SPREAD OF INFECTION…
INTRODUCTION…
Occurrence of infectious disease is
determine by the interaction of host, the
organism & the environment…
Odontogenic infection can originate in the
dental pulp
root canal of tooth
periapical tissue..
Periodontal tissue
spongy bone
outer cortical plates
tissue spaces
mucous membrane
skin surface
Routes of infection…..
• The lymphatic system
• Blood stream
• Directly through the tissues
CELLULITIS…
• Cellulites is a diffuse inflammation of soft
tissue which is not circumscribed or
confined to one area, but which in
contrary to the abscess tends to spread
through tissue spaces & along facial
planes…
• Microorganisms…..
• Streptococci
• Streptokinase
• Hyaluronidase
• fibrinolysin
• Streptococci is the potent producer of
Hyaluronidase.
• They consume local oxygen & metabolize
nutrients to produce acidic environment.
• Anaerobes such as prevotella &
porphyromonas spp. destroy collagen.
• Cellulitis of face & neck is very common.
• It occurs due to infection following tooth
extraction, injection either with an
infected needle or through an infected
area.
CLINICAL FEATURES….!
•
•
•
•
•
•
Elevated temperature
Leukocytosis
Painful swelling
Inflammatory edema
Orange peel like appearance of skin
Maxilla involve swelling of the upper ½ of
the face & spread towards eye because of
cavernous sinus thrombosis through the
vein of inner canthus of eye..
• If the infection tends to spread in the
mandible it perforates the outer cortical
plate below the buccinator.
• Leads to diffuse swelling in the lower ½ of
the face, which leads to cervical spread &
may cause respiratory discomfort.
HISTOLOGICAL
FEATURES..!
• Microscopic section through an area
shows only a diffuse exudation of PMN
leucocytes & occasional lymphocytes,
with serous fluid & fibrin.
• It causes separation of connective
tissue & muscle fibers.
TREATMENT…!
• Cellulitis can be treated with
administration of antibiotics & removal
of cause of infection….!!!
TISSUE SPACES…!!
• Tissue spaces or facial spaces, are
potential spaces situated between
planes of fascia that form natural
pathway along which infection may
spread ..
• These potential spaces are
compartment that contain structure
such as salivary glands ,fat or lymph
nodes
SPREAD OF INFECTION
FROM MAXILLARY TEETH
• Maxillary incisors------ labial, palatal
abscess, vestibular abscess.
• Canine ------ labial or vestibular
abscess, canine space.
• Premolar------ buccal or palatal side,
Canine space
Molars-----buccal or palatal space, buccal
space abscess..
SPREAD OF INFECTION FROM
MANDIBUBULLAR TEETH
• Mandibular incisor---- labial abscess, sub
mental spaces abscess
• Canine root ------ labial or vestibular
abscess.
• Premolar ----- vestibular abscess.
• Molars---- vestibular abscess, sublingual
spaces, pterygomandibular abscess.
CANINE SPACES
• The CANINE SPACES is the region
between the anterior surface of maxilla
& the overlying levator muscle of the
upper lip.
• Infection of space manifest as swelling
with obliteration of the nasolabial fold.
BUCCAL SPACES
• Medially ------ buccinators,
buccopharyngeal fascia.
• Laterally ----- skin &subcutaneous
tissues.
• Anteriorly ---- the posterior border of
zygomaticus major, anguli oris.
• Posteriorly ----- anterior edge of
masseter muscle.
• Superiorly ---- zygomatic arch.
• Inferiorly ---- lower border of mandible.
INFRATEMPORAL SPACES
• Anteriorly ----- maxillary tuberosity.
• Posteriorly ---- lateral pterygoid muscle,
condyle, & temporal muscle.
• Laterally --- tendon of temporal muscle
& coronoid process.
• Medially ---- lateral pterygoid plate &
inferior belly of the lateral pterygoid
muscle.
