Definition

Inflammatory lesions of the maxillary and the

mandible determined by the penetration of the
pathogen agent
Periostitis – inflammatory reactions of the outer
coating of the bone (periosteum)

Osteitis – inflammatory reaction of the cortical bone

and the alveolar process
Osteomielitis - extensive infection that that
includes all bony structures
Periostitis
 High frequency in children and
adolescents
 High frequency in the mandible,
especially in the molar area
 Frequent associated with
hypermineralization of the bone and
even with bone deformation
Etiopathogeny
 Microbian, odontogenic – periapical septic
processes, periodontal or pericoronaritis
(complications of the dental eruption)

 Chemical trauma

 Physical trauma – tempestuous surgical

interventions carried out on bone and/or soft tissue
Histopathology
 Odontogenic periostitis appears following
a vasodilation with periostal thickening,
serous and purulent discharge that
elevate the periosteum.

 Posttraumatic periostitis appears following

a subperiostal hematoma that can
suprainfect or following the osteogenetic
action that produces neo-aposition seen
macroscopically as bone deformation.
 Clinically
a.) Acute periostitis
Subjective: - severe spontaneous pain
-pressure determines exacerbated pain

Percution; - axial sensitivity

- lateral sensitivity
b.) Chronic periostitis
Subjective : - moderate spontaneous pain
- palpation determines exacerbated pain
Palpation: bone deformation
Radiographs – without relevant modifications with the exception of
displaying the odontogenic cause/factor
 Positive and differential
diagnosis

 Based on the anamnesis, etiopathogenesis

simptoms and radiographs
 Diff. diagnosis – perimaxillar or perimandibular
infections
- deforming chronic osteomielitis
- tumours that determine hiperplasia
(peripheral osteoma, cementoma, fibrous
dysplasia)
Treatment
 Acute microbian periostitis – incision,
drainage and treatment of the cause
 Chemical and physical periostitis that
have an uneventful evolution: treatment of
the cause, wait and see, follow up, boost
the immune system.
Osteitis
 Infection localised and the level of the
cortical maxillary or mandibular bone
 Osteitis of the alveolar process is
known under the definition of alveolitis
etiopathogenesis - osteitis
 Direct (odontogenic, open trauma)
 Odontogenic:
 Dental pulp gangrene
 Cystic granuloma/radicular cyst
 Dental extraction
 Periosseous wunds
 Third molar pericoronaritis

 Open trauma:
 Open fractures
Histopathology

 The acute form is characterised by the

presence of pus, cellular debris,
necrosis, pmn cells diapedesis and
fibroblasts and the edge of the process
 The chronic form is characterised by
hipocellularity, decrease in the number of
newly formed capillaries and growth in
the number of colagen fibers
 Chronic sclerosing
form presents
osseus
condensation
produced by
inflammatory
stimulation of the
osteoblastic activity
in the area
Clinically
1. Acute suppurating osteitis
The debut is associated with acute apical periodontitis
- sharp pain
Subjective: - pulsating pain
- the tooth may seem elevated
Palpation: - small local and painful tumefaction
- inflammatory reaction of the lymph nodes
- trismus (in case of involvement of the last
molars)
RX: - radiotranslucency around the apex of the tooth
involved with diffuse margins, inhomogeneous
Differential diagnosis
In the acute state:
- Acute apical periodontitis
- Chronic periapical infection infection
reentering the acute phase

In the chronic state

- Chronic periapical infection
Differential diagnosis
 Radiological a difference is seen
between the osteolytic process witch is
diffuse, and the radicular cyst,
homogeneous and well circumscribed
Evolution and treatment
 Favorable evolution if the cause is
treated
 Left untreated it can complicate with
diffusion of the infection in the
perimaxillar and perimandibular soft
tissues.
 The treatment in conservative,
endodontic and endodontic surgery
 In case of conservative treatment failure,
dental extraction is the elective treatment.
OSTEOMYELITIS

Definition – extensive infectious process that

involves all bony structures
Classification (LASKIN):
-SUPURATIVE – ACUTE
- CHRONIC
-NONSUPURATIVE - chronic sclerosing
osteomyelitis - osteomyelitis Garre
-Chronic speciffic
*particular forms – post chemical necrosis
- electric
- irradiation.
 Etiopathogenesis :
- 50% of bony infections ale localised at
the maxilla and the mandible:
- teeth
- anatomic vicinity relationships
- gingival mucosa adherence
- mand>max:
- bony structure
- terminal type circulation
- mandibular canal
- third molar
 MICROBIOLOGY:
- Staphylococcus aureus
nonpigmented

- Staphylococcus haemolyticus
- Streptococcus pneumoniae
- E.Coli.
 WAYS OF PENETRATION:
I. Direct:
- Acute apical periodontitis.

