CERVICO-FACIAL CELLULITIS OF DENTAL ORIGIN
INTRODUCTION, DEFINITION : Odontogenic cervicofacial cellulitis (of dental origin) is an infection of the cellulo-fatty spaces (cellulo-adipose or conjunctivo-cellular) of the perimaxillary region and neck, propagated from a septic inoculation whose causal etiology is a tooth. These are soft tissue infections, characterized by their location, severity and progression . They constitute by far the first complication of dental infectious foci and represent the main emergency in Dental Medicine .
Certainly the most frequent cause of these conditions remains the tooth, nevertheless, there are other non-odontogenic causes, which contribute to and even trigger them.
Clinically, the circumscribed (limited) forms are the most frequent, however, although they are rare, the diffuse and diffused (malignant) forms can compromise the vital prognosis.
Diagnosis is based mainly on questioning and clinical examination.
Prevention remains the best way to combat this disease, but the emergence and progress of antibiotics have completely changed the profile of these conditions.
The cure of this pathology can only be possible and complete through adequate medical-surgical therapy: rapid, symptomatological and etiological.
Cellulite can affect both sexes at all ages, but it is much more common in children and young adults.
I. ANATOMICAL BASES AND DATA : the cellulo-fatty tissue occupies the areas of least resistance in different spaces, delimited by the musculo or osteo-aponeurotic insertions on the maxillary and mandibular bone cortices. It occupies the subcutaneous and submucosal tissues on the surface.
1. Composition of the cellular-fatty tissue : this facial tissue is formed of loose connective tissue and blood and lymphatic vessels constituting several anatomical lobules and compartments, communicating with each other.
2. Distribution of cellular-fatty tissue : the different cellular spaces can communicate with each other, making the spread of infection possible; they are divided into several regions:
nasal, orbital, labial, chin, submental, jugal (genial), vestibular, zygomatic fossa, temporal, masseteric, floor of the mouth, supra and submylohyoid), pharyngo-mandibular, parotid, retropharyngeal region.
The palatine region does not contain cellular-fatty tissue, but between the bone and the fibromucosa, subperiosteal abscesses can develop there.
3. Relationships of the apices of the teeth with the neighboring anatomical structures:
3.1. Relationships of the apices with the bony tables : the situation of the dental apices in relation to the tables and the musculoaponeurotic insertions determines the location of cellulitis. Exp: the apex of the upper lateral incisor is closer to the palatine table, hence the high frequency of subperiosteal abscesses caused by the latter.
3.2. Relationship of the apices to the muscle insertions on the maxillary bones: in the vertical direction, the length of the root and the location of the apex in relation to the muscle insertions play a very important role in determining the spread of the infection.
Rhizalized roots of transitional teeth and resorbed roots of permanent teeth often cause localized abscesses at the gum level, called parulias.
II. BACTERIOLOGY : the germs usually involved in orofacial infections of dental origin are multiple (multibacterial infection) and generally reflect the oral flora present.
1. The commensal oral flora : it is composed on average of 70% of aerobic or aerobic-anaerobic bacteria. The vast majority of these germs are found in dental plaque where they live together in perfect symbiotic, physiological coherence, constituting a part of the oral ecosystem.
2. The flora encountered in the cellulite process : during cellulitis, the physiological relationship between the bacteria of the oral flora is reversed. We then observe a majority of strict anaerobic bacteria; among the aerobic germs, there is a predominance of streptococci.
The flora responsible for the cellulite process is therefore polymicrobial and most often mixed aerobic-anaerobic, although sometimes only strict anaerobic bacteria or only aerobic bacteria are highlighted.
III. PHYSIOPATHOLOGY : the entry point for perimaxillary cellulitis is most often a dental infection (pulp gangrene) leading to a periapical complication . Penetration of the infection into the subcutaneous, submucosal cellulo-fatty tissue or the cervico-facial compartments occurs mainly by osteo-periosteal, lymphatic, hematogenous or direct route. Cellulitis developed in this way therefore has the particularity of being deep infections, originating from a periapical lesion, secondarily disseminated to the cellulo-fatty tissues of the face.
The location or topography of the infection depends mainly on five factors: the causative tooth, the thickness of the alveolar bone, the length of the roots, the situation of the apex in relation to the bony tables and the relationship between the site of the bony fenestration and the various muscular insertions of the maxilla and mandible.
Dental or peridental infection reaches the cellular tissue by several routes:
1. The osteo-periosteal route: this is the main route of spread of infection, microorganisms that have reached the periapex cross the bone and the periosteum to reach the bucco-facial cellular tissues.
2. The direct route : during anesthesia, the needle and/or the anesthetic can bring germs into the cellular tissues. The same is true in maxillofacial trauma accompanied by wounds.
