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Science, Technology and Medicine open access publisher.Publish, read and share novel research. Non-Odontogenic Oral and Maxillofacial InfectionsPetr Schutz1 and Hussein Hassan Hamed Ibrahim1[1] Al-Adan Dental Center, Al-Adan Hospital, Ministry of Health, State of Kuwait1. Send Home Our method Usage examples Index Contact StatisticsWe do not evaluate or guarantee the accuracy of any content in this site.
Clinical presentation of acute postseptal orbitocellulitis with chemosis, proptosis and ophthalmoplegia.
IntroductionWhile odontogenic infections are daily encountered in dental and oral and maxillofacial surgery practices, some practitioners may be unfamiliar with the wide range of other infections of diverse etiology, some of them relatively uncommon, or even rare. Note progression of infection to right paranasal area.Furuncles can occur anywhere on hairy skin.
It is usually a superficial infection of the moist areas of the body and is generally caused by candida albicans.
Asian countries,[18] United States (including Hawaii), Canada ,[19] and Scotland)[20] due to bacterial resistance.
The outcome of the infection can be mouth ulcers, tongue ulcers, mouth pain, tingling mouth, dental disorders, Gingivitis, throat infection or tongue pain.
32y old female underwent cheek augmentation by injections of unknown substance in a cosmetic salon 3 years earlier. Abscessed submandibular lymph node in 4y old boy with a 10-day history of submandibular swelling treated by amoxicillin. 35y old male presented with a 6-month history of lasting recurrent abscesses in the left submandibular area.
36y old man had a 3-month history of lasting submandibular swelling not responding to antibiotic therapy.
40y old female patient presented with painful infiltrate of right sublingual area and trismus. 55y old diabetic man presented with a 2-week swelling of the right parotid gland treated via antibiotics. 16y old male hospitalized in ENT department was referred to rule out odontogenic source of his right sided pansinusitis. 40y old diabetic woman was referred by a dentist for evaluation of non-healing wound after extraction of tooth 26 done 6 months earlier. Ten day orbital cellulitis in a previously healthy young man, unsuccessfully treated by antibiotics and corticosteroids.B. Female patient treated by chemotherapy for acute myeloid leukemia was referred for evaluation of extensive palatal necrotic ulcer.
Patients so affected come to their attention either through referrals from primary care providers or due to patients’ uncertainty about where to seek help for diseases manifesting themselves in the orofacial area. A carbuncle is the coalescence of several furuncles with pus draining from multiple follicular orifices. Various tests for diagnosis of the infection are swab culture of the ulcer, mucosal biopsy, blood test and physical examination. MRI scan revealed proptosis with stretching of the optical nerve, deformation of the bulbus, thickening of ocular muscles, inflammatory changes of orbital fat, homolateral ethmoid cells and temporal fossa. Also in hospital environment, where majority of oral and maxillofacial surgeons practice, one regularly receives requests for consultations about patients who need interdisciplinary cooperation despite the fact that their conditions primarily belong to the sphere of specializations like ENT surgery, ophthalmology, dermatology and others. Carbuncles frequently develop on the nape and are more likely to be seen in diabetic patients [3]. Orrifice of Stensen’s duct is slightly erythematous and expressed saliva contains whitish floccues.
CT examination revealed partial opacification of the maxillary sinus and signs of osteomyelitis. The purpose of this chapter is to provide an update on such conditions and demonstrate the ways oral and maxillofacial surgeon can participate in their diagnosis and management. These were removed after incision of distal portion of the duct, which was irrigated by saline. HA = hyaluronic acid, CHA = Calcium hydroxylapatite, BDDE = butanediol diglycidyl ether, NASHA = nonanimal stabilized hyaluronic acid, PLL = Poly-L-lactic acid, PMM = polymethylmetacrylate3.2. C.Large amount of foreign material mixed with sanguinopurulent exudate drained from the left buccal space. Complications of tissue fillersComplications can be attributed to the product properties, method of delivery and reaction of the recipient's immune system.
Groccot-Gomori stain of biopsy specimen depicted hyphae of zygomycete, which was classified by subsequent culture as Apophysomyces elegans. Clinical presentationIn the face, furuncles are frequently seen on the chin, upper lip and paranasal area. Despite orbital exenteration and Amphotericin B therapy the patient died 5 days later due to intracranial invasion. Each lesion consists of an inflammatory nodule and an overlying pustule through which hair emerges. The form of impetigo that penetrates deeper into the dermis and may leave a scar is called ecthyma.
