, diagnosis, differential diagnosis, management, special consideration in management,controversies prognosis, conclusion.
This lecture present to you the very basics of dental management of asthmatic patient in dental clinics. I kept it short and comprehensive as I can, for more info please refer to the reference mentioned in the lecture
Definition of periodontal pocket, classification, Histopathology of periodontal pocket, microflora involved, pathogenesis, periodontal pocket as a healing lesion, microtopography of root surface, treatment of periodontal pocket
Definition of periodontal pocket, classification, Histopathology of periodontal pocket, microflora involved, pathogenesis, periodontal pocket as a healing lesion, microtopography of root surface, treatment of periodontal pocket
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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
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New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
3. ⮚ formative organ of tooth
⮚ builds primary dentin
during development of tooth
⮚ secondary dentin after
tooth eruption
⮚ reparative dentin in response
to stimulation as long as
odontoblast remain vital
Pulp
4. ⮚ most common cause of
dental pain
⮚ loss of teeth in younger
persons
⮚ usual cause is caries
penetrating the dentin
Pulpitis
7. ⮚ (a) Mechanical Cause
A. trauma
a) accident (contact sports)
b) iatrogenic damage due to dental procedure
(during cavity or crown preparation)
B. Pathologic wear ( atrrition, abrasion)
C. Cracked tooth syndrome
D. Barometric changes
Causes of Pulpal
Inflammation
8. ⮚ (b) Thermal Cause
✔ uninsulated metallic
restoration
✔ during cavity preparation
✔ polishing
Causes of Pulpal
Inflammation
9. ⮚ (2) Chemical Cause
✔ arise from erosion
✔ or inappropriate use
of acidic dental material
Causes of Pulpal
Inflammation
10. ⮚ (3) Bacterial Cause
✔ can damage pulp
through toxins secreted
by bacteria from caries
✔Microbial colonization in
the pulp by blood borne
microorganisms
(anachoresis).
Causes of Pulpal
Inflammation
11. ⮚ (1) Based on Severity of
Inflammation
⮚ (2) According to Involvement
Classification
12. ⮚ (1) Reversible Pulpitis
⮚ (2) Irreversible Pulpitis
⮚ (3) Pulp Degeneration
⮚ (4) Pulp Necrosis
(1) Based on Severity
of Inflammation
13. ⮚ (1) Reversible Pulpitis
✔ Symptomatic (acute)
✔ Aysptomatic (chronic)
⮚ (2) Irreversible Pulpitis
✔ Acute
• Abnormally responsive to cold
• Abnormally responsive to heat
(1) Based on Severity
of Inflammation
14. ⮚ (2) Irreversible Pulpitis
✔ Chronic
• Asymptomatic with
pulp exposure
• Hyperplastic
• Internal resorption
(1) Based on Severity
of Inflammation
15. ⮚ (3) Pulp Degeneration
✔ Calcific
⮚ (4) Pulp Necrosis
(1) Based on Severity
of Inflammation
16. ⮚ (1) According to extent of inflammation
⮚ (2) According to Severity
⮚ (3) According to presence or
absence of direct
communication
between dental pulp +
oral environment
(2) According to
Involvement
17. ⮚ (1) According to extent of inflammation
✔ Focal or Subtotal or
Partial Pulpitis
✔ Total or Generalized
Pulpitis
(2) According to
Involvement
18. ⮚ (2) According to Severity
✔ Acute
✔ Chronic
(2) According to
Involvement
19. ⮚ (3) According to presence or
absence of direct
communication
between dental pulp +
oral environment
✔ Pulpitis Aperts (open pulpitis)
✔ Pulpitis Clausa (closed pulpitis)
(2) According to
Involvement
20. ⮚ mild to moderate inflammatory
condition of pulp
✔ caused by noxious stimuli
✔ pulp is capable of returning
to un-inflammed state following removal of stimuli
Reversible Pulpitis
22. ⮚ Clinical Features
✔ sharp pain lasting for
a moment
✔ often brought on by cold
than hot food or beverages
and by cold air
Reversible Pulpitis
23. ⮚ Clinical Features
✔ does not continue
when the cause has been
removed
✔ tooth responds to electric
pulp testing at lower
current
Reversible Pulpitis
24. ⮚ Management
✔ prevention
✔ periodic care
✔ early insertion of filling
if a cavity has developed
✔ removal of noxious
stimuli
Reversible Pulpitis
25. ⮚earliest form
⮚ also known as pulp hyperemia
⮚ excessive accumulation of
blood within pulp tissue
⮚ leads to vascular congestion
Focal Reversible
Pulpitis
26. ⮚ Clinical Features
✔ sensitive to thermal
changes
✔ particularly to cold
✔ application of ice or cold
fluids to tooth result in pain
Focal Reversible
Pulpitis
27. ⮚ Clinical Features
✔ disappears upon removal
of thermal irritant or
restoration .