3. The lymphatic and venous route : it is found in severe forms, for example in diffuse cellulitis and thrombophlebitis.
IV. ETIOPATHOGENESIS OF CELLULITIS
1. Dental etiology : it corresponds to pulp necrosis. This can have several origins.
1.1. Carious origin
1.2. Traumatic origin (accidental and occlusal trauma)
1.3. Iatrogenic origin : it corresponds to all the practitioner’s maneuvers which can lead to irreversible pulp inflammation: Exp aggressive cutting of teeth and the use of certain harmful biomaterials (thermal conductors, exothermic or toxic setting reaction), anesthesia and dental extractions and even endodontic and periodontal care.
2. Peridental etiology :
2.1. During dental eruption : this is essentially pericoronitis of the mandibular wisdom tooth where the infection can spread to the surrounding cellulo-fatty cells.
2.2. periodontitis, especially deep periodontitis
3. Factors promoting the spread of infection : the factors triggering cellulitis are the bacteria in the oral flora, but there are local and/or general factors promoting the spread of this infection:
3.1. Local factors : for a given tooth, the location of the infection is determined by two major factors:
* the position of the apex relative to the bone table;
* the situation of the apices with respect to the musculo-aponeurotic insertions
3.2. General factors :
3.2.1. The physiological terrain : age does not seem to play an important role in cellulite, however, pregnancy with the hormonal changes it causes can promote the infectious process (acid pH of saliva and immune depression).
3.2.2. The pathological terrain : all pathologies leading to an immune deficiency will promote the appearance or development of cervico-facial cellulitis: diabetes and AIDS.
3.2.3. Medications : certain medications administered for general pathologies or certain treatments instituted when cellulite appears can aggravate the process of diffusion of cervico-facial cellulitis.
* Antibiotic therapy: it can in fact promote the spread of infection when it is absent or when it is unsuitable.
* Corticosteroid therapy and immunosuppressants
* Nonsteroidal anti-inflammatory drugs
* Cancer chemotherapy
3.2.4. Malnutrition
3.2.5. Drug addiction
CERVICO-FACIAL CELLULITIS OF DENTAL ORIGIN
V. CLASSIFICATION OF CELLULITE : Cellulite is classified according to the clinical form:
*depending on the evolution and severity
*depending on the topography (the seat)
*according to the extent (circumscribed or diffuse)
A. CIRCUMSCRIBED CELLULITES
1. ACCORDING TO THE DEVELOPMENT AND SEVERITY : it reflects the development of the condition and includes acute, subacute and chronic cellulitis, non-serious and serious.
1.1. ACCORDING TO THE EVOLUTION
1.1.1. Common forms with common germs
1.1.1.1. Acute cellulitis
* Acute serous cellulitis
* Acute suppurative cellulitis
* Acute gangrenous cellulitis (severe)
1.1.1.2. subacute cellulitis
1.1.1.3. chronic cellulite
1.1.2. Forms with specific germs: they are generally subacute or chronic.
1.1.2.1. Actinomycotic cellulitis
1.1.2.2. Woody cellulite
1.2. ACCORDING TO THE SEVERITY: there are:
* non-serious forms: especially circumscribed cellulitis;
* severe forms: gangrenous cellulitis and diffuse or spread cellulitis (which spreads from the circumscribed cellulitis).
2. ACCORDING TO THE TOPOGRAPHY : perimaxillary cellulitis is rarer and less serious than perimandibular cellulitis.
2.1. In the maxilla : each tooth communicates with several anatomical lodges, the latter therefore give rise to cellulitis in different sectors. The infection can develop either towards the vestibular side or towards the palatal side.
2.1.1. Palatine evolution : the apex of the lateral incisor, the palatine root of the 1st PM and the 3rd molars are located closer to the palatine vault. The infection from these apices therefore spreads across the alveolar bone table and ends up directly under the fibromucosa (region poor in cellular tissue) creating subperiosteal abscesses.
2.1.2. Vestibular evolution : the central incisor and the vestibular roots of the other teeth are close to the external table, the infection will then spread, either by the vestibular route or by the nasolabial route in the anterior region. Cellulitis then bears the name of the infected region.
2.1.2.1. For the central incisor : the infection crosses the vestibular table and progresses towards the upper lip to give either upper labial cellulitis or subnasal cellulitis
2.1.2.2. For the lateral incisor: in the small percentage where the apex of this tooth is closer to the vestibular table, the infection is nasolabial and the edema fills the nasolabial fold.
2.1.2.3. For the canine : due to the length of its root, the infection affects and fills the nasolabial fold and even the subpalpebral region (eye tooth).