- Chronic apical infections reentering an

acute phase
 WAYS OF PENETRATION
I. Direct:
- Dental inclusion

- Post extraction wounds

 WAYS OF PENETRATION:
I. Direct:
- Maxillary or mandibular fractures
teeth present at the fracture site

- Infection source in the vicinity

 WAYS OF PENETRATION:
II. Indirect- hematogenous
- primary infections
- infecto-contagious disease

- Lymphatic
Factors favoring infection: immune
reaction….immune suppresion

 DEBUT: bone marrow=> cancellous bone=>compact bone=>

periosteum
 PATHOLOGY– 4 phases

1. Bone congestion

2. Bone suppuration

-> ->

Microvascular Medullar Periostal

section section section
 Pathological anatomy
3. osseous necrosis squestrum - fistula

4. Osseous repair

- internal
- external !!~ form. pseudotumoral
 SUPPURATIVE OSTEOMYELITIS

 ACUT:
A) Debut: HISTORY – dental
+ systemic disorders => Hematogenous Osteomyelitis .
B)The clinical picture depends on the anatomico-pathological phase
I. DEBUT – osseous congestion:
 Subjective: local- pain general- F~40°
- swelling - shiver
- trismus -malaise
- functional disorder
 Objective: -exooral: I - swelling
- teguments
- trismus
P - pulping
- sensibility
- osteo-periosteal thickening
-endooral: I –oral mucosa - congestion
- periosseous notches – wiped off
- interdental papillae- edema
P- painfull- teeth become mobile
- osteo-periosteal thickening
 PARACLINICAL:
1) Blood tests :- ESR(ERYTHROCYTE
SEDIMENTATION RATE )>
- leukocytosis…. neutrophilia
2) Bacteriological test
3) Rx.
II. Disease state phase supuration + osseous necrosis
 Subjective: - general – remission
- pain <

 Objective: - exooral I- abscess --- fistula ( pus)

- swelling <
- swelling:
*max. - sinus max. => maxillary sinusitis
phenomena
- infraorbital N. => paresthesia/ anesthesia
*mand. – inf alv. N. => VINCENT D’ALGER S.
P – fistula patency

- endooral I “+”fistula
P – teeth mobility >>
- osteo-perosteal thickening
- vitality tests ”-”
 PARACLINIC:

* Scintigraphy:
- ”cold” zones

* Biopsy

* CT
A. SUPURATIVE OSTEOMYELITIS. –STATE PHASE
*Radiography: - first 6-8 days: ~ scintigrafia
- “stained bone” “bread crumb”

-“ sequestrum” sarcophagus
.

III. REMISSION PHASE  OSSEOUS REPAIR-

Improved symptoms
- Evolution – osseous regeneration

C) DIAGNOSTIC – Clinical ex
- rx.
- bact. ex.
D) Dif. Dg. – Cortical osteitis

- periosseous suppuration
 E) Evolution: depends on the organism
reactivity

- Chronic --- rebound

--- pseudotumoral proliferation
- a-la-long treatment
F) Complications:

- abscess

- diffuse suppuration
F) Complicaţii:

- Orbital suppuration

- Suppuration of the maxillary sinus

F) Complicaţii:

!!! - septic metastases

F) Complications:
- pathological bone fractures
F) Complications:
- TMJ disorders

- Facial asymmetry
CHRONIC OSTEOMYELITIS
-usually in childhood; eruption of decidous teeth- more
frecvently

A) ETIOPATHOGENITY:-subviral bacterial flora

-consequence of acute suppurative
osteom.

