As age affect the our body parts similary it also affect the periodontium. To treat people with different age efficiently we need to understand the changes associated with periodontim.
This presentation describes the gingival recession, its classifications and theories of pathogenesis and different etiological factors in its progression.
Furcation involvement is a common sequela of severe chronic periodontal disease. Its effective management has a profound influence on the outcome of periodontal therapy.
The defense mechanism of gingiva includes GCF, Saliva, epithelial barrier and connective tissue cells. All these protect the periodontium from bacterial invasion.
Periodontitis is a complex infection initiated by bacteria –tissue destruction.
Host: the organism from which a parasite obtains its nourishment/ an individual who receives a graft
Modulation: the alteration of function or status of something in response to a stimulus or an altered physical or chemical environment
This presentation describes the gingival recession, its classifications and theories of pathogenesis and different etiological factors in its progression.
Furcation involvement is a common sequela of severe chronic periodontal disease. Its effective management has a profound influence on the outcome of periodontal therapy.
The defense mechanism of gingiva includes GCF, Saliva, epithelial barrier and connective tissue cells. All these protect the periodontium from bacterial invasion.
Periodontitis is a complex infection initiated by bacteria –tissue destruction.
Host: the organism from which a parasite obtains its nourishment/ an individual who receives a graft
Modulation: the alteration of function or status of something in response to a stimulus or an altered physical or chemical environment
Esthetic considerations in implant placement Esthetic considerations in implant placementEsthetic considerations in implant placementEsthetic considerations in implant placementEsthetic considerations in implant placementEsthetic considerations in implant placementEsthetic considerations in implant placementEsthetic considerations in implant placementEsthetic considerations in implant placement
Understanding of etiology and pathogensis of periodontal pocket will help to treat periodontal pocket successfully. Here I have descried the entire process with diagrams.
lecture 1
Dental implant introduction
1- implant history
2-micro and macro inplant desigen features
3- patient medical evaluation
4- introduction to treatment planning
Frailty syndrome and periodontal disease pptjegede lilian
this document contains a seminar presentation on frailty syndrome
and its relationship with the periodontics and how to manage a patient with this condition.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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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.
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
3. AGING :- It is defined as the sum of all
morphologic & functional alterations that occur
in an organism and lead to functional
impairment which decline the ability to survive
stress.
GERONTOLOGY:- Is the study of aging in all its
aspects biologic, physiologic, sociologic &
psychologic.
Definitions
3
9. Hay flicks limit/ Telomere
shortening
Hayflick, an American microbiologist.
Replicative senescence the number of
progenitor cells.
The decreased cellular component has a
concomitant effect to decrease cellular reserve
and protein synthesis.
This affects the oral epithelium in that the
tissue becomes thin, with reduced
keratinization.
9
10. Stochastic changes
Due to changes within the cell
Structure become stiffer
Loss of elasticity and
Increased mineralization (fossilization).
With loss of regenerative power,
structures become less soluble and
more thermally stable.
10
11. Somatic mutations lead to decreased protein
synthesis and structurally altered proteins.
Free radicals contribute to the accumulation of
waste in the cell.
All these changes produce a decline in the
physiological processes of the tissue.
Primarily: due to aging
Secondarily: due to physiological deterioration.
11
12. Physiologic changes
Gingival epithelium:
Thinning and
decreased
keratinization
Increase in epithelial
permeability to
bacterial antigens
Flatting of rete pegs
and altered cell
density
Decreased resistance
to functional trauma
12
13. Gingival connective
tissue:
Quantitative &
Qualitative changes in
collagen.
Coarser and denser
gingival connective
tissue.
↑ denaturing
↑ rate of conversion of
soluble to insoluble
collagen
↑ mechanical strength
13
14. Periodontal ligament:
Decrease in the no of
collagen fibers: reduction
or loss in tissue elasticity.
Increased amounts of
elastic fiber.
Decreased organic matrix
(mucopolysaccharides)
production
Decreased Epithelial cell
rests
14
15. Cementum:
Increase in cemental
width/ thickness
Upto 5 to 10 times with
increasing age
The increase in width is
greater in apically and
lingually.