Furuncles of the nasal vestibule can be insidious and not obvious upon cursory examination and their symptoms, namely swelling of upper lip and infiltrate of upper oral vestibule, can lead to false impression of odontogenic infection. They include palpable or visible implants due to superficial injection, uneven distribution, overcorrection, undercorrection and hypersensitivity. Impetigo occurs most frequently among economically disadvantaged children aged 2–5 years, although older children and adults may also be afflicted under conditions of poor hygiene, high humidity and warm temperatures.
The most serious immediate complication is vascular compromise by mechanism of either direct arterial embolization of filler or local overfilling leading to venous compression in the treated area [28].Early onset complications appear between 2 – 3 days or weeks after injection.
Prospective studies of streptococcal impetigo have demonstrated that the responsible microorganisms initially colonize the unbroken skin.
Lesions are extremely painful and they are surrounded by area of cellulitis and collateral edema. Inoculation of surface organisms into the skin happens after a mean interval of 10 days by abrasions, minor trauma, or insect bites [2].
If there is any fluctuation or impending skin erosion, incision and drainage with culture should be performed. Empiric antibiotic treatment should begin with a macrolide or tetracycline and should be continued for 4 to 6 weeks [29].


Also gentle removal of overlying crust and necrotic central plug can be helpful; however attempts to express purulent content should be discouraged.
Late (several weeks to 1 year) or delayed (>1 year) complications usually present as nodules or subdermal masses. The lesions of non-bullous impetigo begin as papules that rapidly evolve into vesicles surrounded by an area of erythema. Conservative management is preferable and only rarely cases of furuncles or carbuncles progressing into subcutaneous abscess require incision and drainage. Stimulatory fillers such as polylactic acid and calcium hydroxylapatite, or silicone may give rise to fibrotic nodules. Then they become pustules that gradually enlarge and break down over a period of 4–6 days to form characteristic golden yellow crusts [3]. In the face, whenever possible, this should be done through intraoral route to avoid facial scarring.
Immune response to filler material or chronic infection can lead to formation of granulomas [30-34].
Systemic antibiotics are necessary in instances of substantial collateral cellulitis, alteration of general condition and signs of developing facial thrombophlebitis. They should be treated as foreign body infections with macrolide or tetracycline, and strong consideration should be given to two-drug therapy. If there is no response in 7 to 10 days, intralesional corticosteroids can be injected while maintaining the patient on oral antibiotics [29]. Until recently, staphylococcal infections acquired outside of the healthcare setting have been frequently methicillin-sensitive and responsive to a wide range of antibiotics.
Since 1980, methicillin-resistent staphylococcus aureus (MRSA) infections have been reported in community outbreaks. These organisms have been called community-acquired or community-associated MRSA, as opposed to hospital acquired MRSA [9]. Biofilms are defined as a structured community of microorganisms encapsulated within a self-developed polymeric matrix and irreversibly adherent to a living or inert surface [36]. Hospital acquired MRSA is usually resistant to at least three ?-lactam antibiotics and is usually susceptible only to vancomycin, sulfamethoxazole, and nitrofurantoin.
They are also often characterized by structural heterogeneity, genetic diversity and complex community interactions. Community acquired MRSA is more likely to be susceptible to clindamycin and has varying susceptibility to tetracycline, fluoroquinolone, erythromycin and vancomycin [10].Outbreaks of furunculosis may occur in families and other groups involved in close personal contact, like prisoners, members of sports teams or outdoor recreation groups [3,11]. Extracellular polymeric matrix of biofilms may interfere with macrophage phagocytosis and allow for easier exchange of extrachromosomal DNA plasmids encoding antimicrobial resistance.
TreatmentThe therapeutic approach to impetigo depends on the number of lesions, their extent and location (in a face proximity to eyelids or mouth), and the need to limit spread of infection to other individuals.
Control of outbreaks may require bathing with antibacterial soaps, thorough laundering of clothing, towels, bed spreads, separate use of towels and washcloths.
