Updated: May 19, 2009
A fistula is an abnormal pathway between 2 anatomic spaces or a pathway that leads from an internal cavity or organ to the surface of the body. A sinus tract is an abnormal channel that originates or ends in one opening. An orofacial fistula is a pathologic communication between the cutaneous surface of the face and the oral cavity.
In the literature, the terms fistulas and sinuses are often used interchangeably. Stedman's Medical Dictionary defines a sinus as a fistula or tract leading to a suppurating cavity. Orofacial fistulas are not common, but intraoral sinus tracts due to dental infections are common. When infection or neoplasia is involved, immediate treatment is necessary. Dental infections, salivary gland lesions, neoplasms, and developmental lesions cause oral cutaneous fistulas, fistulas of the neck, and intraoral fistulas.
Chronic dental periapical infections or dentoalveolar abscesses cause the most common intraoral and extraoral fistulas. These dental periapical infections can lead to chronic osteomyelitis, cellulitis, and facial abscesses. Infection can spread to the skin if it is the path of least resistance. Fascial-plane infections, space infections, and osteomyelitis can cause cutaneous fistulas. Fascial-plane infections often begin as cellulitis and progress to fluctuant abscess formation. Compared with the other conditions, fluctuant abscess formation is more likely to result in cutaneous fistulas.
Rarely, a cutaneous lesion such as a furuncle can be misdiagnosed as a sinus tract to the skin of the face. One case report1 demonstrates this occurrence from a periapical infection from the right central mandibular incisor, which drained to the patient's chin. Because the tooth could not be restored, it was extracted, which resolved the lesion.
Another case with cutaneous manifestations involved a 44-year-old woman with a draining lesion to the skin just lateral to the nasofacial sulcus. Oral antibiotics did not help resolve the lesion. The patient had poor dentition, and a panoramic radiograph showed 2 periapical radiolucencies of the maxillary right lateral incisor and canine. The teeth were extracted, which resolved the lesion. Sheehan et al2 recommend a dental examination and radiographs to rule out infection of dental origin to the cutaneous face or neck.
For general information on dental infections, see Infections, Dental.
Origins and spread, salivary gland fistulas, oral antral and oral nasal fistulas, iatrogenic fistulas (eg, dental implant placement), and miscellaneous orocutaneous fistulas are addressed here.
Origins and spread
Dentoalveolar abscesses originate from direct extension or continuity from an acute irreversible pulpitis that spreads beyond the apex of the tooth. Another cause of dentoalveolar abscesses is an acute exacerbation of a chronic apical periodontitis or periapical granuloma. Periapical granulomas may remain quiescent because the inflammatory cells are walled off by connective tissue. A periapical granuloma may be exacerbated if the patient's resistance to the organism decreases or if the number of microorganisms increases. This condition is also termed a phoenix abscess.
Unusual dental malformations may lead to periapical dental infections. Dens in dente or dens evaginatus, an axial invagination of enamel and dentin into the dental papilla, frequently develops periapical infections, which can lead to sinus tract formation.3,4,5 Even more rarely, taurodontism6 consisting of elongated crowns or apically placed furcations with pulp chambers with increased occlusal-apical height can cause periapical disease, leading to a sinus tract or parulis.
Most of these dental infections remain intraoral, and they most often spread to the facial or buccal side of the alveolar ridge. If the dental roots are closer to the lingual side, as they often are with the maxillary anterior teeth and the lingual roots of the maxillary molars, a palatal sinus tract may develop. When a sinus tract appears as an intraoral papule or pustule, it is called a parulis. When a chronic infection is acutely exacerbated or persistent, the infection can spread to the facial skin, most commonly in the area of the chin. Numerous barriers, including bone, muscle, and facial planes, determine the path of infection spread.
Yasui et al7 reported a cutaneous fistula of dental origin. A 75-year-old Japanese woman presented with the chief complaint of a left-cheek skin lesion with mild pain. A subcutaneous nodule with erythematous skin was on her left cheek. Dental examination demonstrated a radiolucent area in the left-lower first molar periapical region. The tooth was asymptomatic. Antibiotic therapy and endodontic therapy eliminated the subcutaneous nodule. The authors recommend a complete dental evaluation be performed when a subcutaneous facial nodule is encountered.