Increasing surface
irregularity.
15
16. Alveolar bone:
Decrease in bone density
Increase in bone resorption
Decrease in vascularity.
Irregular periodontal surface
of bone
Less regular insertion of
collagen fibers.
Healing rate of bone in
extraction sockets appears
to be unaffected by
increasing age.
16
17. Dentogingival plaque accumulation has been
suggested to increase with age-
Increased hard tissue surface area resulting from
gingival recession
Surface characteristics of the exposed root surface
compared to enamel
Subgingival plaque: increased numbers of rods
and pseudomonads
Periodontal pathogens:
Increased Porphyromonas gingivalis
Decreased Actinobacillus actinomycetemcomitans
Relation of Bacterial plaque with aging
periodontium17
18. Relation of Immune responses with
aging periodontium
Immunosenescence
Difference between young and older
individuals can be demonstrated for T and B
cells, cytokines and natural killer cells, but not
for polymorphonuclear cells and macrophage
activity.
McArthur in 1999: no evidence for age related
in host defenses correlating with periodontitis
in an elderly group of individuals, with and
without disease.
18
19. Functional changes
Abnormality in T cell function: more susceptible
for viral and fungal infection.
Inflammation, when persist, develops more
rapidly and more severely.
Decrease the healing capacity and rate.
19
20. Clinical changes
Migration of junctional epithelium from its
position in healthy individual (on enamel) to
more apical position on the root surface with
accompanying gingival recession.
The consensus is that gingival recession is not
an inevitable physiologic process of aging but
is explained by cumulative effects of
inflammation or trauma on the periodontium.
20
23. Xerostomia
Saliva plays an essential role in maintaining
oral health.
Antimicrobial activity
Buffering capacity
Lubrication of the oral cavity
Transport of taste sensors
Digestive function
23
24. Loss of acinar cells with aging.
Medications: tricyclic antidepressants,
antihistamines, antihypertensives, and
diuretics.
Radiation treatment, Sjohren’s syndrome,
poorly controlled diabetes, bone marrow
transplantation, thyroid disorders, and
depression-
24
25. Xerostomia screening by
Sialometry
Oral examination
Sialometry:
Precise collection of saliva for 5 to 15 min from
gland
Parotid gland-Stensen’s duct: modified Carlson-
Crittenden collectors
25
28. Candidiasis
Cause by Candida albicans.
A pathogenic infection occurs when C.
albicans infiltrates into the oral mucosal layers.
Any condition compromising a patient’s
immune system can be considered a risk
factor for candidiasis.
Pseudo membranous
candidiasis.
Chronic atrophic candidiasis
28
29. Periodontal disease in older
adults
Age is either nonexistent or provides a small
and clinically insignificant increased risk of
loss of periodontal support.
29
30. Chronic periodontitis
Prevalence of periodontal disease is expected
to increase with age, as a result of cumulative
disease progression over time, not
susceptibility.
Severe or moderate chronic periodontitis???
Systemic disease
30
31. On progression of periodontal
disease
Greater inflammatory response in older adults-
Greater size of infiltrated connective tissue
Increased gingival crevicular fluid flow
Increased gingival index
Increased loss of connective tissue:
Chronic mechanical trauma from toothbrushing
Iatrogenic damage from unfavorable restorative
dentistry or repeated scaling and root planing
31
32. Periodontal treatment planning
Prevention, comfort, function, esthetics and
ease of maintenance are the criteria for
successful management of an older adult.
To preserve
function
Eliminate or
prevent the
progression of
inflammatory
disease.
32
33. Factors which influence periodontal treatment
outcome or progression of the disease :
medical and mental health status,
medications,
functional status,
lifestyle behaviors that.
Periodontal disease severity, ability to perform
oral hygiene procedures and ability to tolerate
treatment should be evaluated.
33
34. The risks and benefits of both surgical and non
surgical therapy should be considered.
Nonsurgical approach is often the first
treatment choice.
Age alone is not a contraindication of surgery.
Maintenance of surgical results.
