Spread of Oral Infection (2009)
Copyright 2009 by Department of Oral Medicine
University of Dental Medicine, Yangon
Feel free to request to take it down this slide if you are copyright owner.
Tuberculosis is a disease characterized by granulomatous lesions caused by Mycobacterium Tuberculosis. A German scientist Robert Koch discovered the causative organism of TB in 1882.
Since time immemorial, it has been a global health problem. TB has shown a decline in its prevalence globally; however, it is still highly prevalent in Asian countries.
TB is usually overlooked in the differential diagnosis of oral lesions as it is supposed to be a rare entity.
Oral manifestations of TB occur either due to infected sputum or due to hematogenous spread.
TB is an age old disease and has been known to mankind for thousands of years.
Spread of Oral Infection (2009)
Copyright 2009 by Department of Oral Medicine
University of Dental Medicine, Yangon
Feel free to request to take it down this slide if you are copyright owner.
Tuberculosis is a disease characterized by granulomatous lesions caused by Mycobacterium Tuberculosis. A German scientist Robert Koch discovered the causative organism of TB in 1882.
Since time immemorial, it has been a global health problem. TB has shown a decline in its prevalence globally; however, it is still highly prevalent in Asian countries.
TB is usually overlooked in the differential diagnosis of oral lesions as it is supposed to be a rare entity.
Oral manifestations of TB occur either due to infected sputum or due to hematogenous spread.
TB is an age old disease and has been known to mankind for thousands of years.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
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This seminar consisits of description of various bacterial diseases along with their oral manifestations,diagnosis and treatment.an addition of suitable case reports for better understanding and associated disorders
Dr. Ahmed M. Adawy, Professor Emeritus, Dep. Oral & Maxillofacial Surgery. Former Dean, Faculty of Dental Medicine
Al-Azhar University. The Pathogenesis of infection in oro-facial region due to odontogenic origin is a common clinical issue. bacterial invasion to deeper tissues usually a spread from diseased dental pulp. Recent evidences indicated a multi-microbial nature. The spread of infection is governed by the thickness of the investing bone and the anatomical relation of the tooth root to the attached muscle. Infection could spread from one facial space to another, and the condition may be aggravated to life threatening situations.
BACTERIAL INFECTCTIONS OF ORAL CAVITY i /certified fixed orthodontic courses ...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
This seminar consisits of description of various bacterial diseases along with their oral manifestations,diagnosis and treatment.an addition of suitable case reports for better understanding and associated disorders
Dr. Ahmed M. Adawy, Professor Emeritus, Dep. Oral & Maxillofacial Surgery. Former Dean, Faculty of Dental Medicine
Al-Azhar University. The Pathogenesis of infection in oro-facial region due to odontogenic origin is a common clinical issue. bacterial invasion to deeper tissues usually a spread from diseased dental pulp. Recent evidences indicated a multi-microbial nature. The spread of infection is governed by the thickness of the investing bone and the anatomical relation of the tooth root to the attached muscle. Infection could spread from one facial space to another, and the condition may be aggravated to life threatening situations.
BACTERIAL INFECTCTIONS OF ORAL CAVITY i /certified fixed orthodontic courses ...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Infection- microbiology and pathology in orofacial infectionPunam Nagargoje
INTRODUCTION
Oral and maxillofacial infections are commonly caused by teeth they are referred as odontogenic infections.
The etiological agents may be bacteria viruses or fungi.
The infection may spread directly from the tooth or secondary infections of cyst or tumours or infection of surgical wound or by contaminated needles.
Infection may be defined as invasion and multiplication of microorganisms in body tissues, especially that causing local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response.
Aerobic bacteria
Gram positive cocci –
Streptococcus species
S.Milleri
S.sanguis
S.Salivarius
S.Mutans
Staphylococcus species
Gram negative cocci –
Neisseria spp.
- N. subflava
N. sicca
Gram positive rods-
Dipetheroids
Lactobacillus spp
Gram negative rods-
Moraxella catarrhalis
Actinobacilllus actinomycetemcomitans
Campylobacter spp.
Capnocytophaga spp.
Eikenella corodens
Helicobactor pylori
Anaerobic bacteria
Gram positive cocci –
Peptococcus species
Pepto Streptococcus species
Gram pasitive bacilli –
Actinomycosis spp
Eubacterium spp
Gram negative species-
veillonella spp.
