This document discusses aggressive periodontitis, a rare and severe form of periodontitis. It is characterized by early onset, rapid progression, and familial aggregation. There are two main types: localized aggressive periodontitis, which mainly affects first molars and incisors, and generalized aggressive periodontitis, which affects at least three teeth across the mouth. Risk factors include certain bacteria like Aggregatibacter actinomycetemcomitans, genetic factors, and immune system abnormalities. The document provides details on the clinical features, causes, and differences between the chronic and aggressive forms of periodontitis.
Furcation involvement is a common sequela of severe chronic periodontal disease. Its effective management has a profound influence on the outcome of periodontal therapy.
Phase I periodontal therapy is the first in the chronologic sequence of procedures that constitute periodontal treatment. It is also referred to as cause related therapy or non-surgical periodontal therapy.
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
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Furcation involvement is a common sequela of severe chronic periodontal disease. Its effective management has a profound influence on the outcome of periodontal therapy.
Phase I periodontal therapy is the first in the chronologic sequence of procedures that constitute periodontal treatment. It is also referred to as cause related therapy or non-surgical periodontal therapy.
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
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
AGGRESSIVE PERIODONTITIS
PRESENTER
DR. REBICCA RANJIT
DEPT. OF PERIODONTOLOGY & ORAL IMPLANTOLOGY
Why is there localisation of disease to 1st molars and incisors in LAP?
Often subjects present with attachment loss that does not fit the specific diagnostic criteria (AP or chronic periodontitis).
Schenkein et al. 1995: cigarette smoking was shown to be a risk factor for patients with generalized forms of AgP.
Smokers with GAP had more affected teeth and greater mean levels of attachment loss than patients with GAP who did not smoke.
IgG2 serum levels as well as antibody levels against A.a. are significantly depressed in subjects with GAP who smoked.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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
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!
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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.
2. CONTENTS
INTRODUCTION
HISTORY
AGGRESSIVE PERIODONTITIS
DIFFERENCE BETWEEN CHRONIC AND AGGRESSIVE
PERIODONTITIS
CLINICAL FEATURES
LOCALIZED AGGRESSIVE PERIODONTITIS
GENERALIZED AGGRESSIVE PERIODONTITIS
DIFFERENCE BETWEEN LAP & GAP
RISK FACTORS
o MICROBIOLOGIC FACTORS
o IMMUNOLOGIC FACTORS
o GENETIC FACTORS
o ENVIRONMENTAL FACTORS
CONCLUSION
REFERENCES
3. INTRODUCTION
Periodontitis is defined as an inflammatory
disease of the supporting tissue of the teeth
caused by specific microorganisms, resulting in
progressive destruction of the periodontal
ligament and alveolar bone with pocket
formation, recession, or both.
4. HISTORY
1923, Gottlieb -- Case of epidemic influenza
“Diffuse atrophy of the alveolar bone”
Loss of collagen fibers in the periodontal
ligament
Replacement by loose connective tissue
Extensive bone resorption,
Resulting in a widened periodontal
ligament space.
The gingiva apparently was not involved.
5. In 1938 Wannenmacher described incisor-first
molar involvement and called the disease
Parodontitis marginalis progressiva.
Finally in 1967, Chaput and colleagues and by Butler
in 1969 introduce the term Juvenile Peridontitis.
In 1989 the World Workshop in Clinical
Periodontics categorized this disease as ‘Localized
Juvenile Periodontitis’ (LJP)
Most recently , it is named as Aggressive
Periodontitis.
6. AGGRESSIVE
PERIODONTITIS
Aggressive periodontitis (AgP) comprises a
group of rare, often severe, rapidly
progressive forms of periodontitis often
characterized by an early age of clinical
manifestation and a distinctive tendency for
cases to aggregate in families.
(Clinical Periodontology and Implant Dentistry
4th edition)
7. Aggressive periodontitis describes three of
the formerly classified as “early-onset
periodontitis”
They are:
LOCALIZED AGGRESSIVE PERIODONTITIS
GENERALIZED AGGRESSIVE PERIODONTITIS
RAPIDLY PROGRESSIVE PERIODONTITIS
8. CHRONIC
PERIODONTITIS
AGGRESSIVE
PERIODONTITIS
AGE More prevalent in adults
but may be present in
children & adolescents
Circumpubertal onset in
LAP & under 30 years of
age in GAP
RATE OF
PROGGRESSION
Slow rate of progression Rapid rate of progression
with pronounced episodic
events of attachment and
bone loss
MICROBIAL
AETIOLOGY
Consist of both aerobic &
anaerobic gram positive &
gram negative
microorganisms
Key microorganisms are
Aggregatibacter
actinomyctemcomitans &
Prevotella intermedia
IMMUNOLOGICAL
AETIOLOGY
No abnormalities detected Hyper responsive
macrophage phenotype &
phocyte abnormalities
9. CHRONIC PERIODONTIS AGGRESSIVE
PERIODONTITIS
DISTRIBUTION Localized when less than 30%
of sites involved
Generalized when more than
30% of sites are affected
Localized when 1st molar &
incisors & no more than two
permanent teeth are
involved
Generalized when at least
3 permanent teeth other
than 1st molar & incisor are
involved
LOCAL FACTORS Presence of local factors
directly relates to the
amount of destruction
present
Presence of local factors
does not commensurate
with the amount of
destruction present
FAMILIAL
AGGREGATION
Lacks strong evidence of
correlation between
particular genes and
periodontitis
Evidence of strong familial
aggregation
10. FEATURES OF AGGRESSIVE
PERIODONTITIS
(by lang et al. in 1999)
PRIMARY FEATURES
Non contributory medical history
Rapid attachment loss and bone loss
Familial aggregation
11. SECONDARY FEATURES
Amount of microbial deposits does not
commensurate with the severity of periodontal
tissue destruction
Elevated proportions of aggregatibacter
actinomycetemcomitans (Aa)
Hyper responsive macrophage phenotype with
exaggerated response to bacterial endotoxin
Phagocyte abnormalities
13. LOCALIZED AGGRESSIVE
PERIODONTITIS
Clinically, it is characterized as having
"localized first molar/incisor presentation with
interproximal attachment loss on at least two
permanent teeth, one of which is a first molar,
and involving no more than two teeth other
than first molars and incisors” .