B) CLINICAL PICTURE : Subjective: debut- mild

general- discomfort
facial asymmetry gradual
CHRONIC OSTEOMYELITIS

B) CLINICAL PICTURE:
Objective: I -swelling ; fistula
P- osseous thickening

Rx: radioopacitaty wiht

radiotrasparency

C) POZITIV Dg : clinical and radilogical exam

D) Dif Dg. :- fibrous dysplasia

- specific osseous infection

Maxillary chists
D) Dif. Dg.
- Osseous benign tumours

Osseous malign tumours

E) EVOLUTION- LONG TERM

F) COMPLICATIONS:
-infectious:- periosseous suppuration of the soft
tissues
F) COMPLICATIONS:
*infectious:
- tromboflebitis s. cavernous

- pulmonary suppuration

- septicemia
F) COMPLICATIONS:
-osseous:- pseudartrosis
F) COMPLICATIONS:
*osseous:
- pathological bone fractures

Facial asymmetry

Mandibular constriction
F) COMPLICATIONS:
*osseous:
- oro-nasal fistula

Oro-antral fistula
TREATMENT
 PROPHYLACTIC
 CURATIVE
*MEDICAMENTOUS: AC O.- Penicilina
CR O.- AB gen IV !! Aggressive
treatment
*SURGICAL:
AC O..- objective…
- means - Sequestrectomy - perle
genta perls
CR O.. Aggressive treatment– objective..
- means: corticotomy

 Repair-sequelae
 GARRÉ'S SCLEROSING
OSTEOMYELITIS
= inflammation – periosteal thickening+ neoformation bone deposition;
- Young patients
A) ETIOPATHOGENY: stafilococ aureus+ causal tooth
B) CLINIC: I- facial asymmetry, swelling P:- firm consistency
- Celsius signs -pain- caract.
Rx- osseous thickening intermittent
GARRÉ'S SCLEROSING
OSTEOMYELITIS
C) Dif. Dg..- periostitis
- infant hyperostosis CAFFEY
- fibrous dysplazia
- osseous malign tumours

D) TREATMENT:- Dental extraction

- curettage
NEW BORN OSTEOMYELITIS
- Etiop. Staf. Aureus

- Clinical pic.: sudden debut

st gen-
- exooral I: local- genio- palpebral swelling
- endooral I: fistule
Rx- after 10 days – osseous demineralization

- Treatm: sequestrectomy + removal of affected deciduous

teeth
- Sequelae: max development
eyeball mobility
Dental management of
patients treated with
bisphosphonates
 What are biphosphonates(BF)?
• Structural analogs of anorganic pyrophosphates, utilized for
reducing the osseous resorbtion sau or for ectopic calcifications;
• Rezistent to enzymatic hydrolysis;
• 2 Forms- with and without amino- structure ;
• Administration: iv and orally.
 Istoric
• Au fost cunoscuti de la sfarsitul sec.
XIX (Germania 1865), utilizati ca
inhibitori ai coroziunii in industria
textila si cea a uleiului;

• In medicina inca de la inceputul

secolului XX au fost recunoscuti ca
factori declansatori in boala
profesionala a minerilor din minele
de fosfor sau a lucratorilor in fabricile
de chibrituri (fosfor alb);

• In medicina dentara analogii

pirofosfatilor au fost utilizati ca
agenti antitartru in pastele de dinti
sau radionucleotide specifice osoase
(Technetiu 99m metilen difosfonat).
Marx R.E: Oral and Intravenous Bisphosphonate-Induced Osteonecrosis of the Jaws. History, Etiology,
Prevention and Treatment. Quitessence Books, 2011.
 Way of action

Marx R.E: Oral and Intravenous Bisphosphonate-Induced Osteonecrosis of the Jaws. History, Etiology,
Prevention and Treatment. Quitessence Books, 2011.
 Way of action
Inhibit osseous resorbtion, also the turnover-ul and osseous
regeneration:
•through inhibition/cellular death of osteoclasts;
•Death of osteocyte leaving behind non-vital bone;
•Secondary death through BF, adds mineral matrix to the bone
structure=> hipermineralization -> osseous sclerosis seen
radiologically

Marx R.E: Oral and Intravenous Bisphosphonate-Induced Osteonecrosis of the Jaws. History, Etiology,
Prevention and Treatment. Quitessence Books, 2011.
 • Farmacokinetics
The accumulation of BF in the mineral matrix can not be avoided
because of the repeated doses during the treatment plan , the long half-life
of the drug ( 11 years) and the unique removal of bisphosphonates from the
bone structure through an osteoclastic process
per os adminisration:
•0,64% absorbed in the small bowel:
•30-40% renal excretion=>
•only 0,50% of the dose reaches the bone
IV administration:
•Direct disponibility;
•Rapid skeletal accumulation;
•High accumulation dose.
 Farmacokinetics
Tropism for maxillary bone
Favorable Factors:
• The alveolar process remodels itself
with a rate 10x > then tibial bone,
5x > then manibular bazal bone =>
• High concentrations BF in the
alveolar process
• The alveolar bone is dependent of
the resorbtion/osteoclastic
remodeling for repairing the wear of
masticatory function;