✔ responds to electrical test
stimulant at lower level
of current
Focal Reversible
Pulpitis
28. ⮚ Clinical Features
✔ indicates lower pain
threshold than that of
adjacent normal
teeth
Focal Reversible
Pulpitis
29. ⮚ Clinical Features
✔ teeth show:
• deep carious lesion
• large metallic restoration
• restoration with defective
margins
Focal Reversible
Pulpitis
30. ⮚ Management
✔ removal of irritants
before the pulp is
severely damaged
Focal Reversible
Pulpitis
32. ⮚ Causes
✔ bacteria involvement of
pulp through caries
✔ chemical
✔ thermal
✔ mechanical injury
Irreversible Pulpitis
33. ⮚ Clinical Features
Early Stage
✔ paroxysm of pain
caused by:
• sudden temperature
changes like cold,
sweet, acid foodstuffs
Irreversible Pulpitis
34. ⮚ Clinical Features
Early Stage
✔ pain often continues
when cause has been
removed
✔ may come and go
spontaneously
Irreversible Pulpitis
35. ⮚ Clinical Features
Early Stage
✔ pain
• sharp
• piercing
• shooting
• generally severe
Irreversible Pulpitis
36. ⮚ Clinical Features
Early Stage
✔ pain
• bending over exacerbates pain which
• lying down is due to change in
• change of position intrapulpal pressure
Irreversible Pulpitis
37. ⮚ Clinical Features
Late Stage
✔ pain
• more severe as if tooth is under
• throbbing constant pressure
Irreversible Pulpitis
38. ⮚ Clinical Features
Late Stage
✔ pain
• patient is often awake
at night due to pain
• increased by heat and
sometimes relieved by cold,
although continued application
of cold may intensify pain
Irreversible Pulpitis
39. ⮚ Management
✔ complete removal of pulp
or pulpectomy
✔ if the time is a factor, pulpotomy
should be done as an emergency
procedure
✔ Surgical removal should be considered if the tooth
is not restorable.