PTERYGOMANDIBULAR
SPACES
• The inferior portion of the infra
temporal space is called the
pterygomandibular space & it lies
between the internal pterygoid muscle
& ramus of mandible.
• The post zygomatic space extending
antero medially from the infra temporal
space.
LATERAL PHARYNGEAL
SPACE BOUNDARIES
• The lateral pharyngeal space is
bounded anteriorly by the
buccopharyngeal aponeurosis, the
parotid gland & pterygoid muscles.
• Posteriorly ---- prevertebral fascia
• Laterally ---- carotid sheath
• Medially ---- lateral wall of the pharynx
RETROPHARYNGEAL SPACE
• The retropharyngeal space is bounded
anteriorly -----the wall of the pharynx.
• Posteriorly --- prevertebral fascia
• Laterally ---- lateral pharyngeal space &
carotid sheath…
PAROTID SPACE
• The parotid space contain the parotid
gland & all associated structures,
including the facial nerve, the
auriculotemporal nerve, the posterior
facial vein, & the external carotid,
internal maxillary, & superficial
temporal arteries.
SPACE OF BODY OF MANDIBLE
• The space of the body of the mandible is
enclosed by a layer of fascia derived from
the outer layer of the deep cervical fascia,
which attaches to the inferior border of the
mandible and then splits to enclose the
body of the mandible. Superiorly, it
becomes continuous with the alveolar
mucoperiosteum and muscles of facial
expression, which have their attachment
on the mandible.
SPACE OF BODY OF MANDIBLE
• The space contains, the mandible
anterior to the ramus as well as the
covering periosteum, fascia, muscle
attachments, blood vessels, nerves,
teeth, and periodontal structures.
Shapiro pointed out that infections in
this space may be dental. Periodontal or
vascular in origin, or may arise from
fractures or by direct extension from
infection in the masticator or lateral
Submasseteric Space
• Boundaries. The submasseteric space is
situated between the masseter muscle and
the lateral surface of the mandibular
ramus. The masseter attaches to the ramus
at three sites: the deep part on the lateral
surface of the eoronoid process, the
middle part in a linear pattem on the
lateral surface of the ramus extending
upward and backward, and the superticial
part close to the angle of the mandible.
Submasseteric Space
• The submasseteric space is a narrow
space that parallels the middle
attachment by extending upward and
backward between tl1e middle and
deep attachments. The posterior
boundary of this space is the parotid
gland, and anteriorly it adjoins the
retromolar fossa
Clinical Features
• Infection of this space usually occurs
from a mandibular third molar, the
infection passing through the
retromolar fossa and into the
submasseteric space. The patient may
suffer from severe trismus and pain,
and there may be facial swelling . The
patient is often seriously ill.
SUBMANDIBULAR OR
INFRAMANDIBULAR SPACES
• Ther are three chief spaces in the submandibular
region:
• 1. the submanibular space
• 2. the sublingual space
• 3. the submental space
SUBMANDIBULAR SPACE
• BOUNDARIES:
• THE SUBMANDIBULAR SPACE IS
LOCATED medial to the mandible and
below te posterior portion of the mylohyoid
muscle.
• It is bordered medially by hyoglossus and
diagastric muscle and laterally by superficial
fascia and skin.
• This place encoses the submandibular
salivary gland and lymph nodes.
CLINICAL FEATURES
• Infection of the submandibular space usually
originates from the mandibular molars and
produces a swelling near the angle of the jaw.
• The space abscess is triangular, begins at lower
border of the mandible, and extends to the level
of the hyoid bone.
• It is one of the most commonly involved facial
and cervical tissue spaces.
• The infection spreads locally to involve the other
submandibular spaces like the lateral pharyngeal
space, the carotid space etc.
SUBLINGUAL SPACE
• BOUNDARIES:
• The sublingual space is bound by the mucosa
of the floor superiorly
• The inferior border is mylohyoid muscle,
anteriorly and laterally by the body of
mandible.