Dixon R.B et al: Bone turnover in elderly canine mandible and tibia. J. Dent. Res. 1997, 76:336.
• Because of the impossibility to remodel the lamina dura,
biphosphonates accumulate determining hypermineralization wich
represents a PATHOGNOMONIC SIGN for osteomyelitis induced by
biphosphonates
 Farmacokinetics
Why the jaw bone?

The accumulation of a sufficient dose of BF:

• Trauma(prosthetic decubitus, extrations, surgical treatment

etc.) determines the need for repair wich is not possible
with the lack of osteoclasts => osseous necrosis;
• Afterwards the bone necrosis will determine mucosal
dehiscence and the bone will be exposed in the oral cavity.
Medical indications

Marx R.E: Oral and Intravenous Bisphosphonate-Induced Osteonecrosis of the Jaws. History, Etiology,
Prevention and Treatment. Quitessence Books, 2011.
 Medical indications

Osteoporosis

Neoplastic osseous metstasis

Paget Disease
 Biphosphonates related osteonecrosis of the jaw
(BRONJ)
The presence of exposed maxillary or mandibular bone in the
oral cavity, for more than , on a pacient who is treated or
undergone a treatment with biphosphonates and didn’t have
any radiotherapy

Ruggiero S.L et al, Task Force on Bisphosphonates-Related Osteonecrosis of the Jaw: American Association of Oral and Maxillofacial
Surgeons position paper on bisphosphonates-related osteonecrosis of the jaw - 2009 update. Aust. Endod J 2009, 35 (3), 119-130.
BRONJ administered iv

Dental comorbidities:
• Periosseous absceses;
• Active periodontitis detrmines
intraosseous inflammation
similar to occlusal trauma
which needs bony repair ,
impossible in this case. Thus
bony necrosis will develop.
 BRONJ iv administration

 Triggers:
 Surgical trauma or osseous inflammation
The risk of developing BRONJ through
therapeutic procedures :
• 25% spontaneous;
• 75% dental procedures:
• 36% extractions;
• 9,2% periodontal surgery;
• 2,6% dental implants insertion;
• 0,7% apical surgery.

Marx R.E: Oral and Intravenous Bisphosphonate-Induced Osteonecrosis of the Jaws. History, Etiology,
Prevention and Treatment. Quitessence Books, 2011.
 BRONJ iv administration
Clinical staging- depending on :
•The degree of bony exposure on a hemiarch;
•Rx evaluation of bony resorbtion ;
Clinical stages:
•Stage 0 –bone impegnated with BF without bone exposure;
•Stadiul I – bone exposed on a hemiarch or less, the
osteolisis doesn t go beyond the alveolar process
•Stadiul II – bone exposed on 2 or more hemiarches, the
osteolisis doesn t go beyond the alveolar process
Stadiul III – the osteolisis overcrosses the alv. proc. ,
produces pathologic bone fracture/sinusal implication/
cutaneous fistula Marx R.E: Oral and Intravenous Bisphosphonate-Induced Osteonecrosis of the Jaws. History, Etiology,
Prevention and Treatment. Quitessence Books, 2011.
 Intravenously bisphosphonates treatment
induced maxillary osteonecrosis

Stade 0 - os
impregnat cu BF
permeated bone,
without bone
exposure.
Only Rx signs
f
Intravenously bisphosphonates treatment
induced maxillary osteonecrosis

Stade I – exposed bone

on one hemiarch or less,
the osteolysis doesn’t
exceed the alveolar
process
Intravenously bisphosphonates treatment induced
maxillary osteonecrosis
Stadiul II – one ore two hemiarch exposed
bone, the osteolysis doesn’t exceed the
alveolar process.
Intravenously bisphosphonates treatment induced
maxillary osteonecrosis
Stade III - the osteolysis
exceeds the alveolar
process, leads to
Pathological bone fracture
Maxillary sinus pathology
Cutaneous fistula
 Intravenously bisphosphonates treatment
induced maxillary osteonecrosis