If the infection originates from a region of the maxillary molar, intraoral spread of the infection occurs buccally. When the infection spreads inferior to the superior attachment of the buccinator muscle, it remains in the oral cavity. If the infection path moves superior to this attachment, cutaneous spread with fistula formation is possible. Infection from the maxillary molar teeth can spread to the palate and into the maxillary sinus, depending on the position of the lingual roots of the teeth.
Maxillary dental infections also may spread to the canine fossa, buccinator space, lateral pterygoid space, and infratemporal space. Spread of infection to the lateral pterygoid and infratemporal spaces is associated with trismus. Infection of maxillary premolars almost always stays confined to the oral cavity and most commonly spreads to the buccal side of the alveolar ridge. Infection from the maxillary anterior teeth is usually contained within the oral cavity. Spread of infection superior to the levator anguli oris muscle or orbicularis oris muscle may result in cutaneous spread.
Infection from the mandibular molars is usually confined to the lingual aspect of the oral cavity by the mylohyoid muscle and to the buccal aspect by the inferior attachment of the buccinator muscle. If the infection penetrates to the lingual area inferior to the mylohyoid muscle, infections of the submandibular, sublingual, and submental spaces may result. If the infection spreads inferior to the buccinator muscle attachment, cutaneous spread may occur with fistulation.
Infection of the mandibular premolars is almost always confined by the buccinator muscle in the oral cavity and most commonly spreads to the buccal side. Infection of the mandibular anterior teeth is usually confined to the oral cavity and spreads facially. If the infection spreads below the mentalis muscle, cutaneous spread may occur. Mandibular space infections may involve the submandibular, submental, pterygomandibular, masseteric, lateral and posterior pharyngeal, parotid, and carotid spaces.
Chronic osteomyelitis more frequently drains through an extraoral sinus opening than through an intraoral opening. Osteomyelitis is more likely to develop in patients with uncontrolled diabetes, in those who have undergone jaw irradiation because of a previous malignancy (osteoradionecrosis), and in those with metabolic bone diseases such as Paget disease (osteitis deformans) or Albers-Schönberg disease (osteopetrosis).
Garré osteomyelitis is a unique chronic osteomyelitis with a prominent periosteal inflammatory reaction that follows periapical disease or tooth extraction. It is uncommon, with average age of 13 years. Elimination of pulpal periapical infection through endodontic therapy without endodontic surgery was shown to be an effective treatment. In this case report,8 total bone healing was observed 1 year later.
Lymphatic spread is also common. Lymphadenopathy with movable tender nodes is a common finding with dental infections. Inflammatory lymph nodes caused by dental infection rarely result in cutaneous fistulas.
Salivary gland fistulas
Salivary gland fistulas are rare except with minor salivary gland mucocele. Saliva from damaged salivary glands or ducts finds the path of least resistance but rarely escapes through the skin or mucosa. The parotid duct or Stensen duct comes close to the cutaneous surface as the duct crosses the outer surface of the masseter muscle. A rare submandibular fistula was reported in association with a ranula of the submandibular gland. A case was reported with a cutaneous opening caused by an ectopic salivary gland. This instance mimicked a branchial cleft or branchial cyst fistula. Gerhard et al9 state that ectopic salivary gland fistulas should be in the differential diagnosis of branchial fistulas.
One interesting case is of a 4-year-old boy with an anterior cervical fistula, which secreted salivalike fluid while he was eating. Head and neck examination revealed an opening posterior to the hyoid bone. The fistula ascended superficially to the anterior cervical muscles, with a cyst anterior to the hyoid bone, continuing to the left submandibular gland. According to Hayasaka et al,10 no previous reports have described the Wharton duct running from the submandibular gland to the anterior cervical skin.