2.1.2.4. For premolars and molars : for vestibular roots there are two cases:
* if the apices are located below the upper insertion of the buccinator , a real barrier to the spread of infection, we will have upper vestibular cellulitis . The cheek is swollen, thus erasing the vestibular groove. The vestibule opposite the causative tooth appears red and pasty.
* if the apices of these teeth are located above the insertion of the buccinator , the infection progresses towards the subcutaneous cellular tissue, we will then have high genial cellulitis which can diffuse downwards by overlapping with the low genial.
2.2. In the mandible
2.2.1. Linguistic developments
2.2.1.1. Submylohyoid or submandibular cellulitis : it is mainly the lateral part of the submylohyoid floor (the submaxillary compartment) which is affected. It manifests itself by a swelling adherent to the basilar edge and to the internal table in relation to the responsible molars. The cheek is spared while the sublingual region is edemaciated.
On endooral examination, the vestibule is free, the floor of the mouth is hard and infiltrated and trismus is still present.
2.2.1.2. Supramylohyoid or sublingual cellulitis : the infection moves towards the sublingual space, which is rich in cellular tissue. The functional signs are much more significant and give it a certain degree of severity.
The pain is intense and radiates towards the mandibular angle, towards the ascending branch or towards the ear. The trismus is intense from the outset.
This form of cellulitis manifests itself as a firm and painful swelling, pressed against the internal table and it pushes the tongue towards the opposite side, limiting all of its movements. Phonation and swallowing are disturbed.
2.2.1.3. Cellulitis of the lower wisdom tooth with lingual evolution : several types of cellulitis are linked to the mandibular wisdom tooth either during its eruption or after the mortification of its pulp. We distinguish:
* cellulitis of the base of the tongue
* ESCAT pterygomandibular cellulitis
* pterygopharyngeal cellulitis
2.2.2. Vestibular developments : the apices of the incisors, canines and 1st PM are very close to the external table. Cellulitis related to these teeth always develops on the vestibular side.
2.2.2.1. Cellulitis of the incisor-canine region : it is the anatomy of the muscles of the tuft and the square of the chin that directs the different forms of cellulitis of this labio-mental region. In this region the traumatic origin of pulp mortification is frequent .
2.2.2.2 . Cellulitis related to PM and M: the 1st PM most frequently gives vestibular cellulitis, while the 2nd gives vestibular and floor of mouth infections with roughly equal frequency.
The length of the roots, the position of the posterior teeth will have a fundamental importance in the development of the suppurative collection.
* lower genial cellulitis : the collection develops below the buccinator and is located subcutaneously. On exo-oral examination, a low swelling is observed deforming the genial region and reaching but not exceeding the basilar edge of the mandible. The integuments are often red and edemaciated and palpation is very painful.
The vestibule opposite the causative tooth is often filled with a hard and painful ridge. The floor of the mouth and the internal bony table are unaffected.
* lower vestibular cellulitis : the collection migrates to the side of the external mandibular bony table and above the insertion of the buccinator . Isolated, it manifests itself on intraoral examination by a simple lifting of the vestibular mucosa opposite the causative tooth and neighboring teeth.
2.2.2.3. Complications of the evolution of the lower wisdom tooth : infectious accidents of the lower wisdom tooth are the most frequent. In addition to the lingual evolutions seen above, these infections can also evolve vestibularly.
When the external table is involved, the infection invades the virtual space between the bone and the masseter in the subcutaneous fat panniculus, we will then have masseter cellulitis. The evolution can also extend to the temporal region to give temporal cellulitis.
CHOMPRET ‘s buccinato-maxillary abscess and HIRONDEL or genian cellulitis (with vestibular evolution): This is the migratory abscess of the lower vestibule. It was described for the first time in 1925 by Chompret and Hirondel . It is the result of suppurative pericoronitis of the lower wisdom tooth . . It is located at the bottom of the vestibule in front of the masseter. The starting point of the collection is located at the level of the pericoronal sac of the wisdom tooth. The pus then “slides” along the external face of the body of the mandible and collects opposite the premolars. After a few episodes of retromolar pain, a lower genian swelling forms. The intraoral examination reveals a red swelling, limited behind by the masseter, in front by the depressor muscle of the angle of the mouth (triangular muscle of the lips), above by the edge of the buccinator and below by the basilar edge of the mandible. This quadrilateral of least resistance is in direct contact with the cellular tissue of the genial region. The abscess fills the vestibule, and takes the elongated shape of a club whose end is attached to the mesial and vestibular faces of the hood of the tooth in question. The terminal swollen part is located at the level of the PM. The mucous hood of the wisdom tooth is constantly red, painful at the slightest touch. The pressure of the lower genial swelling causes pus to flow under the mucous hood of the wisdom tooth in question. This is a pathognomonic sign of this migratory abscess. The classic evolution of this abscess is towards spontaneous fistulization of the mucosa, leading to a transient regression of the symptoms.