Gram negative bacilli-
Bacteroids
Prevotella species
Porphyromonas species
Fusobacterium
There are three stages in progression of acute odontogenic infections
Stage I – Innoculation
Stage II – Cellulitis
Stage III – Abscess
Stage IV – Space infection
TYPES
Acute stage - 3 forms
1.Abscess
2.cellulitis
3.fulminating infection
FULMINATING INFECTIONS
Here the infection involves secondary spaces involving vital structures.
Chronic stage
C/c fistulous tract or sinus formation
Abscesses neglected for a long time may discharge intraorally or extra orally
Spread of oral infection
Routes of spread
Direct continuity through tissues
By lymphatics to the lymph nodes.From lymph nodes to tissues results in secondary areas of cellulitis or tissue space abscess.
By blood stream-local thrombophlebitis may spread via the veins entering the cranial cavity producing cavernous sinus thrombosis. It may cause septicemia.
Invasion of dental pulp by bacteria after
decay of a tooth
¯
Inflammation, edema & lack of collateral
blood supply
¯
Venous congestion or avascular necrosis
(pulpal tissue death)
¯
Reservoir of bacterial growth(anaerobic)
¯
Periodic egress of bacteria into surrounding
alveolar bone
Factors influencing spread
General factors
Host resistance
Virulance of micro organism
Combination of both
Local factors
Anatomic barriers-
Alveolar bone
Periosteum
IgA preven
Granulomatous diseases of the head & neckMammootty Ik
covers all the important granulomatous diseases of head and neck region with a brief and to-the-point description of pathogenesis, clinical features , differential diagnosis and management of each disorder
This Presentation will help ou to compare the spectrum of pathologies in ulcerated versus non-ulcerated exophytic oral mucosal lesions and explore the significance of surface ulceration as an indication of various oral diseases
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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2 Case Reports of Gastric Ultrasound
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,
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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.
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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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- Prix Galien International Awards Ceremony
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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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1.
2. Tuberculosis is still one of the most life threatening
infectious diseases, resulting in high mortality in
adults.
The World Health Organization (WHO) estimates
that worldwide there are approximately 20 million
active cases, of them approximately 3 million people
die each year from tuberculosis, of which 80% are in
developing countries.
3. It is very common in India and South-East Asia,
where the prevalence rate is about four in every
1,000 people.
India alone accounts for nearly one fifth of the global
burden of tuberculosis .
4. Every year, approximately 2.2 million individuals
develop tuberculosis in India, of which around
0.87 million are infectious cases and it is estimated
that annually there are around 330,000 deaths due
to TB.
5. The incidence of TB in the underdeveloped countries
is increasing, and this is thought to be because of
associated poor hygienic conditions and a greater
prevalence of acquired immunodeficiency syndrome
(AIDS).
8. Extrapulmonary tuberculosis is rare, occurring in
10% to 15% of all cases.
Oral manifestations occur in approximately 3% of
cases involving long standing pulmonary and/ or
systemic infection.
9. May be as
Ulcers
Erythematous patches
Indurated lesions with granular surface
Nodules
Fissures
Plaques
Granulomas
Vemicous proliferations
Jaw lesions in the form of tuberculous osteomyelitis.
10. Most commonly affected site:
Tongue(the lateral border, tip, anterior dorsum and
the ventral surface)
Other sites include:
Lip
Cheek
Soft palate
Uvula
Gingiva
Alveolar mucosa
Tooth socket
Jaw involvement may present as osteomyelitis
11. Two main types of tubercular infections of oral tissues
are recognized –
Primary
Secondary.
12. Primary lesions develop when tuberculosis bacilli are
directly inoculated into the oral tissues of a person who
has not acquired immunity to the disease and in fact,
any area that is vulnerable to direct inoculation of
bacilli from exogenous source can be a potential site.
13. These frequently involve
• Gingiva
• Tooth extraction sockets
• Buccal folds.
Primary oral tuberculous lesions are extremely rare
and generally occur in young adults with associated
caseation of the dependent lymph nodes; the lesion
itself remains painless in most cases. Primary lesions
of tuberculosis manifest in the oral cavity as non
healing chronic ulcers.
14. 1. An intact oral mucosa
2. Cleansing action of saliva
3. Salivary enzymes
4. Tissue antibodies
5. Oral saprophytes
Any breach in these defense mechanisms, such as
abrasions, tears, chronic inflammation,
poor oral hygiene, tooth eruption, extraction sockets,
periodontal disease, and carious teeth with pulp
exposure may lead to infection by tubercle bacilli.