• Medially by the median raphae of the tongue.
• Posteriorly by the submandibular space.
CLINICAL FEATURES
• Infection in the sublingual space produces an
obvious swellin in the floor of the outh and
may cause both dyspnea and dysphagia.
• Extension of the infection takes the same path
as infection of submandibular space.
Submental space
• BOUNDARIES:
• The submental space extends from the
anterior border of the submandibular space to
the midline and is limited in depth by the
mylohyoid muscle.
CLINICAL FEATURES
• Infection in this area presents an anterior
swelling in the submental area. This may
cause dyspnea and dysphagia.
• The spread of infection is similar to that in the
submandibular and sublingual spaces.
Ludwig’s Angina
• Ludwig’s angina is an acute, toxic
cellulitis, beginning usually in the
submandibular space and secondarily
involving the sublingual and submental
spaces as well. The disease is not
usually considered to be true Iudwig’s
angina unless all submandibular spaces
are involved. It is most commonly a
disease of dental origin..
Ludwig’s Angina
• The chief source of infection is
involvement of a mandibular molar, either
periapical or periodontal.
• It may also result from submandibular
glandsialadenitis, oral soft tissue
lacerations, a penetrating injury of the
floor of the mouth, such as a gunshot or
stab wound, or from osteomyelitis in a
compound jaw fracture.
• However, this has become rare since the
advent of antibiotics
Ludwig’s Angina
• The second and third molars are the teeth
most commonly cited as the source of
infection. The study of Tschiassny showed
that of 30 teeth involved in 24 cases of
ludwig’s angina, 20% were first molars,
40% were second molars, and 40% were
third molars.
• The explanation for this phenomenon lies
in the fact that when an infection
perforates bone to establish drainage, it
seeks the path of least resistance
• Since the outer cortical plate of the
mandible is thick in the molar region, the
lingual plate is the one most frequently
perforated. According to the studies of
Tschiassny initial infection of the
submandibular space, particularly in cases
of the second and third molars, is due to
the fact that the apices of these teeth are
situated below the mylohyoid ridge in
65% of cases.
Ludwig’s Angina
• He also noted that because the apices
ofthe roots of the first molar are above
this ridge in about 60% of the cases,
infection of the sublingual space is most
common in cases of infection of this
tooth.
Clinical Features
• The patient with Ludwig’s angina manifests
a rapidly developing boardlike swelling of
the floor of the mouth and consequent
elevation of the tongue. The swelling is firm,
painful and diffuse, showing no evidence of
localization and paucity of pus. There is
difficulty in eating and swallowing as well as
in breathing.
• Patients usually have a high fever, rapid
pulse and fast respiration. A moderate
leukocytesis is also found.
Clinical Features
• As the disease continues, the swelling
involves the neck, and edema of the glottis
may occur. This carries the serious risk of
death by suffocation. Next, the infection
may spread to the parapharyngeal spaces,
to the carotid sheath or to the
pterygopalatine fossa.
• Cavernous sinus thrombosis with
subsequent meningitis may be sequela to
this type of spread of the infection.
Laboratory Findings
• Most cases of Ludwig’s angina are
mixed infection, but streptococci are
almost invariably present .
• Fusiform bacilli and spiral forms,
various staphylococci, diphtheroids and
many other microorganisms have been
cultured on different occasions.
Laboratory Findings
• Prevotella melaninogenicus,Prevotella
oralis, have also been isolated from
patients with Ludwig's angina.
• There are no apparent specific
organisms associated with the etiology
of this disease. It appears to be a
nonspecific mixed infection.
Treatment and Prognosis.
• Management consists of early recognition
of incipient cases, maintenance of airway;
intense and prolonged antibiotic therapy;
extraction of the affected tooth, and
surgical drainage.
• Before the advent of antibiotics, the
disease carried an exceedingly high
mortality rate, primarily due to
asphyxiation and severe sepsis.
Treatment and Prognosis.