RISK EVALUATION:
Radiological examination:
•Lamina dura sclerosis;
•Periodontium enlargement.
 IBTMO prevention in iv BF
treated patients
BEFORE BEGINNING THE BF THERAPY:
• close cooperation between oncologist and dentist / OMF
surgeon;
• Guide of oncological patients in the dentistry / OMF surgery
for examination and rehabilitation;
• The postponing initiation of BF therapy for 2-3 months (if
possible) for recovery and healing;
• If delays are not possible, restoration begins anyway, with
ITBMO being installed more frequently after 3 doses (3
months);
• For patients who do not require surgery for rehabilitation,
BF therapy should not be delayed.
Marx R.E: Oral and Intravenous Bisphosphonate-Induced Osteonecrosis of the Jaws. History, Etiology,
Prevention and Treatment. Quitessence Books, 2011.
 IBTMO prevention in iv BF treated
patients
ORAL CAVITY CLEANSE:
Scaling, oral hygiene, oral hygiene training
extraction of non-recovering teeth from which they have priority:
massive coronary destruction, periapical pathology, periodontal
disease.
Odontectomy of teeth included superficially; it is not for the
profoundly included teeth!
Periodontal disease treatment
Endodontic therapy;
Restoration of dental caries;
Eliminating occlusal trauma;
Proprosthetic treatment of the bone support (torus);
dental implants are not indicated!
Marx R.E: Oral and Intravenous Bisphosphonate-Induced Osteonecrosis of the Jaws. History, Etiology,
Prevention and Treatment. Quitessence Books, 2011.
 IBTMO prevention in iv BF treated
patients
• DURING BF THERAPY:
Careful examination of the oral cavity for detection of possible lesions by
IBTMO;
Rx Examination for Detection of: radiological signs of IBTMO, inflammatory
lesions of the maxillary bones, osteolysis.
MAIN PURPOSE: Obtaining / maintaining optimal dental / oral health to
prevent IBTMO.
Avoiding, as far as possible, any surgical intervention: extraction, periodontal
surgery, dental implants, prosthetic system, apex resections, etc.
In case of irrecoverable teeth through crown destruction there will be
performed endodontic treatments, coronary amputation, not extraction!
In the case of periodonthic teeth with I or II degree mobility- immobilization, not
extraction!
In the case of periodonthic teeth with IIIrd mobility, abscesses, antibiotic
protection extraction - necessity solution;
If the extraction takes place the bone will be discovered- what the patient should
be informed about!
 IBTMO prevention in iv BF treated
patients

DURING BF TREATMENT: covering polishing

• Scaling/ oral hygiene – brushing, carious lesions, prosthetic treatments
and any other non-invasive procedures can be performed and are
required to maintain dental / oral health.
• The existing periodontal disease- there will be performed only non-
surgical treatments: supragingival scaling, chlorhexidine 0.12% oral
wash.
• Antibiotic treatments - if necessary.
• In case of occlusal trauma, selective polishings will be performed.
• Careful monitoring of mobile / mobilizable prostheses - is necessary to
detect possible decubitus;
• In cases where recoverings are needed, they will be silicone-lined.
 IBTMO prevention in iv BF treated
patients

BEFORE THERAPY INITIATION:

• Close cooperation between medical specialties and
dentist / OMF surgeon;
• Initial assessment of dental / oral status;
• Oral cavity traeatments - just like in iv administered BF;
• There is enough time for recovery - significant risk from
ITBMO - after 2 years;
• Implant therapy is possible:
• There is a risk but low (Grant B.T. et al., 2008, Bell B. M.
et al, 2008, Bedogni A. et al., 2010);
• Patient information and explicit written consent of the
patient.
 ITBMO treatment in iv
administered BF

• 25% of the ITBMO is spontaneous, despite

prophylactic measures;

• iInforming the patient about the disease;

• Coworking with the treating physician;

• Treatment according to the clinical stage.

Marx R.E: Oral and Intravenous Bisphosphonate-Induced Osteonecrosis of the

Jaws. History, Etiology, Prevention and Treatment. Quitessence Books, 2011.
 ITBMO treatment in iv
administered BF

The exposed bone is not problematic:

it does not hurt - it is denervated;
but becomes symptomatic by
infection;
THERAPEUTICAL DESIRES:
prevention and control of local
infection;
accepting the presence of the
denuded bone.