Trauma, microorganisms, neoplasms, xerostomia, immunosuppression, and malnutrition usually are the cause of infections that result in fistulas from salivary glands. Iatrogenic causes include surgery and radiation therapy. Patients who are ill or debilitated may be prone to these infections. Actinomycosis, syphilis, tuberculosis, salivary calculi, and malignancy are other etiologic agents that cause salivary gland infections. Staphylococcus aureus, Streptococcus viridans, and Escherichia coli most commonly are found in these infections.
Sjögren syndrome, which has a female-to-male ratio of 10:1, is an immunologic disease that causes xerostomia. Patients with this disease have dry eyes, a dry mouth, and, in the secondary form, immunologic connective-tissue disorders, most commonly rheumatoid arthritis. Patients with Sjögren syndrome may be more prone to parotid gland infection, but this infection rarely results in sinus tract formation to the skin or oral mucosa.
Salivary gland stones or sialoliths can be a site of infection. These are most commonly associated with the Wharton duct, the major duct for the submandibular gland. Any gland can be affected. The sialolith blocks the ductal secretion of saliva, causing a fluid buildup that creates a potential site for infection. A ranula or mucous retention phenomenon of the floor of the mouth results from this blockage; when this is large, it is treated by marsupialization. This technique exteriorizes a cyst or other such enclosed cavity by resecting its anterior wall and suturing the cut edges of the remaining wall to adjacent edges of the skin, thereby creating a pouch.
Drage et al11 presented 3 cases of a migrating salivary stone or sialolith to adjacent tissues, resulting in cutaneous fistulas from salivary gland origin. Two patients were treated successfully surgically, which resulted in resolution of the fistulas.
A mucocele or mucous retention phenomenon occurs when minor salivary gland ducts are damaged. The walling off of mucin with granulation tissue causes a cystlike structure; on the floor of the mouth, this structure is called a ranula. This lesion is usually painless, and the patient often reports that it swells and breaks with a fluid discharge. More than 50% of patients with a mucocele or mucous retention phenomenon are younger than 21 years, and it occurs equally in males and females. Patients may remember biting their lip.
Clinically, the mucocele appears as a clear or bluish fluctuant vesicle. It is most common on the lower lip and can be found in minor salivary glands of the palate and retromolar pad area. It is extremely rare on the upper lip. Physical trauma to the lower lip is the most common cause of mucoceles. Most upper lip swellings are due to cysts, odontogenic infections, and salivary gland tumors. The differential diagnoses include salivary gland neoplasms, especially mucoepidermoid carcinoma, vascular malformation, hemangiomas, and fibrous nodules or fibroma.
Oral antral and oral nasal fistulas
Tooth extraction, tuberculosis, syphilis, leprosy, malignant neoplasms, phycomycoses, midline granuloma (a form of lymphoma), and developmental clefts may cause oral antral and oral nasal fistulas. The most common cause of oral antral fistulas is tooth extraction. Maxillary first molars account for 50% of oral antral fistulas caused by extractions. Maxillary second and third molar extractions account for the other 50%. Prior to extraction, infection of these teeth may create a communication with the antrum. Approximately 10% of all sinusitis cases have a dental origin.
Lopatin et al12 concluded that an endoscopic approach to chronic maxillary sinusitis of dental origin is a dependable technique associated with less morbidity and a lower rate of complications.
When patients ingest food and liquids, these may enter the nasal cavity and antrum, causing an unpleasant salty taste and fetid breath. Infection may cause sinusitis, which results in throbbing headaches that are aggravated by head movement. Nocturnal cough and epistaxis may result from drainage of exudate to the oropharynx and nose. Swelling and redness over the sinus and pain beneath the eye, especially with palpation, may occur.
In all cases of idiopathic sinusitis, causes such as infection, polyps, and neoplasms should be excluded. Neoplasms, such as squamous cell carcinoma, may manifest as sinusitis until the neoplasm enlarges enough to show signs of malignancy. By this stage, metastasis may have occurred.
Miscellaneous orocutaneous fistulas
An oral cutaneous fistula leads to esthetic problems due to the continual leakage of saliva from the oral cavity to the face. Malignancy, inflammation, and trauma are the most common causes.