15. Secondary infection of oral tissues can result from
either haematogenous or lymphatic spread or from
autoinoculation by infected sputum and direct
extensions from neighbouring structures.
Intraoral sites frequently involved include:
Tongue
Palate
Lips
Alveolar mucosa
Buccal mucosa
Gingiva
Frenula
and jaw bones
18. Lowered host resistance
Increased virulence of the organisms
19. The mechanisms that prevent activation of latent
M.tb and those that bring active TB infection under
control are poorly characterized.
CD4+ T cells play an essential role in controlling
active M.tb infection, but only a minor role in
preventing re-activation of latent M.tb infection.
CD8+ T cells provide immunity against re-activation of
latent infection, but make only a limited contribution to
the containment of active M.tb infection.
20. Primary M.tb infection
Mycobacteria phagocytosed by macrophages
Activate CD4+ T cells
Cytokines are secreted
Activate lymphocytes and mononuclear phagocytes
Fuse into multi-nucleated giant cells
Forms immunoinflammatory granuloma (tubercle)
21. Reactive nitric oxide metabolites produced by
activated macrophages play an important role in the
intracellular neutralization of the bacteria.
CD8+ cytotoxic T effector cells recognize M.tb
antigens on infected macrophages in the context of
MHC class1 molecules and induce either killing of the
intracellular pathogens or lysis of the infected cells by
means of granzymes, granulysin or perforin.
Furthermore a Th-1cytokine profile is important for
building up a protective immunoinflammatory response
to M.tb infection.
22. Persistent productive or unproductive cough
Evening rise of temperature
Gradual weight loss
Malaise
23. An ulcerative lesion of the mucosa is seen. The
lesion may be preceded by an opalescent vesicle or
nodule which may break down as a result of
caseation necrosis to form an ulcer.
The typical tuberculous ulcer is an irregular lesion
with ragged undermined edges, minimal induration
and often with a yellowish granular base.
Tiny single or multiple nodules called 'sentinel
tubercles' may also be seen surrounding the ulcer.
24. Ulcer of the right buccal
mucosa Intra orally photograph shows an ulcer with well
defined margins on the left buccal mucosa
covered by a yellow pseudomembrane
27. Sputum examination(smear microscopy)
{ Ziehl-Neelsen, PAS staining}
Chest radiograph (PA view)
Intraoral radiograph
Biopsy
Tuberculin (Montoux) test
Mycobacterial culture
Special staining(Grocott-Gomori stains, Auramine-Rhodamine
stain)
C-reactive protein test
Evaluation of immunoglobulins
ESR
FNAC
DNA probes
Polymerase Chain Reaction(PCR) assays
ELISA test
28. Multiple confluent and discrete granulomas composed
of epithelioid histiocytes and Langhans giant cells
with central caseous necrosis, surrounded by
lymphocytes and few plasma cells.
29. Low magnification micrograph Higher-magnification micrograph of
showing numerous noncaseating granulomatous process with
granulomas. Langhan’s giant cells and epithelioid
cells.
30. Histopathological slide shows Langhan’s cells containing nuclei
granulomatous inflammation with arranged in a horseshoe shaped
Langhan’s giant cells and focal caseous pattern at cell periphery
necrosis (hematoxylin and eosin stain)
32. Chest radiograph without Postero-anterior chest radiograph
abnormal findings. showing bilateral upper lobe
consolidation and cavitation,
consistent with pulmonary tuberculosis
33. Standard antitubercular therapy with isoniazid,
rifampicin ,pyrazinamide and ethambutol.
WHO recommended category 1 anti-
tubercular therapy DOTS (Directly
Observed Treatment, Short Course) :
Rifampicin (450 mg), Isoniazid (600 mg), Ethambutol
(1200 mg) and Pyrazinamide (1500 mg) for two
months, with three times doses per week, followed
with a continuation phase with Isoniazid (300 mg) and
Thioacetazone (150 mg) for six months.
35. A 30-year-old female came with a painful sore on the
upper left labial mucosa of about 2 weeks duration.
36. Age: 30yrs
Sex: Female
Chief complaint: Patient complains of a painful sore
on the upper left lip region of about 2 weeks
duration.
Habits: No habit of smoking or drinking
37. Built: Moderate
Past medical history: Claimed to be HIV-
seronegative as tested for HIV infection 2 months
back.