B: DIFFUSE CELLULITE : these are malignant (serious) cellulitis, these are rare conditions but which remain dangerous despite antibiotics and modern means of resuscitation. They cause general toxic-infectious syndromes with extensive tissue necrosis.
CERVICO-FACIAL CELLULITIS OF DENTAL ORIGIN
VI. CLINICAL FORMS AND DIAGNOSIS OF CELLULITE
1. The diagnostic approach
In Medicine D usual consultation from which everything else will flow.
Making a diagnosis means recognizing the disease based on the symptoms the patient experiences and which the practitioner observes during the clinical examination.
When examining a patient with perimaxillary cellulitis, the main part of the observation is based on the physical examination. Color and warmth of the skin, flexibility or hardness of the swelling, its circumscribed or diffuse appearance, whether or not the general condition is affected. To achieve this, a general outline is required:
* the interrogation
* exobuccal examination : inspection and palpation
* the intermediate examination : it specifies the degree of mouth opening (presence or absence of trismus)
* the intraoral examination : especially the examination of the causal tooth, the vestibule and the floor of the mouth opposite.
Important: percussion of the causative tooth is always painful if the cellulitis is acute.
* the paraclinical assessment (additional examination): it is important to arrive at the diagnosis but it is not always essential and obligatory. It is radiological and biological.
1. biological assessment : it includes blood culture, bacteriological sampling, antibiogram, formula count which shows hyperleukocytosis (increased polymorphonuclear neutrophils), ESR and sometimes C-reactive protein (CRP).
2. radiological assessment : the diagnosis of cellulite is generally clinical.
– The retro-alveolar radiograph and the panoramic scan do not give the diagnosis of cellulitis, but that of its dental origin.
– The injected scanner or computed tomography , constitutes a second-line examination. It allows to carry out an exhaustive extension assessment, to search for the entry point, to characterize the elementary lesions that are the abscess, the cellulitis, the fasciitis, the myositis and the tissue necrosis. The injected scanner is the optimal examination for the diagnosis of cellulitis, especially diffuse.
– MRI and ultrasound may also be exceptionally requested.
The clinical examination leads to the diagnosis, that is to say to recognize the disease, their type according to the evolutionary mode, their topography and their cause after having eliminated the different differential diagnoses.
2. DESCRIPTION AND CLINICAL FORMS OF CELLULITE
A. CIRCUMSCRIBED CELLULITES
1. EVOLUTIONARY FORMS
1.1. Acute forms
1.1.1. Serous cellulitis : This is the initial stage of inflammation of the cellular tissue.
Symptoms: The external manifestations of the condition are easily detectable despite the absence of general signs. The pain is pulsating, stabbing and relieved by analgesics.
After a dental episode or following it, a recent swelling appears filling the furrows of the face, erasing the flat spots and covered with tight, pink skin.
On exobuccal palpation , it is noted that the contact is slightly painful, the swelling is elastic, mobile, hot. The pressure exerted on the lesion does not leave a pit.
On intraoral examination , the swelling raises the mucosa which may be congested in the region where the cellulitis is located, it is very painful to the touch; we can recognize the causal tooth which does not respond to vitality tests. Percussion is too painful.
The progression is towards sedation if the treatment is well conducted, otherwise the condition can progress towards suppuration.
Differential diagnosis : concomitant dental signs allow us to eliminate:
* lymphadenitis
* osteitis (increased dental mobility)
* sialites
* the only delicate diagnosis is with suppurative cellulitis, clinically characterized by the limitation of the swelling and the positive pit; in addition, the intensity of the pain, the local heat and the importance of the general signs are in favor of the latter. Puncture can be useful.
Positive diagnosis: as in all cellulitis, it will be based on the clinical assessment. It must be topographical and must specify above all the evolutionary mode of the infection. The search for the etiology is more than essential.
Example : circumscribed serous cellulitis, nasolabial, caused by 13
1.1.2. Suppurative cellulitis : this is the unfortunate continuation of the previous stage. This is the stage of abscessation, characterized by the circumscribed suppurative inflammation of the cellular tissue, giving rise to a hot collected abscess.
CERVICO-FACIAL CELLULITIS OF DENTAL ORIGIN
Symptomatology:
* general signs : high temperature, fatigue (asthenia), pallor, headaches, etc.
* functional signs : they are marked by pain which becomes throbbing, resistant to analgesics with various irradiations plus insomnia.