Irreversible Pulpitis
40. Clinical Difference
Reversible Pulpitis Irreversible Pulpitis
⮚ pain generally lasts for few
seconds
⮚ the pain produced by thermal
stimulus disappears as soon as
the stimulus is removed
Pain may last several
minutes or later
⮚ pain lingers even after
the stimulus is removed
⮚ pain may come without
any apparent stimulus
41. ⮚ extensive acute inflammation
of pulp
⮚ frequent sequel of focal
reversible pulpitis
Acute Pulpitis
42. ⮚ Causes
✔ tooth with large carious
lesion
✔ defective restoration
where there has been
recurrent caries
✔ pulp exposure due to
faulty cavity preparation
Acute Pulpitis
43. ⮚ Clinical Features
✔ severe pain is elicited by
thermal changes
✔ pain persists even after
thermal stimulus
disappears or been
removed
Acute Pulpitis
44. ⮚ Clinical Features
✔ may be continuous
✔ intensity may be increased
when patient lies down
✔ application of heat
may cause acute
exacerbation of pain
Acute Pulpitis
45. ⮚ Clinical Features
✔ tooth reacts to electric
pulp vitality tester at a
lower level of current
than adjacent normal
teeth
Acute Pulpitis
46. ⮚ Clinical Features
✔ pressure increases
because of lack of
escape of inflammatory
exudate
✔ rapid spread of inflammation
through pulp with pain
+ necrosis
Acute Pulpitis
47. ⮚ Management
✔ early stages of acute pulpitis pulpotomy
(removal of coronal pulp)
✔ placing material that
favors calcification such
as:
• calcium hydroxide
over entrance of
root canals
Acute Pulpitis
48. ⮚ Management
✔ root canal filling with
inert material like
gutta percha should be
done
Acute Pulpitis
49. ⮚ may develop with or
without episodes of
acute pulpitis
⮚ many pulps under large
carious cavities die painlessly
⮚ 1st indication is then
development of periapical
periodontitis, either with pain
or seen by chance in radiograph
Chronic Pulpitis
50. ⮚ Clinical Features
✔ dull aching type
✔ more often intermittent
than continuous
Chronic Pulpitis
51. ⮚ Management
✔ root canal therapy
✔ followed by crown
restoration
Chronic Pulpitis
52. ⮚ also called as pulp polyp
or pulpitis aperta
⮚ essentially an excessive
exuberant proliferation
of chronically inflammed
dental pulp tissue
Chronic Hyperplastic
Pulpitis
53. ⮚ pulpal inflammation due
to an extensive carious
exposure of a young pulp
⮚ development of granulation
tissue
⮚ covered at times by epithelium
⮚ resulting from long standing
low grade infection
Chronic Hyperplastic
Pulpitis
55. ⮚ Clinical Features
✔ most commonly involved
are deciduous molars +
1st permanent molar
• excellent blood supply
• large root opening
Chronic Hyperplastic
Pulpitis
56. ⮚ Clinical Features
✔ asymptomatic
✔ seen only in teeth of children
+ young adults
Chronic Hyperplastic
Pulpitis
57. ⮚ Clinical Features
✔ polypoid tissue appears
• fleshy
• reddish pulpal mass filling
most of pulp chamber
or cavity
• or even extend beyond
confines of tooth
Chronic Hyperplastic
Pulpitis
58. ⮚ Clinical Features
✔ polypoid tissue appears
• sometimes, if mass is
large enough
• interferes with closure
of mouth
Chronic Hyperplastic
Pulpitis
59. ⮚ Clinical Features
✔ polypoid tissue appears
• may cause discomfort
during mastication
• due to pressure of food
bolus
Chronic Hyperplastic
Pulpitis
60. ⮚ Clinical Features
✔ polypoid tissue appears
• tissue easily bleeds
because of rich network
of blood vessels
• tooth may respond or
not at all to thermal test
Chronic Hyperplastic
Pulpitis
61. ⮚ Management
✔ elimination of polypoid tissue
✔ followed by extirpation of pulp
✔ hyperplastic tissue bleeeding
can be controlled by pressure
✔ pulpectomy or extraction of tooth can also
be done if the tooth is not restorable.
Chronic Hyperplastic
Pulpitis
62. ⮚ death of pulp
⮚ may be partial or total
depending on whether part
or the entire pulp is
involved
Necrosis
63. ⮚ Causes
✔ sequeala of inflammation
✔ can also occur following
trauma
• pulp is destroyed before
an inflammatory reaction
Necrosis
73. References:
⮚Baume, L.: Transactions of the Fourth
International Conference on Endodontics.
Philadelphia: University of Pennsylvania
press, 1968, p. 66 .
⚫Baume, L.J.: Monogr. Oral Sci.,8:1-
220, 1980.