14. Clinical features:
1. Age of onset at about puberty.
2. Affects both the sexes
3. Main characteristic
feature affects mainly the
FIRST MOLARS and INCISORS
4. Lack of clinical inflammation
despite the presence of
deep periodontal pockets.
15. 5. Plaque that is present forms
thin biofilm on the teeth.
6. Plaque contains elevated
levels of :
Aggregatibacter
actinomycetem-comitans
(Serotype b)
Porphyromonas gingivalis
(in some pts)
7. Disease progresses rapidly and Plaque that is
present forms a thin biofilm on the teeth
and rarely mineralizes to form calculus
16. 8. The rate of bone loss is 3 to 4 times
faster than in chronic
periodontitis.
9. Robust serum antibody response. to
infecting agents
17. Other Clinical Findings:
1. Maxillary incisors migrate disto-labially that
results in diastema formation.
2. Increasing mobility of the
affected teeth
3. Sensitivity of denuded root surfaces to
thermal and tactile stimuli
4. Deep, dull radiating pain during mastication.
5. Periodontal abscess may form.
6. Regional lymph node enlargement may occur.
18. Radiographic finding:
o Classic diagnostic sign VERTICAL LOSS of
alveolar bone around the first molars and incisors.
o Other finding “Arc-shaped” loss of alveolar bone
extending from the distal surface of 2nd premolar
to the mesial surface of the 2nd molar.
o Bone defects are usually wider than usually seen
with chronic periodontitis.
19. Generalized aggressive
periodontitis
“Characterized by generalized interproximal
attachment loss affecting at least three
permanent teeth other than first molars and
incisors”
20. FEATURES
Usually affecting persons under 30 years of
age, but patients may be older.
Poor serum antibody response to infecting
agents.
Generalized interproximal attachment loss
affecting at least three permanent teeth
other than first molars and incisors.
Pronounced episodic nature of the destruction
of attachment and alveolar bone.
21. Radiographic features
No definitive pattern of distribution. Ranges
from severe bone loss associated with the
minimal no. of teeth, to advanced bone loss
affecting the majority of teeth in the
dentition.
Patients with GAP demonstrate osseous
destruction of 25% to 60% during a 9 week
period and other sites show no bone loss.
22. Localized aggressive
periodontitis (LAP)
Generalized aggressive
periodontitis (GAP)
AGE OF ONSET Circumpubertal Under 30 yrs of age but
older patients may be
affected
DISTRIBUTION Localized 1st molar or incisor
presentation with
interproximal attachment
loss & not involving more
than 2 permanent teeth
Generalized interproximal
attachment loss affecting at
least three permanent teeth
other than 1st molars &
incisors
SEVERITY Rapid & severe loss of
alveolar bone
Episodic in nature
AETIOLOGY Predominantly Aa Predominantly P. gingivalis
IMMUNOLOGICAL
Robust serum antibody
RESPONSE
response to infecting agent
Poor serum antibody
response to infecting agent
PRESENCE OF
LOCAL FACTORS
There is minimal amount of
local factors present on the
affected teeth
There is marked plaque &
calculus accumulation
FAMILIAL
PATTERN
Strong association Unclear association
23. Localized Aggressive
Periodontitis
Generalized Aggressive
Periodontitis
GINGIVAL
INFLAMMATION
Lack of clinical
inflammation despite the
presence of deep pockets
and advanced bone loss
Clinical signs of gingival
inflammation are evident
RADIOGRAPHIC
APPEARANCE
Vertical or arc-shaped
bone loss around 1st molars
and incisors
There is generalized
extensive destruction or
bone loss around involved
teeth
24. Risk factors for aggressive form of
periodontitis
Microbiologic factors
Immunologic factors
Genetic factors
Environmental factors
25. Microbiologic factors
Presence of Aggregatibacter
actinomycetemcomitans (Aa) is a key agent in
LAP as it is present in high nos. & the patient
has high titre of serum antibodies against Aa.
Virulence factors possessed by Aa, such as
leucotoxin, lipopolysaccharide, proteases,
collagenases, surface associated material
affect the immune response & lead to
connective tissue destruction and bone
resorption.
26. Immunologic factors
Defective chemotaxis due to functional defect
of PMNs.
Hyper responsive monocytes that increase
prostaglandin, IL-1 α IL-1βproduction, which
result in one resorption.
Human leucocyte antigen (HLA) A9 & B 15 are
recognized as candidate markers of aggressive
periodontitis.
27. Genetic factors
Tendency to occur in families: familial
aggregation
Segregation & linkage analysis have shown that
presence of specific gene is responsible for
neutrophil abnormalities
Transmission through autosomal- dominant
mode of inheritance
28. Environmental factors
Smoking has a significant influence in the
progression of generalized aggressive
periodontitis. Smokers have greater
attachment loss than non smokers.
29. CONCLUSION
Aggressive forms of periodontitis are currently
considered to be multifactorial diseases developing as a
result of complex interactions between specific host
genes and the environment.
Interactions between the disease process and
environmental factors and genetically controlled
modifying factors are thought to contribute to
determining the specific clinical manifestation of the
disease.
For a successful treatment outcome the conventional
therapy is to be combined with a wide range of
therapeutic procedures to increase the chances of
disease resolution.