38. Twoulcers:
1.On the upper left labial mucosa(painful)
2.On the ventral surface of the tip of the
tongue.
The dorsal surface of the anterior margin of
the tongue was hyperaemic with a lobulated
appearance.
39. Both ulcers were surrounded by a wide area of
erythema.
The margins of both ulcers were slightly elevated &
indurated.
Ulcer on the ventrum of the tip of the
Dorsum of anterior one-third of the
tongue,with slightly elevated margins
tongue with erythematous, lobulated
and a wide zone of surrounding
appearance.
erythema.
40. Histological examination showed necrotic tissue and
chronically inflamed granulation tissue.
Scattered epithelioid cells were present, and Ziehl-
Neelsen staining revealed the presence of acid fast
bacilli leading to the final diagnosis of oral
tuberculosis.
41. The chronic granulomatous lesion in
Ziehl-Neelsen stain showing two
the sub mucosa of the lip (H&E stain,
acid-fast bacilli(×1000).
×300).
42. Patient proved to be HIV-seropositive with CD4+T
cell count of 429 cells/mm3.
General physical examination: Unremarkable
Chest radiograph: Didn’t show any evidence of
tuberculosis
Other laboratory investigations: All within the
range of normality
43. The diagnosis of primary oral TB was made by biopsy
since the clinical features of the oral lesions were
nonspecific.
On microscopical examination, typical tuberculous
granulomas were not evident.
The presence of epithelioid cells prompted the Ziehl-
Neelsen stain which revealed the acid-fast bacilli.
Failure to express well-defined granulomas with giant
cells is the result of immune suppression due to HIV co-
infection.
44. A nine-month anti-TB drug regimen of
isoniazid,rifampicin, pyrazinamide, and ethambutol
was prescribed.
The patient did not receive antiretroviral treatment
because in government hospitals this is allowed only
to patients whose CD4+ T cell counts are lower than
200cells/mm3.
Unfortunately our patient could not afford the
medication privately.
45. The same site, four weeks after The same region, four weeks after
starting antitubercular treatment. starting antitubercular treatment.
47. Infection with HIV is the greatest single
risk factor either for the progression of latent
infection to active TB or for acquisition of new M.tb
infection.
Subjects with HIV-M.tb co-infection more frequently
have extrapulmonary TB than do HIV-seronegative
subjects, lymph nodes and central-nervous system
being the sites most commonly affected.
There is a synergistic relationship between
tuberculosis and HIV infection: each accelerates the
progression of the other; and HIV-seropositive
subjects with TB have a shorter life than TB-free HIV-
seropositive with comparableCD4+ T cell counts.
48. Complex
Multifactorial.
The profound HIV-associated cellular immune
suppression has several identifiable
characteristics:
A progressive decrease of CD4+ T cells
Functional impairment of surviving CD4+ T cells
Functional impairment of macrophages and
polymorphonuclear neutrophils
Dysregulation of the cytokine network
CD8+ T cell exhaustion.
49. M.tb-specific chronic activation of the
cellular arm of the immune response adds to the
existing HIV-associated CD4+ T-cell and CD8+ T-
cell exhaustion.
M.tb promotes HIV replication by upregulating
CXCR4 surface receptors on alveolar macrophages
thus permitting the more virulent X4 strains of HIV to
enter and replicate in these cells.
This leads to further immune exhaustion and
impairment, resulting in the perpetuation of
a pernicious cycle of HIV-M.tb co-infection.
50. The diagnosis of TB in HIV-seropositive subjects is
not always straightforward as the clinical signs and
symptoms of TB in these subjects are not as well
defined as in HIV-seronegative subjects.
HIV-M.tb co-infected subjects are frequently
negative to tuberculin skin testing.
Acid fast bacilli are very scant in their sputum
although sputum culture invariably confirms
pulmonary TB,and pulmonary TB granulomas are
not always present.
51. If highly active antiretroviral therapy (HAART) is
introduced early in the course of HIV disease and if
concurrent TB is treated expeditiously, then this
pernicious cycle will be arrested.
The outcome of treatment of TB in either HIV-
seropositive subjects or HIV-seronegative subjects is
similar, but recurrence of, and mortality rates from TB
are greater in HIV-seropositive subjects .
52. TB may also sometimes present as an
immune reconstitution inflammatory syndrome shortly
after HAART has brought about a decrease in the
HIV load with consequential significant elevation of
the CD4+ T cell count.