* physical signs : they are also important. The patient whose face reflects the feverish state, presents a more or less significant swelling covered by congested tissues. These tissues are tense, shiny and reddish-purple in color. Palpation is too painful; the mass adheres to the above and below underlying planes, it allows a fluctuation to be perceived and it keeps the pit (persistence for a moment of a depression at the pressure point).
The opening of the mouth , which may be hampered by trismus, shows a more or less significant lifting of the external or internal table of the vestibule opposite the causative tooth with infiltration of the floor of the mouth.
Evolution : if untreated or poorly managed at this stage, the condition most often develops into spontaneous fistulization of the skin or mucous membrane or becomes chronic and sometimes even widespread.
Overall, the diagnosis is not difficult to make.
Differential diagnosis : depending on the location of the cellulite, it will be discussed with:
*an infected radiculo-dental cyst
* osteitis
* a stone of the Warton canal
* parotitis
* a subperiosteal abscess in children
* an adenophlegmon
* maxillary sinusitis
Positive diagnosis: it is based on the clinical assessment. Intra-oral and extra-oral radiography can be useful to highlight the causative tooth. In case of doubt, a puncture should be performed.
1.1.3. Gangrenous cellulitis : this is a rare acute lesion. In this form, necrosis is very marked.
1.2. Subacute and chronic cellulitis
1.2.1. Common germs : the starting point is acute, circumscribed cellulitis which has developed either spontaneously or after poorly conducted treatment into fibrosis or sclerosis.
CERVICO-FACIAL CELLULITIS OF DENTAL ORIGIN
Symptomatology
General and functional signs are nil. It is aesthetic concerns, repeated injuries during shaving (men) or warming that push the patient to consult.
*On inspection : a nodule protruding under the skin, rounded, oval or polycyclic in shape, the size of a walnut, is observed. The covering integuments are thin and purplish.
* On palpation : there is no pain or heat; the nodule is firm with sometimes more flexible punctiform areas, it adheres but remains mobile despite the presence of a hard cord which connects it to the area in question.
* Opening the mouth : the gingivo-jugal mucosa is raised by an elongated, renitent or fluctuant mass, pressed against the bone. Trismus is absent.
* Evolution :
Spontaneously , the lesion has no tendency to improve, on the other hand it can worsen:
it can be done towards warming, it is the return to the acute picture; or the passage to the chronicity with the perception by the patient of a core in his cheek, then insidiously a fistula forms. The exit orifice is generally unique, episodically giving rise to a few drops of pus.
* Differential diagnosis : it is made with genial and submaxillary adenitis, with common or specific germs (tuberculosis), with sebaceous cysts, with boils and with cellulitis with specific germs such as actinomycotic cellulitis.
1.2.2. Specific germs: actinomycotic cellulitis
Actinomycotic cellulitis is a rare variety of facial cellulitis that remains difficult to diagnose. It is caused by certain actinomycetes, which are saprophytes of the mouth that enter the body through a caries cavity or by breaking into the mucous membrane. Finally, most often actinomycosis begins with inflammatory accidents of dental origin.
* Symptomatology : the lesions generally begin in the perimaxillary cellular tissue and whatever the location of the lesion, the symptoms and the evolution remain more or less the same.
It is observed in men in more than half of cases and particularly in young subjects with poor oral hygiene.
Most often, the lesion has a clear inflammatory appearance: it is suppurative, progressing towards the skin and not towards the mucous membrane, with ulcerations and fistulas which discharge a seropurulent liquid with yellow grains.
The five classic characteristic signs of actinomycosis are found : pain, trismus, swelling, fistulas and pus containing yellow grains. The general condition is late altered.
* positive diagnosis : direct examination is delicate, classically the presence of yellow grains in the pus is pathognomonic. Sometimes, cultures are necessary to detect actinomycetes and determine the variety.
2. TOPOGRAPHICAL FORMS : depending on the starting point or the region of diffusion of the condition, the clinical picture locally takes on particular forms and various names.
We thus distinguish different types of cellulite.
2.1. Perimandibular cellulitis
2.1.1. Labiomental cellulitis : if the infection develops below the mentalis and lower lip muscles, the picture is that of a mental abscess that can open to the skin. Spread above these muscles gives a lower labial abscess that can open intraorally, at the level of the lower vestibule.
2.1.2. Lower vestibular cellulitis : the collection has migrated to the side of the external mandibular bone cortex and above the insertion of the buccinator muscle. Isolated, it manifests itself on intraoral examination by a simple arching of the vestibular mucosa opposite the causative tooth and neighboring teeth. It may accompany other cellulitis (lower genial, lower labial or chin).