• Most studies reported a death rate of
40-50%. Antibiotics have greatly
reduced the occurrence of cases of
Ludwig’s angina, and the seriousness of
the cases that do arise is attenuated by
the antibiotic therapy.
• The edema of the glottis, which may
develop rapidly, often necessitates
emergency tracheotomy to prevent
suffocation.
Complications of
Dental Infection
• A variety of intracranial complications
may occur as a direct result of dental
infection or dental extraction. Haymalter
reviewed a series of28 fatal infections
occurring after tooth extraction noting that
the infection process proceeded along
fascial planes to the base of the skull and
then traversing the skull by one or more
routes, spreading to the intracranial cavity
despite combative measures.
Complications of
Dental Infection
The specific complications included:
• Subdural empyema: 1
• Suppurative encephalitis and epyndimitis: 1
• Transverse myelitis: 1
• Subdural empyema and brain abscess 2
• Leptomeningitis: 2
• Leptomeningitis and brain abscess: 2
• Brain abscess: 8
• Sinus thrombosis: 11
Complications of
Dental Infection
• The majority of these cases occurred
after extraction of maxillary teeth.
Interestingly only 8 of the 28 cases
occurred in patients whose mouths
were classified as being in poor
hygienic condition. Furthermore, in 19
of the 28 cases the dental extraction
involved only a single tooth.
Cavernous Sinus Thrombosis of
Thrombophlebitis
• Cavernous sinuses are bilateral venous
channels for the content of middle
cranial fossa, particularly the parotid
gland. Areas drained by cavernous
sinus include the orbit, paranasal
sinuses, anterior mouth, and middle
portion of the face.
Cavernous Sinus Thrombosis of
Thrombophlebitis
• Cavernous sinus thrombophlebitis is a
serious condition consisting in the formation
of a thrombus in the cavernous sinus or its
communicating branches. Infections of the
head, face and intraoral structures above the
maxilla are particularly prone to produce this
disease.
• There are many routes by which the
infection may reach the cavernous sinus. The
facial and angular veins carry infection from
the face and lip, while dental infection is
carried by way of the pterygoid plexus.
Cavernous Sinus Thrombosis of
Thrombophlebitis
• Gram-positive organisms(specifically S.
aureus) are usually the pathogens in
this setting.
• It has been emphasized by Mazzeo that
infection spreading by the facial or
external route is very rapid with a short
fulminating course because of the large,
open system of veins leading directly to
the cavernous sinus.
Cavernous Sinus Thrombosis of
Thrombophlebitis
• ln contrast, infection spreading through
the pterygoid or internal route reaches
the cavernous sinus only through many
small, twisting passages and has a
much slower course, often with a lack
of obvious symptoms early in the
disease.
Clinical Features.
• The patient with cavernous sinus
thrombophlebitis is extremely ill and
manifests the characteristic features of
exophthalmos with edema of the eyelids
as well as chemosis. Paralysis of the
exteral ocular muscles is reported, along
with impairment of vision and sometimes
photophobia and lacrimation. There are
also headaches, nausea and vomiting,
pain, chills and fever..
Clinical Features.
• Orbital cellulitis and cavernous sinus
thrombosis can have similar signs and
symptoms, and differentiation between
them sometimes is impossible on
clinical basis alone. Neuroimaging with
C11 MRI or magnetic resonance
angiography may help distinguish
these entities
Treatment and Prognosis.
• A combination of intravenous
antibiotics, anticoagulants. and surgery
is the optimal treatment for cavernous
sinus thrombosis.
• The primary site of infection may
require early drainage, especially when
acute sinusitis is the cause of infection.
Treatment and Prognosis.
• The disease was once almost invariably
fatal, death occurs as a result of brain
abscess or meningitis. The use of
antibiotics has decreased this mortality
but the condition is still serious, with a
mortality rate of upto 30%.