Pallative support periodontal care.
34
35. Response to treatment of the
periodontium
The successful treatment of periodontal
requires both meticulous plaque control by the
patient at home and meticulous supragingival
debridement by therapist.
Despite the histologic changes in the
periodontium with aging, no differences in
response to nonsurgical or surgical treatment
have been shown for periodontitis
35
36. Prevention of periodontal disease and
maintenance of periodontal health in older
adults
Oral hygiene maintenance
Chemotherapeutic agents
Antiplaque agents
Fluoride
Saliva substitutes
36
38. Fluoride:
Natural cavity fighter
Reduce enamel solubility
Promotes remineralization of early carious
lesions
Is bactericidal to bacterial plaque
OTC: 230-1500 ppm
Professional: 9050-22,600 ppm
38
39. Saliva substitutes
They are intended to
match the chemical and
physical traits of saliva.
Composition: salt ions, a
flavoring agent, paraben
(preservative), cellulose
derivative or animal
mucins and fluoride.
ADA approved: Salivart
Xylitol chewing gum
Parotid-sparing radiation
therapy
39
40. 5 golden rules for healty teeth
1. Brush your teeth twice daily
2. Rinse your mouth after every meal
3. Eat fresh fruits and vegetables
4. Do not eat sweet in between meals
5. Visit your dentist every six months
40
Oral cavity example in aging…teeth wear
Gerentology….periodontology…
Why want to study aging in periodontium??
Do you think there will be change in young like you ppl and older adults??
In oral cavity what all changes you can see???
Increasing in the life expectancy of population more older adults…
Due to advance in maintenance of oral cavity increase tooth survival/retained…
So here as a periodontologist come into picture…
Also a upcoming brach is coming geriatric dentistry…interdiscipinary treatment approach…
Physician nurse psychiatrist….also the dentist….so you should know all changes that can be seen in older alduts..also know as geriatric person
interdisciplinary
Healthy periodontium
What changes you can think that will be there for older adults???
Cells are of three types: contionous diving, stable, permanent/ terminally differentiated
Epthelium of gingiva…continous diving cells
Layers of epithelium…4 layers…basal, spinosum, granulosum, corneum..
Basal cells have progenitor cells…
cell divide by mitotic cell division…
One cell give rise to 2 daugther cells
1- amplifying cell…contious division
2- become keratinocyte
Balance between cell division and cell shedding
In older adults…
Decrease in cell renewal
Fewer cell…decrease in regenerative process…
Reason..hay flick…
Due to changes with in the cells…crosslinking…morphological and physiological changes
Try to retain what is there…..
Loss of elasticity and increased resistance of tissue..decreased permeability..decreased nutrition….accumulation of waste
Decreased blood flow secondarily decrease cellular function.
Indicate increased collagen stabilization
Greater collagen contain in older adults despite of decreased collagen synthesis
Decrease in vascularity
Parallel to the gingival fibroblasts
Decrease in width of periodontal ligament space
Less remodeling capacity….resorption bays
Bone resorption and bone formation in a balanced manner
Before going to functional changes….
Decreased in renewal and vascularity…decreased healing
Recession is exposure of the root surface by an apical shift in the position of the gingiva.
Apparent: visible
Actual: hidden + visible
The width of the attached gingiva would be expected to decrease with age, but the opposite appears to be true .
Passive eruption
Diagram of dry mouth
Long term use of antibiotics
Steroid therapy
Chemotherapy
DM
Head and neck radiation therapy
HIV
Wipe by guaze psedomembranous
More suspectibile to severe periodontal disease but..advanced disease site have lost teeth earlier in life..suggesting older adults is not a risk factor.
Cardiovascular disease and diabetis
Periodontal healing and recurrence of disease are not influenced by age.
Implants….
Reduced osteogentic potential of the bone graft…
Older adults may have difficulty performing adequate oral hygiene
The newer, lightweight, electrical powered toothbrushes may be more benifical
because of compromised health, altered metal status, medications, or altered mobility and dexterity.
Dispensed in spray bottle, rinse bottle or oral swab stick