All surgical implants like orthopedic appliances, heart valves, indwelling catheters, stents or other forms of foreign material may be compromised by biofilms. The best topical agent is mupirocin, although resistance has been described; other agents, such as bacitracin and neomycin, are considerably less effective.
Active clinical infections can flare up weeks, months and even years after initial surgery. Topical therapy with mupirocin is equivalent to oral systemic antimicrobials and may be used when lesions are limited in number. The prevalence of nasal staphylococcal colonization in the general population is 20–40%, but not all carriers develop recurrent skin infections.
Bacteriemia caused by dental treatment, contaminated surgery, or trauma can activate infective response of a chronic biofilm. Patients who have numerous lesions or who are not responding to topical agents should receive oral antibiotics effective against both S. Eradication of nasal colonization can be achieved by application of mupirocin ointment twice daily in the anterior nares for the first 5 days each month [12]. The active infection can be controlled with antibiotic therapy, but the underlying biofilm can persist and generate a recurrence [27,37,38].
The preferred antibiotics are penicillinase resistant penicillins or first- generation cephalosporins, because S. CellulitisCellulitis is diffusely spreading soft tissue infection not associated with underlying suppurative foci. It involves rapidly spreading areas of edema, erythema, and may be accompanied by lymphangitis and regional lymphadenitis [13]. Folliculitis Folliculitis is defined as purulent infection of hair follicles limited to the epidermis.
Clinical presentationIn orofacial areas cellulitis is routinely seen as an early stage of odontogenic infections and it is present also at the periphery of other defined skin infections and infected traumatic wounds (Figure 6). Clinical presentation and etiologyFolliculitis is characterized by clusters of small, erythematous papules or pustules, usually in body areas prone to friction and heavy perspiration.
The most common form of folliculitis is sycosis barbae a staphylococcal infection related to shaving. Predisposing factors for these infections include conditions that make the skin more fragile or local host defenses less effective, such as obesity, previous cutaneous cuts, venous insufficiency, lymphatic obstruction or other causes [3].Cellulitis of non-odontogenic origin is most commonly caused by ?-hemolytic streptococci (usually group A) but may also be caused by other streptococcal species. Other possible etiological agents include Enterobacteriaceae (often associated with prolonged antibiotic therapy), Pseudomonas aeruginosa (associated with hot tubs and wet suits) [6], Malassezia furfur, herpes simplex virus, varicella-zoster virus and Demodex mites.
Non-infectious folliculitis include eosinophilic folliculitis thought to be an autoimmune process directed against the sebocytes [7] and a papulopustular follicular eruption after treatment with epidermal growth factor receptor (EGF-R) inhibitors [8]. TreatmentUncomplicated superficial folliculitis may respond to improved hygiene supported by use of antibacterial soap.
Selection of appropriate antibiotic is based on knowledge of the common microorganisms involved in the particular type of infection before results of microbiology examination and antibiotic sensitivity tests are available. Parenteral therapy is indicated for severely ill patients or for those unable to tolerate oral medications. Reasonable choices include a penicillinase-resistant penicillin such as nafcillin, a first-generation cephalosporin such as cefazolin, or clindamycin or vancomycin for patients with penicillin allergies [3].
Eosinophilic folliculitis may respond to isotretinoin, metronidazole, UV-B phototherapy, indometacin or itraconazole [1].
Erysipelas Erysipelas is a well-demarcated, painful skin infection characterized by intense erythema.


Infectious folliculitis may progress to involve deeper layer of the dermis and finally spread to subcutaneous tissue. The term erysipelas is often used inconsistently and some physicians use it to describe simple cellulitis. Furuncle and carbuncle Furuncle is purulent infection involving the hair follicle and extending to surrounding subcutaneous tissue. The distinction between these two terms relates to the depth of inflammation; erysipelas affects the upper dermis, including the superficial lymphatics, whereas cellulitis involves the deeper dermis and subcutaneous fat.
In practice however, distinguishing between cellulitis and erysipelas clinically may be difficult [3].
Clinical presentationErysipelas is distinguished clinically from other forms of cutaneous infection by the following two features: The lesions are raised above the level of the surrounding skin, and there is a clear line of demarcation between involved and uninvolved tissue [15]. Vesicles, bullae, and cutaneous hemorrhage in the form of petechiae or ecchymoses may develop. Systemic manifestations like fever, tachycardia, hypotension, and leukocytosis may occur, even before the skin abnormalities appear.