Traumatic fistulas may be due to injury or surgical repair in areas where mucosal and epidermal surface epithelia line the fistula wall. No inflammation is associated with this type of fistula unless an infection develops (see Media File 2).
Actinomycosis has been documented as a cause of continual, recurrent, periapical disease associated with endodontically treated teeth. One case presented by Jeansonne16 demonstrated persistent periapical disease with recurrent sinus tracts. No pain or swelling was present after clinically acceptable initial endodontic treatment, but a periapical lesion developed. After routine endodontic retreatment, the periapical lesion persisted and a sinus tract developed. The sinus tract healed with antibiotic therapy but recurred within a few months. The sinus tract recurred and disappeared with antibiotic therapy over a period of 5 years. After histological diagnosis confirmed actinomycosis, the lesion was treated with antibiotics and periapical surgery. It finally resolved in 5 months.
Fistulas may arise from developmental cysts of the neck region, such as thyroglossal duct, dermoid, sebaceous, preauricular, and branchial arch cysts. Nasopalatine duct cysts occasionally secrete fluid to the anterior palate and the site of the duct.
Intracranial extension and a cutaneous sinus tract are rarely seen with craniofacial dermoid cysts. Scolozzi et al17 reported a case of a 1-year-old girl who was initially seen with a cutaneous fistula of the frontotemporal region, from an intracranial dermoid cyst. The patient was treated surgically with a right lateral orbitotomy by a bicoronal approach. The cyst was seated within the lateral orbital wall, with intracranial extension through the temporal and sphenoidal bones to the dura of the temporal lobe. Histopathologic analysis confirmed the diagnosis of a dermoid cyst. Craniofacial dermoid cysts may rarely be associated with a cutaneous sinus tract and/or intracranial extension. Failure to identify and treat these lesions may lead to recurrent infection with a potential for meningitis or cerebral abscess. The authors strongly recommend CT scanning and MRI before surgical treatment of any cutaneous fistula in the head and neck region.
The thyroglossal duct cyst is the most common of the developmental cysts of the neck. In embryonic development, the duct follows a path from the tongue to the normal position of the thyroid. These cysts have an equal incidence in females and males, and they usually are observed within the first 2 weeks of life. Proliferation of duct tissue may continue, causing enlargement of the thyroglossal tract. If a sinus opening to the neck occurs, the most frequent location is just below the hyoid bone. The epithelial lining may consist of squamous or pseudostratified columnar epithelium. Infection may occur anywhere along the duct tract, causing purulent exudate. Complete surgical removal of the thyroglossal duct epithelium is the treatment of choice; however, complete removal is difficult and recurrence is frequent.
The lateral branchial arch cyst is the most common developmental cyst of the lateral neck. It occurs when the second branchial arch or second pharyngeal pouch is not eliminated in normal development. The endoderm of this pouch normally becomes the tonsil. A cutaneous sinus, a mucosal sinus, or both may occur. Lateral branchial arch cysts occur equally in males and females, and they may be familial. They can be unilateral or bilateral. They may occur in children; ruptured cysts may occur in adults. Usually, the opening is near the anterior border of the sternocleidomastoid muscle just above the sternoclavicular joint. The differential diagnosis includes a fistula or sinus from an infected or cancer-containing lymph node.
Preauricular fistulas or sinuses occur in approximately 1% of the population. They are observed more commonly in blacks and Asians than in whites and occur equally in males and females. Approximately one fourth of preauricular fistulas are bilateral. They may be associated with other congenital anomalies such as Treacher-Collins syndrome. Preauricular fistulas originate from the abnormal development of the first and second branchial arches from the external ear. The most common site is the marginal helix of the ear at the junction with facial skin. Usually, preauricular fistulas are asymptomatic and require no treatment unless they become secondarily infected. They can be differentiated from first branchial arch anomalies because the first branchial arch usually opens into the external auditory canal and has a purulent discharge.
Lymph nodes infected with mycobacteria cause scrofula, a condition in which infection spreads from the node to the skin through a sinus tract. This infection most commonly occurs in the neck. Cat scratch disease is another consideration in the differential diagnosis of sinus tracts from lymph nodes.