2.1.3. Low genial cellulitis : the collection develops below the buccinator and is located subcutaneously. On exobuccal examination, a low swelling is observed deforming the genial region and reaching, without going beyond it, the basilar edge of the mandible. The deformation is significant, it raises the often red and edemaciated integuments. Palpation, which is very painful, easily reveals a fluctuation. The vestibule, opposite the causal tooth, is often filled. The floor of the mouth and the internal bony surface of the mandible are free.
2.1.4. Cellulitis of the floor of the mouth : a distinction must be made between supramylohyoid cellulitis and submylohyoid cellulitis.
2.1.4.1. supramylohyoid cellulitis or sublingual cellulitis or Ludwig’s angina: this is typical. It corresponds to the spread of the infection above the mylohyoid muscle; the infection moves towards the sublingual space. The functional signs are much more significant. The intense pain radiates towards the mandibular angle, towards the horizontal branch or towards the ear. The trismus is intense from the outset. The cortico-lingual (pelvi-lingual) groove is erased. The swelling is adherent to the internal cortex. The tongue is deviated to the opposite side.
This cellulitis, although limited below by the mylohyoid muscle, can however reach the submandibular region.
2.1.4.2. submylohyoid cellulitis or submandibular cellulitis : this corresponds to the infection of the compartment of the same name. The trismus is immediately significant, hampering the clinical examination and feeding. The exobuccal examination shows a swelling under the mandibular rim, adherent to it, and to the internal mandibular cortex in its lower part. On the intraoral examination, the vestibule is free.
2.1.5. Cellulitis of 38 and 48 : Chompret and Hirondel buccinato -maxillary migratory abscess : See above.
2.2. Perimaxillary cellulitis
2.2.1. Palatine abscess: due to the absence of cellular tissue, the infection immediately leads to a subperiosteal purulent collection, detaching the fibromucosa. The latter, not very extensible, explains the very painful and early nature of this abscess.
On intraoral examination, a palatal watchglass swelling was found opposite the causative tooth.
2.2.2. Upper vestibular cellulitis : the short roots of the molars are located under the upper insertion of the buccinator, a real barrier to the spread of infection. Damage to the connective tissue located between the internal face of the buccinator and the oral mucosa then defines upper vestibular cellulitis. Diagnosis is made by eye and finger. The cheek is swollen in the middle part, the vestibular groove is erased, with the presence of a more or less fluctuating thickening depending on the evolution. The mucosa opposite the causative tooth is red.
2.2.3. High genial cellulitis and nasolabial cellulitis : the PM and the canine have their roots above the insertion of the buccinator muscle. The infection then progresses to the subcutaneous cellular tissue. It lifts the jugal mucosa, which is then called high genial cellulitis. The canine, due to the length of its root and its location, causes nasolabial cellulitis. The cellulitis can go up to the lower eyelid, hence its name “eye” tooth.
2.2.4.: Upper lip and subnasal cellulitis : they are related to the central incisors.
2.2.5. Cellulitis of 18 or 28 : necrosis or pericoronitis of the upper wisdom tooth can develop into upper vestibular cellulitis, high genial cellulitis or a subperiosteal palatal abscess, but also into pterygomaxillary cellulitis which develops behind the tuberosity.
2.3. Complications of circumscribed cellulitis
2.3 . 1. Locoregional complications
2.3.1.1. Facial thrombophlebitis : facial and cerebral thrombophlebitis constitute an extremely rare but very serious complication of the dental infectious process.
NB. Unsightly cutaneous fistulas constitute a chronic locoregional complication following cellulitis.
2.3.1.2. Osteitis, sinusitis, adenophlegmon, meningitis etc.
2.3.2. General complications are dominated by sepsis or septicemia : by definition sepsis is a generalized septic state whose etiology can be dental or thrombotic.
All dental and periodontal foci in contact with the bloodstream are likely to cause bacteremia and therefore septicemia.
Clinically, two distinct situations may occur:
2.3.2.1. Acute septicemia : in this case the temperature is the first sign that appears, it is often very high ( 40°C and more), and accompanied by shivering. Hypothermia is sometimes found.
Headaches, drowsiness sometimes interspersed with episodes of excitement and tachycardia quickly indicate the progression.
The occurrence of such a state of shock has a poor prognosis, even today with the various antibiotics available.