Marx R.E: Oral and Intravenous Bisphosphonate-Induced Osteonecrosis of the Jaws. History, Etiology,
Prevention and Treatment. Quitessence Books, 2011.
 ITBMO treatment in iv
administered BF

STAGE 0:

No clinical lesions, only Rx signs;

Only PROFILACTIC MEASURES are

required
 ITBMO treatment in iv
administered BF
STAGE I AND II:
The exposed bone does not require therapy. Oral wash with 0,12%
chlorhexidine or application of bioadhesive ointment with antibiotics for
protection can be performed (Rotaru H., Dinte E.);
 ITBMO treatment in iv
administered BF

STAGE I AND II:

In the case of a local infection, oral lavage with 0.12% chlorhexidine
and ATB treatment by general route will be performed
 ITBMO treatment in iv administered
BF
STAGE III:

Palliative treatment - similar to Stage I or II:

Oral lavages with 0,12% chlorhexidine;
ATB treatment by general route;
Surgery:
Extended resection of alveolar proc.;
Segmental jaw bone resection.
Bone Reconstruction:
Microsurgical flaps may be used but they present a risk of tissue
necrosis
Reconstruction with titanium bar;
Without reconstruction.
ITBMO treatment in iv
administered BF
ITBMO treatment in iv
administered BF
ITBMO treatment in iv administered
BF
 ITBMO treatment in iv
administered BF

INTERRUPTION OF THERAPY WITH BF ADM. IV

It can only be done by the oncologist!
The necrotic bone does not detach after BF interruption;
BF> 11 years life;
IT IS NOT MANDATORY IN ITBMO TREATMENT !!!
BF can be and must be discontinued if it is no longer
necessary for metastatic control!
 ITBMO treatment in iv
administered BF

• Orally administrered ITBMO is less extensive (often only

Std I or II);
• responds well to BF administration interruption;
• positive diagnosis of the affection;
• working with the prescribing physician to discontinue BF
for one year or to replace it with alternative medication;
• Do NOT make bone debridement in the initial phase =>
disease extension!

Marx R.E: Oral and Intravenous Bisphosphonate-Induced Osteonecrosis of the Jaws. History, Etiology,
Prevention and Treatment. Quitessence Books, 2011.
 ITBMO treatment in iv administered
BF

Prophylaxis of soft tissues infection either anti-inflammatory and

ATB treatment is performed (Std I and II);
After 6-12 months spontaneous detaching occurs;
Sequestrectomy is practiced only when the detached fragment
is clinically mobile and clearly visible radiological !!
Healing is then spontaneous, with epithelial covering;
After healing, stopping BF (if not needed) or restoring BF
therapy in discontinuous therapy (2 years / 1 year)
Upon completion of the recovery, the patient will be placed in a
prosthetic rehabilitation program.
ITBMO treatment in iv administered
BF
ITBMO treatment in iv
administered BF
 Nonspecific cervicofacial
inflammatory lymphadenitis
Characteristics of the cervicofacial
lymphatic network

 Numerous ganglion groups witch drain the

lymph from well individualized teritories

 Lymphatic vessels cross each other

Lymphatic drainage of oral
and maxillofacial structures
 Mastoid lymph nodes
 Parodit lymph nodes
 Buccal lymph nodes
 Submandibular lymph
nodes
 Submental lymph
nodes
 Tonsilar
(jugulodigastric) lymph
nodes
 Lateropharingeal lymph
 Occipital lymph
nodes
 Mastoid lymph
nodes
 Parotid lymph
nodes
 Submandibular
lymph nodes
 Submental lymph
nodes
 Parapharingeal
lymph nodes
 Tonsilar lymph
nodes
 Superficial cervical
lymph node chain
 Deep cervical lymph
node chain
Etiopathogenesis
 Dental, periodontal and bone inflammatory
processes
Etiopathogenesis
 Gingivostomatitis
 Tonsilar inflammatory processes
Etiopathogenesis
 Inflammatory lesions of the skin –
piodermitis/furuncles
 Congestive phase:

 Reversibility
 Chronicization
 Suppuration
Symptoms
 Suppurative
phase:

 Healing
 Extension in a
certain space
Acute submandibular
lymphadenitis
 Nodular debut
 The mandibular base is difficult to palpate
 Stretched out skin
 Oral vestibule and floor of the mouth
remain unmodified
 Moderate or absent trismus, dysphagia
Acute submandibular
lymphadenitis
 To find the cause
we will examine the
teeth, tonsils and
maxillary sinus
Acute submandibular
lymphadenitis
 The stretched out
skin can present o
congestive zone at
the level of the
maximum swelling
where a fluctuating
area can be
perceived.
Differential diagnosis of the
submandibular space abcess
 Diffuse tumefaction
 Alteration of the
floor of the mouth
and the oral
vestibule
 Dysphagia
 Intense trismus
(locked jaw)
Acute lithiasic sialadenitis of
the submandibular gland
 Signs of salivary
retention
 Congestion of the
sublingual crest
 Swollen salivary
gland
 Radiologic
Chronic adenitis
 Swollen lymph nodes, firm consistency,
mobile
 Without periadenitis, painless
 Without alteration of the general state of
health
Differential diagnosis
 Specific adenitis
 Bartonellosis (cat-scratch disease, trench
fever)
 Toxoplasmosis
 Besnier-Boeck-Schauman disease
 Leucosis
 Malignant tumours of the lymph nodes
 Hodgkin disease
Satelite metastatic adenopathy
Infectious mononucleosis
 Submandibular and
laterocervical
lymphadenopathy
 Stomatitis type
lesions of the
mucosa
 Monocitosis
Submandibular gland tumours
 Pleomorphic
adenoma
Chronic lymphadenopathy- AIDS
 Kaposi’s sarcoma
Treatment
 In the initial phase,
causal,pharmaceuti
cal treatment
 Incision, drainage
 Chronic adenitis--
vaccines, physical
agents, suppression
of the entrance gate
PERIMAXILAR CHRONIC FISTULA
Etiology
 Dental septic processes
 Lymphadenitis
Etiology
Location
 Maxilla- rare
 Mandible- menton, lower buccal region
Clinical signs
Radiological
Submandibular fistula- after
extraction of 3.6
Differential diagnosis
 Salivary fistula
 Lower lip fistula-the
result of
coalescence
disorders
Differential diagnostic
 Fistula of the
thyroglossal canal
Chist of the thyroglossal canal
Branhial Chists
 laterocervically
Treatment
 It adresses the causal factor, the fistula
togheter with the fistulous canal have to
be excised
 It uses contrast substance
 thyroglossal canal fistula is difficult to
excise because of the fragile and thin
membrane
Specific infections of soft tissues
and jaw bones

Syphilis
Tuberculosis
Actinomicosis
Primary syphilitic ulceration
 Primary Syphiloma
of the lower lip
Primary Syphilis
 Ulcerated mental
primary syphilis
Sifilisul primar
 Hypertrophic
primary
 syphilis
Secondary stage
 Sifilide
Tertiary stage
Gumma,Tubers
 Syphilitic gumma
palatal ulcerated
Maxillary bone
 Circumscribed Syphiloma
 Syphilitic hiperostosis
 Gumma
 Diffuse Syphiloma
Treatment
 Surgical or prosthetic
 Small defects–plasty
 Extensive palatal defects- simple plate or
obturator
Tuberculosis
 Primary tuberculosis
 Secondary tuberculosis
Primary tuberculosis
Primary complex

Ulceration
Adenopathy
Secondary tuberculosis

 Ulceration
 Tuberculosis goma
 Tuberculosis lupus
Tuberculosis goma
 Gomas located in
the laterocervical,
submandibular and
prebreastbone area
Tuberculosis lupus
 Ulcerated
tuberculosis lupus
of the nose and
palat cleft
Tuberculosis lupus
Nose tuberculosis
lupus with a
scarring scar
Tuberculosis lupus
 Plane tuberculosis
lupus with relapsed
tubercules
Treatment
 General specific for the bacillus infection
 Surgery- for the sequelaes
Actinomycosis
 Subacut either chronic evolution infection
 Different stades of development
abscesess
 Mostly affects the soft tissues
Actinomycotc node
 Central area
 Mononuclear cell layer
 Peripheral layer
Clinical signs

 Debut- acute perimaxillary suppurations

 Status period- tough-woody tumefactions
 abscesses in different stades of evolution
 The general condition is not affected
Positive diagnosis

 Clinical and laboratory

 Microbiological examination
 Actinolysate intradermoreaction
Differential diagnosis
 Perimaxillary abscesses
 Osteitis, oeteomyelitis
 Cervicofacial dermatosis
 Pox tuberculosis
Treatment
 Surgery – abscesses opening and
evacuation
 Iodine, antibiotics - penicillin G,
tetracycline, metronidazole intravenous
administration