Maxillary sinusitis
• An acute or chronic inflammation of the
maxillary sinus, is often due to direct extension
of dental infection, but originates also from
infectious diseases due to bacteria, fungus, or
virus such as the common cold, influenza and
the exanthematous diseases; from local spread
of infection in the adjoining frontal or
paranasal sinuses; or from traumatic injury of
the sinuses with a superimposed infection.
Maxillary sinusitis
• The common organisms include
Streptococcus pneumoniae, Hemophilus
influenzae, Moraxella catarrhalis in children,
gram- negative bacilli, anaerobic organisms,
rhinovirus and parainfluenza viruses. etc.
The occurrence of maxillary sinusitis as a
result of the extension of dental infection
known as odontogenic sinusitis, is
dependent, to a great extent, upon the
relation and proximity of the second
premolar, the first and second molar teeth to
the sinus..
Maxillary sinusitis
• When sinusitis is secondary to dental
infection, the microorganisms
associated with the sinusitis are the
same as those associated with the
dental infection. Apart from periapical
infection, foreign bodies, tumors, and
granulomatous lesions of the
nasomaxillary complex may also
produce maxillary sinusitis
Acute Maxillary Sinusitis
• Acute sinusitis may result from an
acute periapical abscess or acute
exaerbation of a chronic inflammatory
periapical lesion. which involves the
sinus through direct extension. In some
cases a latent chronic sinusitis may be
awakened by extraction ofa maxillary
bicuspid or molar and perforation of
the sinus.
Acute Maxillary Sinusitis
• Usually the organisms involved in
acute sinusitis are S. pneumoniae, H.
influenzae, and Moraxella catarrhalis.
• Anerobic organisms are isolated during
acute infections at times.
Clinical Features.
• Patients with acute maxillary sinusitis
suffer from moderate to severe pain with
swelling overlying the sinus or may have
headache. Pressing over the maxilla
increases the pain. Often, the Painful
sensation is one of pressure.
• Pain may be referred to various areas,
including the cheek, posterior teeth, and
ear.
Clinical Features.
• Sometimes patient may feel numbness in
maxillary molars and premolars. Sinus
pain increases when the patient bends
over or is supine. The patient may
complain of a discharge of pus into the
nose and often a foetid breath. Fever and
malaise are usually present.
• The diagnosis of acute maxillary sinusitis
from clinical manifestations alone is quite
difficult.
Diagnosis.
• Clinical signs and symptoms,
transillumination with strong flashlight
in darkroom, sinus view radiograph,
nasal and sinus endoscopy, and
computed tomogaphy are some aids
that can be used in diagnosis.
Histologic Features
• The lining of the maxillary sinus may
show a typical acute inflammatory
infiltrate with edema of the connective
tissue and often hemorrhage. A
squamous metaplasia of the specialized
ciliated columnar epithelium occurs
sometimes.
Treatment and Prognosis
• The prime objective of treatment is the
removal of the infecting locus. This is
particularly efficacious if the infection is
of dental origin. Because of the infection
present, antibiotics should also be
administered.
Chronic Maxillary Sinusitis
• Chronic sinusitis refers to sinusitis of
more than 3 months duration and may
develop as the acute lesion subsides or
may represent a chronic lesion from the
onset. Common predisposing factors
are recent upper respiratory viral
infections or allergic sinusitis.
Chronic Maxillary Sinusitis
• In cases of acute or chronic maxillary
sinusitis, the possibility of
phycomycosis infection (q.v.) must
always be considered, especially in
diabetic patients. In chronic sinusitis,
the organisms are anaerobes and
streptococcus. bacteroides, or
veillonella are the most commonly
involved.
Clinical Features.
• Clinical symptoms of chronic sinusitis
may be generally lacking, and the
condition may be discovered only during
routine examination.
• Sometimes headache, fever, vague facial
pain or upper toothache is present, or
there is a stuffy sensation on the affected
side of the face.
• There may be a mild discharge of pus into
the nose and a fetid breath.