2.3.2.2. Sepsis-pyohemia : in this case the onset is also very rapid and brutal. The febrile peaks correspond to infectious micro-emboli released into the circulation. Secondarily, they are responsible for many systemic and local pathologies:
** OSLERIAN infective endocarditis
** rheumatological manifestations
** ophthalmological manifestations
** neurological manifestations
** pulmonary manifestations etc…
CERVICO-FACIAL CELLULITIS OF DENTAL ORIGIN
B. DIFFUSE CELLULITE
Diffuse or malignant cellulitis can be either secondary to circumscribed cellulitis and we speak of diffuse cellulitis, or diffuse from the outset. Due to its rapid development, it leads early to very serious complications resulting in a toxic-infectious septic shock on a general level with extensive necrosis of the infected tissues, locally. Due to its emergency nature, it requires rapid hospital treatment.
1. Clinical signs
1.1. In general : it is characterized by a toxic infection. The onset is rapid, it is a real infectious shock ( sepsis ). After the appearance of chills, the patient becomes covered in sweat. The face is pale, breathing is shallow and blood pressure is low. In a few hours, diarrhea appears with repeated vomiting. Urine is rare and dark (oliguria). Subicterus sets in. The face becomes earthy, the eyes are sunken. Consciousness is preserved. Meningeal and pleuropulmonary signs may be added. Death is possible at this stage by cardio-respiratory collapse, reflex syncope or hepatic coma.
1.2. Locally : diffuse cellulitis is characterized by rapid and extensive tissue necrosis. Initially, there is a limited, soft, slightly painful but fluctuating swelling.
Very quickly, it spreads and becomes woody hardness. The skin is pale and tight, while the mucous membrane is grayish.
The trismus is tight. Suppuration does not appear until the fifth or sixth day.
The pus, obtained at first in small quantity, is usual: it is greenish in color, sometimes gaseous, containing sphaceous necrotic debris; it then becomes clearer and more abundant.
The muscles and aponeuroses are destroyed, the veins are thrombosed, the arteries are ulcerated and the risks of hemorrhage are major. The edema leads to considerable deformations associated with respiratory disorders (asphyxia).
2. Topographical forms of diffuse cellulite
2.1. Supramylohyoid cellulitis or Gensoul-Ludwic angina : this is septic phlegmon of the floor of the mouth.
2.2. Submylohyoid cellulitis: this is the diffuse phlegmon of Lemaître and Ruppe ; it spreads to the entire floor of the mouth and the cervical region.
2.3. Peripharyngeal cellulitis or Senator’s angina
2.4. Diffuse phlegmon of the face: this is Petit Dutailles phlegmon . Its starting point is the lower wisdom tooth, which causes pterygomandibular cellulitis.
VII. TREATMENT : The treatment of cellulite is medical-surgical. In emergencies, it is necessary to assess:
* the progressive stage (serous, abscessed or diffuse cellulitis);
* localization , in particular severe forms of floor cellulitis, and cervicofacial cellulitis (diffuse);
* the terrain (age and associated diseases);
* clinical severity criteria (dysphagia, dyspnea, trismus, crackles) and biological criteria ( FNS, VS and RCP ).
This clinical and biological assessment makes it possible to decide on hospitalization and the type of treatment, medical, medical-surgical, or even medical-surgical-resuscitation.
Purpose of the processing: the processing is intended to:
* to stop the progression of cellulite and evacuate the suppurative collection if it exists;
* to relieve the patient and cure him by removing the identified cause.
The treatment of cellulitis is first of all preventive (prophylactic), but in the event of an infection being triggered, symptomatic and etiological curative treatment is essential.
Schematically, the treatment of odontogenic cellulitis is as follows:
1. Preventive treatment.
2. Curative treatment
2.1. Symptomatic treatment
2.1.1. Drug treatment
2.1.2. Surgical treatment
2.2. Etiological treatment
2.2.1. Conservative treatment
2.2.2. Non-conservative treatment (extraction of the causative tooth)
1. Preventive treatment : it is essentially based on the prophylaxis of dental caries and therefore involves good oral hygiene and biannual check-ups.
The second step is early treatment of caries and pulp diseases before they lead to cellulitis.
2. Curative treatment : it includes two successive and essential stages: symptomatic treatment and etiological treatment
2.1. Symptomatic treatment : it is both medicinal and surgical
2.1.1. Drug treatment : it will fight against the infection and its consequences (inflammation and pain), it will be represented essentially by the prescription of antibiotics.
* antibiotics : antibiotic therapy will cool the infectious focus, slow down the spread of lesions, without actually stopping it. It prevents the consequences of blood dissemination and allows local treatment to be initiated.
* non-steroidal anti-inflammatory drugs (NSAIDs): their use is not systematic. They must always be stopped 2 to 3 days before stopping antibiotics.
* analgesics : analgesics are symptomatic drugs that act non-specifically on painful sensations, which they alleviate or eliminate without acting on their cause.
* corticosteroids : their main pharmacological properties are anti-inflammatory, anti-allergic, immunosuppressive action. They are used in malignant syndrome or for respiratory disorders due to significant edema.
