one stimulus, general response
oral medicine
periodontitis
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Language: en
Added: May 04, 2024
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Slide Content
Oral –systemic health
interconnection
Overall response-personal treatment
Mohamed Assadawy
https://orcid.org/0000-0001-7901-3303
Lecture outline
summarize the oral disease
Systemic disorders
the nature of the connections between oral and systemic health
Local stimulus elicit overall response
Enhancement the connection between dentistry and medicine
A New Partnership Between Dentistry and
Medicine
Focal infection: new age or ancient history
DEAD TEETH CAN AFFECT YOUR HEALTH
The Oral -Systemic Health Relationship
•Focal infection :
•a localized or generalized infection
caused by the dissemination of organisms
or toxic products from a focus of infection.
It probably would be better defined as a
metastatic infection
A focus of infection :a circumscribed area of tissue
infected with pathogenic organisms.
Foci may be primary or secondary. Primary foci usually are
located in tissues communicating with a mucous or
cutaneous surface. Secondary foci are the direct result of
infections from other foci through contiguous tissues, or at
a distance through the blood stream or lymph channels.
Primary foci of infection may be located anywhere in the
body.
Focal infection versus a focus of infection
❑focal infection implies metastasis from the infected foci, of bacteria or their toxins,
capable of injuring contiguous or distant tissue
❑
A Focus of infection has been defined as; “a circumscribed area infected with
micro‐organisms which may or may not give rise to clinical manifestations.”
Risk Groups
• Immunosupressed patients
• organ transplantation
• HIV
• Cancer
• Prosthetic heart valves
• Hip replacement
• Heart surgery
aurgments
In favor
•Primary foci found in association with secondary
systemic disease, such as tuberculosis
•Transient bacteremia in patients with primary foci and
secondary systemic disease
• selective affinity of certain bacteria for certain
tissues.
•exacerbations of arthritis, myositis, and iridocyclitis
may follow surgical procedures on the primary focus
•improvement may occur in the systemic or secondary
disease when the primary focus is eradicated.
•The flora of the colon can kill the host when the body
defenses are lowered by radiation
•
against
•the infectious agents involved are
unknown
•Patients whose teeth or tonsils are
removed often continue to suffer from
the original disease for which they were
removed
•beneficial effects can seldom be
ascribed to surgical procedures alone
•foci of infection heal after recovery from
systemic disease or when the general
health is improved with hygienic or
dietary measures
Focal infections : attributed to foci of infection have
included arthritis, neuritis, myalgias, nephritis, osteomyelitis,
endocarditis, brain abscesses, prosthetic
joint infections, skin abscesses, pneumonia, asthma,
anemia, indigestion, gastritis, pancreatitis, colitis,
diabetes, emphysema, goiter, thyroiditis, Hodgkin’s
disease, fever of unknown origin, stupidity and
‘nervous diseases of all kinds’, cancer .
Overall effect
Epidemiological studies have identified a range of malignancies associated with
periodontitis; however, in the majority of cancers the available evidence does not allow a
clear conclusion as to whether a true association exists and therefore in these cancers
we conclude that no association exists based on the current evidence . However, in the
case of head and neck/upper aerodigestive tract, lung, stomach and oesophageal cancer,
and pancreatic cancers the available evidence supports an association. Many of the
studies used different methods to assess periodontitis, some of which are potentially
inaccurate such as tooth loss as a surrogate for periodontitis. Inaccuracy in the
assessment of periodontitis would therefore have a major impact on the validity of the
data presented. In both periodontitis and malignancy older age and smoking are major
risk factors; however, the majority of studies adjusted for these.
Oral disease linked to an increased risk for cancer
The potential mechanisms supported by the strongest evidence
include local and systemic inflammation, oral microbiome
dysbiosis and the direct effects of specific periodontal pathogens,
and the effects of the metabolic products of periodontal
bacteria.
●Inflammation and associated oxidative/nitrosative stress have
been shown to contribute to tumorigenesis and tumour
proliferation in multiple ways.
●Should an association between cancer and periodontitis exist
then periodontally induced local and systemic inflammation and
free radical production would appear to be leading candidates to
account for this association.
●Although there is currently no direct evidence for a role in
tumorigenesis or tumour progression of bacterial metabolic
products such as nitrosamines, acetaldehyde and H
2S, a possible
role can be inferred as other exogenous as well as endogenous
sources of these molecules have been implicated in
carcinogenesis.
●The potential causal mechanisms that are supported by less
evidence, either direct or indirect, but which remain of potential
interest include epigenetic changes and shared genetic risk
factors, such as aldehyde dehydrogenase (ALDH),CYP1A1or
cytokine gene polymorphisms.
The complex interplay of periodontitis-induced inflammation and its potential to influence tumorigenesis and
tumor progression. (MMPs = matrix metalloproteinases; NF-κB = nuclear factor kappa-light-chain-enhancer of
activated B cells; RNS = reactive nitrogen species; ROS = reactive oxygen species; TIMPs = tissue inhibitors of
metalloproteinases; TLRs = toll-like receptors.)
connectors
•Cytokines, chemokines and growth factors
•Receptors it was found that LPS induced TLR4 signaling in colorectal cancer
cells and suggested that this might increase metastasis of colorectal cancer.
•Enzymes: TIMP concentrations are reduced in cancers. They also act as
mitogenic growth factors and inhibit apoptosis
•Free radicals: Generation of ROS and RNS leads to a signalling cascade that
triggers the production of pro-inflammatory cytokines and chemokines, thereby
upregulating systemic inflammation, genomic instability
The oral microbiome and specific oral pathogens :
Gastric cancer associated withH. pylori, which has become the model of bacterial-associated
cancer. The oral microbiome is a complex community composed of commensal bacteria as
well as representatives of other microbiological domains. The association of periodontitis
with malignancy
Bacteria
Viruses
Fungi
Host genetics associated with both (focal infection) periodontitis and
malignancy: Polymorphisms in genes encoding other pro-inflammatory
cytokines and receptors have been implicated in periodontitis and are associated
with increased risk of certain malignancies
Postulated cellular and molecular mechanisms accounting for the association between periodontitis and
malignancy. (H
2S = hydrogen sulphide; PADs = peptidylarginine deiminase enzymes; RNS = reactive
nitrogen species; ROS = reactive oxygen species.)
❑sarcoidosis, multiple sclerosis, amyotrophic lateral sclerosis, autism, Guillain–Barre
´ syndrome, pediatric autoimmune neuropsychiatric disorders associated with
streptococcal infections (PANDAS), Tourette’s syndrome, myasthenia
gravis, polycystic kidney disease, obesity, Alzheimer’s
disease, diabetes mellitus and, of particular interest to
dentistry, cardiovascular disease .
❑Many of these are proposed to affect the host by antigenic mimicry: microbial
antigens similar to host antigens that induce
an immune response that damages host tissue.
Systemic diseases (Overall response)
Periodontitis and respiratory diseases
Periodontitis, obesity and diabetes mellitus
Periodontitis and autoimmunity
Periodontitis and rheumatoid arthritis
Periodontitis, pregnancy and fertility
Periodontitis and neurodegenerative disease
The Focal Infection Theory may appeal to those
who desire or require a simple explanation for
biologic events particularly of a catastrophic
nature or when no explanation exists.