Clinical Features.
• Children may have persistent cough,
fever, and purulent rhinorrhea. ln
chronic sinusitis, rarely will there be
dystrophic calcification termed
antrolith, which may be detected
radiographically
Radiographic Features.
• Sinusitis can be seen on the radiograph
as a clouding of the sinus due to the
hyperplastic tissue or fluid present.
Films of both sinuses should be
compared before a diagnosis is
attempted. CT scan may reveal
thickening of the mucosa.
Histologic Features.
• The mucosa lining the maxillary sinus
may show remarkable thickening and
the development of numerous sinus
‘polyps’. These polyps are simply
hyperplastic granulation tissue with
lymphocytic and sometimes plasma cell
infiltration.
Histologic Features.
• This tissue which is usually covered by
ciliated columnar epithelium. tends to
till the sinus and obliterate it. In some
instances there is no remarkable
proliferation of granulation tissue;
rather, there is only a mild lymphocytic
infiltration of the lining tissue with
squamous metaplasia of the epithelium.
Treatment and Prognosis
• The treatment for chronic maxillary
sinusitis consists in removal of the
cause of the disease. The prognosis is
considered good if the disease is due to
dental infection. since it can be
eliminated. Infection from other sites
may be difficult to eradicate.
FOCAL INFECTION
AARUSHI SHAH
Oral infection originates in the dental pulp or in
superficial periodontal tissues
Extend trough the root canals and into the periapical
tissues
Disperse trough the spongy bone
It may perforate the outer cortical bone
Spread in various tissue spaces or discharge onto a free
mucous membrane
INTRODUCTION:
• It has been observed since long time that
infections from the oral cavity can spread to
distant parts of the body and produce fresh
lesions over there.
• A focal infection is a localized or general
infection caused by the dissemination of
microorganisms or toxic products from a focus
of infection
• Moreover, oral tissues are vulnerable to
infections caused by various
microorganisms (e.g. bacteria, virus and
fungus), which produce a wide variety
of lesions in the oral cavity.
• Infections from these primary lesions
may spread to the distant organs to
initiate secondary diseases.
FOCUS OF INFECTION:
• Circumscribed area of tissue, which is
infected by exogenous pathogenic
organisms and is usually located near
the skin or mucosal surface, is called a
“focus of infection”.
MECHANISM OF FOCAL OF
INFECTION:
Two generally accepted mechanisms:
1) Metastasis of microorganisms from an infected
focus by either hematogenous or
lymphogenous spread.
2) Toxins may be carried through the blood
stream or lymphatic channels from a focus to
distant site, where they incite a hypersensitive
reaction in the tissues.
• The spread of microorganisma through
vascular or lymphatic channels is a recognized
phenomenon
• Thus certain organisms have a predilection for
isolating themselves in specific sites in the body
• The production of toxins by microorganisms
and their dissemination by vascular chhanels
are also important
• E.g.: SCARLET FEVER , cutaneous features of
the disease being due to the erythrogenic toxin
liberated by the infecting streptococci.
• RHEUMATIC FEVER: which probably
develops as a result of an altered reactivity or
hypersensitization of the tissue to hemolytic
streptococci.
• A high concentratiion of antibodies to
antigens of the group of hemolytic
streptococci is found in many patients with
rheumatic fever.
• Fact that microorganisms cannot be cultured
from the blood or from any of the tissues
involved in the disease indicates that this is
not a direct bacterial infection.
Oral foci of infection
• Infected periapical lesions:
-periapical cyst
-periapical granuloma
-periapical abcess
• Teeth with infected root canals
• Periodontal diseases with special
refernces to tooth extraction or
manipulaiton
Significance of oral foci of
infection
• Oral foci of infection either cause or aggravate a
great many systemic diseases.
• Most frequently mentioned are:
- Arthritis
- valvular heart disease ( subacute bacterial
endocarditis)
- gastrointestinal diseases
- ocular diseases
• Skin diseases
• Renal diseases
Arthritis
• Rheumatoid type of disease
• Unknown etiology
• Close resemblance to many features of
rheumatic fever.