*anticoagulants : they play an important role in preventing venous thrombophlebitis.
2.1.2. Surgical treatment : this is based on the drainage of the suppurative collection. The prescription of antibiotics should never replace the surgical procedure which remains essential if the lesion is abscessed.
In Oral Medicine , there are two types of drainage (transcanal drainage, non-surgical and surgical drainage) .
In this course we will only cover true surgical drainage which involves the following steps:
* preparation of the material
* disinfection
* anesthesia: local, locoregional or general
* the incision
* the drainage itself
* the dressing + monitoring and control.
CERVICO-FACIAL CELLULITIS OF DENTAL ORIGIN
VIII. THERAPEUTIC CONDUCT: they vary depending on the evolutionary forms.
1. Acute serous cellulitis : without signs of severity, hospitalization is not necessary, treatment includes:
1.1. Oral antibiotic therapy such as Amoxicillin 1g every 8 hours (adult) for a duration of 6-7 days. In case of allergy to penicillins, a Macrolide (Erythromycin 1g 3 times / day or Spiramycin 3 million 2 or 3 times / day) will be prescribed.
1.2. A level 1 analgesic (Paracetamol 1g 3 or 4 times/day “always adult”) or level 2 (Paracetamol + Codeine) if the intensity of the pain requires it.
NB . Pediatric dosages are based on the patient’s weight.
1.3. Local antiseptics in mouthwashes
1.4. Ice packs with skin protection in cellulite with external (cutaneous) development.
NB. only trepanation of the tooth allowing transcanal drainage can be performed in this acute phase.
Conservative or radical treatments with extraction are considered in a second stage after cooling of the lesion (more than a week).
2. Abscessed (suppurative) cellulitis : this is the time for surgery, to flatten and drain the abscess.
2.1. Abscesses with intraoral development : abscesses with intraoral development, of small volume, vestibular and especially palatine, can be incised under contact anesthetic, more or less supplemented by local anesthesia.
The incision with a cold blade 15 or 11 is made at the highest point (the highest or the summit) of the collection, long enough ( about 1 cm) to introduce a closed Kocher clamp, then it is opened and carefully removed into the collection. This action facilitates the evacuation of pus and collapses any septa. Rinsing is carried out with a syringe, with diluted Betadine or even hydrogen peroxide followed by neutralization always rinsed with physiological serum.
In the case of a large abscess, the flattening is sometimes carried out under general anesthesia. Drainage is ensured by placing a Delbet blade (drain), fixed to the mucosa with a stitch. The Delbet blade prevents the wound from closing too early, thus allowing drainage and daily irrigations with a mixture of half Betadine and half physiological serum. It will be removed after 48 hours.
2.1.1. Sublingual lodge abscesses : they are incised near the internal mandibular cortex .
2.1.2. Chompret-L’Hirondel abscesses : they are incised from the vestibular region opposite the PM up to 38 or 48 .
2.2. Abscesses with exo-oral cutaneous developments of the lower genitourinary system: they are incised at the cutaneous level. The incision is limited in its depth ; it is only cutaneous and limited in its length ( 1 to 2 cm ). It is located in the most sloping part of the swelling . Drainage by Delbet blade is associated. A dressing can be put in place and changed every day ( 5 or 6 days ).
3. Acute diffuse cellulitis : parenteral antibiotic therapy is started immediately after bacteriological samples are taken, without the latter delaying its implementation. A 3rd generation cephalosporin-type beta-lactam can be used , sometimes combined with an imidazole (flagyl), or a more “classic” antibiotic therapy such as amoxicillin-clavulanic acid (Augmentin * ). In the event of signs of severity, and in order to obtain a response, an aminoside can be combined. This antibiotic therapy is started for a period of more than 15 days . Any septic shock is prevented or corrected. The patient is usually hospitalized in the intensive care unit. Surgery consists of a wider flattening-drainage with multiple Delbet blades .
CERVICO-FACIAL CELLULITIS OF DENTAL ORIGIN
CONCLUSION
Odontogenic cellulitis nevertheless remains commonplace in its etiology, but formidable in its progression and can even put the patient’s prognosis at risk.
They require great attention and early and adequate management.
The treatment of cellulite necessarily combines three fundamental actions:
* preventive treatment
* symptomatic treatment
* and etiological treatment
Our role will therefore be to prevent these conditions and treat them appropriately, always bearing in mind the dramatic developments that they can lead to in certain cases.
END
CERVICO-FACIAL CELLULITIS OF DENTAL ORIGIN
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Composite fillings are discreet and durable.
Composite fillings are discreet and durable.
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