In older textbooks, pictures of erysipelas of the face characteristically involved the butterfly area, which is nowadays rarely seen.
Craniofacial necrotizing fasciitisNecrotizing fasciitis (NF) is rapidly progressing bacterial infection spreading along the deep fascial planes with relative sparing of skin and underlying muscles [16]. Necrotizing infection may involve any combination of dermis, subcutaneous tissue, fascia or muscle. Blood supply to the fascia is typically more tenuous than that of muscle or healthy skin, making the fascia more vulnerable to infectious processes. Additionally, the propensity for fluid collection between involved fascia and adjacent tissues further weakens fascial immune protection [9]. Most patients with NF have polymicrobial infections with an average of 4.4 organisms isolated per infection [17,18]. Although these polymicrobial infections can spread widely and become life-threatening, they tend to be less aggressive than infections caused by a limited number of highly virulent pathogens. These may cause very rapidly spreading necrotizing infections in an immunologically intact host through production of exotoxins.
Recently, increased awareness of the condition resulted in more reports of cervico-facial NF appearing in the literature.
Cervical NF is characterized more frequently by polybacterial etiology, mainly odontogenic source of infection, predominance of males and higher mortality.
Craniofacial NF does not have gender preference, has lower mortality, but cosmetic and functional consequences are often severe. Clinical presentationCraniofacial NF predominantly originates from periorbital regions;d only one microorganism is usually identified from cultures, most commonly group A hemolytic streptococci. The distinguishing features are fast progression, pain disproportionate to clinical findings, systemic toxicity and presence of gas.
TreatmentThe promptness of initial surgical debridement is considered decisive for favorable outcome [19,20]. The early incision and debridement of all involved spaces can salvage the skin, which later in the progress of disease succumbs to necrosis due to thrombosis of feeding vessels.
All necrotic tissues should be excised, the defects should be kept open and debridement should be repeated until a completely healthy granulating wound is obtained. While the surgical treatment should be performed promptly, it cannot be as aggressive as in the extremities and trunk, where large areas of skin and subcutaneous tissue are often sacrificed. It is necessary to preserve as much of the anatomic structures as possible to avoid significant cosmetic disfigurement and functional limitations. Simultaneous immediate antibiotic therapy should consist of high-dose penicillin G or ceftriaxone in addition to metronidazole and clindamycin for anaerobic coverage. Clindamycin is a potent suppressor of bacterial toxin synthesis, facilitates phagocytosis of S. Numerous recent published reports claim substantial reduction in mortality and length of hospital stay when hyperbaric oxygenotherapy is used as adjunctive treatment [22].3.
Infected tissue fillersInjectable soft tissue fillers (ISTFs) are widely popular in facial rejuvenation. ISTFs are usually injected into the deep dermis or dermal – subdermal junction for wrinkles, skin creases or depressed scars [23]. Recently there is a tendency to more frequent use of fillers injected into deep subcutaneous layers for augmentation [24]. They can be differentiated as volumetric and structural, or fibroplastic, based on the biomechanics of filling effect [27].
Another practically important property is their time of tissue survival differentiating them into temporary, long lasting or semi-permanent and permanent (Table 1).The most commonly used ISTFs are homogenous polymer gels, both degradable and nondegradable. Nondegradable homogenous ISTFs are represented by polyacrylamide hydrogel and silicone gel. Polyacrylamide gel is hydrophilic, consisting of polyacrylamide, to which water molecules are loosely attached. The macrophages enter the gel, become transformed into fibroblasts that connect and eventually form a vascular fibrous network. Silicone gel differs from the other polymer gels by being hydrophobic, which results in dispersion in the tissue in the form of rounded vacuoles or droplets, which do not interact with the host tissue. However they stimulate response of macrophages and foreign body giant cells and are frequently seen within these cells as small round inclusions. Combination or structural ISTFs are composed of two components: Solid microparticles dissolved in a transient carrier gel. Microparticles remain in the tissue after the carrier gel has been degraded and thus, elicit a foreign-body reaction, which results in fibrosis responsible for the final filling effect. Some of the microparticles are nondegradable and add to the resulting filling effect, others are slowly degraded over a period of several years [26].




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