• Microorganisms cannot be cultured
from the joints, the patients frequently
have high antibody titer to group A
hemolytic streptococci.
• This suggests a tissue hypersensitivity
reaction.
• Dental infection is implicated because of the
occurrence of streptococci infection in the
mouth.
• Theory of rheumatoid arthritis which favor
streptococci
1. Streptococcal infection of tonsil. Throat, or
nasal sinuses causes the initial or recurrent
attacks.
2. Removal of septic foci show dramatic
improvement.
3) The pathologic and anatomic features
of lymphoid tissue in tonsillar infection,
sinus infection, root abcesses suggest
that toxic products can be absorbed into
the circulation.
4) A temporary bacteremia may occur
immediately after tonsillectomy or
tooth extraction or after vigorous
massage of the gums.
Points against this theory
• Often no infection focus can be found.
• No dramatic results are produced when a focus
has been extirpated(removed).
• Sulfonamides, antibiotics and vaccines fail to
produce beneficial effects.
• Many person who are I n good health or are
suffering from a disease other than rheumatoid
arthritis may have septic foci.
Subacute bacterial endocarditis
(infective endocarditis)
• Close similarity between the etiologic
agent of the disease and the
microorganisms in the oral cavity, in
the pulp, in the periapical lesions.
• Symptoms of Subacute bacterial
endocarditis have been observed in
some cases shortly after extraction of
teeth.
• Transient bacteremia follows tooth
extraction.
• It is due to accretion (growth or incrase by
accumulation) of bacterial vegetation on heart
valves.
• Streptococci of the viridance type once caused
the majority of the cases of Subacute bacterial
endocarditis
• The advent of the antibiotics has resulted in the
drug resistance microorganisms assuming a
more important role.
• The majority cases of SBE as following tooth
extraction have occurred within a few weeks to
a few months after the dental procedure.
• Premedication with various antibiotics is
usually prescribed to prevent the transient
bacteremias
• This prophylactic measures is considered to be
an absolute necessity in patients who have a
past history of rheumatic fever or evidance of
known vascular damage.
Gastrointestinal diseases
• Periodically related
• Include gastric and duodenal ulcers
• Produced experimentally by the injection of
streptococci
• According to some workers, constant
swallowing of microorganism might lead to a
variety of GI disease.
• Low PH of the gastric secretion is an adequate
defense against such infection.
Ocular disease
• Woods evaluated the role of foci infection in
ocular disease and as pointed out by easlick
1) Many ocular disease occur in which no
systemic cause other than the presence of
remote foci of infection.
2) Dramatic healing of ocular disease are
reported to have followed the removal of these
foci
3) Some reports indicate the presence of blood
stream infection in the early stages of ocular
disease
• Iritis may be produced in animal experiments
by the injection of microorganisms, especially
streptococci.
:OBJECTION TO THESE POINTS:
• Can be found to have focal infection, but no
ocular disease.
• Spontaneous cures frequently occur if nothing
is done.
Skin Disease
• To be related to foci of infection
• Only some forms eczema and possibly urticaria
can be related to oral foci of infection
• A few other dermatoses have been ralted to
focus of infection
• Includes
- erythema mutiforme,
- pustular dermatitis
- lupus erythematosus
- lichen planus
-
• If such relationship does exist, the
mechanism is probably sensitization
rather than metastatic spread of
microorganism
Renal disease
• Microorganisms most commonly
involved in UTI(urinary tract infection)
are:
- Escherichia coli
- staphylococci and streptococci
• Of the streptococci, streptococcus
hemolyticus seems to be most common.
• Oral foci of infection play a small role
even when the possibility of
superimposition on a damaged urinary
tract exists.
• Occurrence of metastatic infections
from the mouth to distant bodily sites is
also not very common.