Preauricular fistulas or sinuses occur in approximately 1% of the population.
Most dental infections are treated with incision and drainage and antibiotics, which result in an excellent prognosis. Usually, no morbidity and mortality occur. Cellulitis can lead to Ludwig angina and cavernous sinus thrombosis.
| Cellulitis | Pulp Polyp |
| Cutaneous Tuberculosis | Squamous Cell Carcinoma |
| Mucocele and Ranula | |
| Necrotizing Sialometaplasia | |
| Oral Cutaneous Fistulas |
The differential diagnoses include any dental and periodontal infection, odontogenic cysts and tumors, salivary gland lesions and neoplasms, and other benign and malignant neoplasms. The most common neoplastic cause of oral cutaneous fistulas is squamous cell carcinoma. Unless secondarily infected, oral cutaneous fistulas rarely, if ever, develop from benign neoplasms and cysts.
With acute infection, histologic sections show a preponderance of neutrophils and necrotic debris. Chronic infections are histologically characterized by numerous plasma cells, lymphocytes, and macrophages; often, a proliferation of blood vessels and connective tissue or granulation tissue is present.
In chronic osteomyelitis, sections of acellular bone are present, sometimes with little inflammatory infiltrate. When histologic sections are processed, decalcification of the specimen for sectioning can remove lacunar cells present in bone. This effect must be considered when histologic sections of bone are viewed.
Actinomycosis has characteristic pseudohyphae appearing as clublike projections that stretch out from a central basophilic-staining core. The absence of this finding does not rule out an actinomycotic infection.
Microscopic sections of mucoceles show minor salivary glands with chronic inflammation and a granulation wall that surrounds a pool of mucin.
To properly treat any infection, drainage is necessary to decrease the number of microbes and reduce the amount of substrate on which they grow. Antibiotic coverage is necessary to eliminate or reduce the number of microbes causing the infection.
The goals of pharmacotherapy are to eradicate infection, reduce morbidity, and prevent complications.
Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.
Inhibits biosynthesis of cell wall mucopeptide. Bactericidal against sensitive organisms when adequate concentrations are reached and most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects. DOC in treating common orofacial infections caused by aerobic gram-positive cocci and anaerobes. Orofacial infections include cellulitis, periapical abscess, periodontal abscess, acute suppurative pulpitis, oronasal fistula, pericoronitis, osteitis, osteomyelitis, and postsurgical and posttraumatic infections. No longer recommended for dental procedure prophylaxis.
250-500 mg PO q6-8h; not to exceed 3 g/d
<12 years: 25-50 mg/kg/d PO in divided doses q6-8h; not to exceed 3 g/d
>12 years: Administer as in adults
Probenecid may increase effectiveness by decreasing clearance; tetracyclines are bacteriostatic, decreasing effectiveness of penicillins when administered concurrently
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in severe renal impairment (modify dosage), history of seizures, or hypersensitivity to cephalosporins; hemolytic anemia reported
Analog of ampicillin with broad-spectrum bactericidal activity against gram-positive and gram-negative microorganisms. Interferes with cell wall mucopeptide synthesis during active multiplication, resulting in bactericidal activity against susceptible bacteria.
250-500 mg PO q6-8h; not to exceed 3 g/d
<3 months: up to 30 mg/kg/d PO divided q12h
>3 months: 25 or 45 mg/kg/d PO divided q12h; alternatively, 20 or 40 mg/kg/d PO divided q8h (higher dose for severe infections)
May reduce efficacy of oral contraceptives; concurrent use with probenecid may increase and prolong blood levels; chloramphenicol, macrolides, sulfonamide, and tetracyclines may interfere with bactericidal effects of penicillin, as demonstrated in vitro (clinical significance not yet understood)
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; may increase risk of candidiasis; if superinfections with mycotic or bacterial pathogens occur, discontinue and initiate appropriate therapy; Amoxil tab has phenylalanine, avoid use in PKU; may cause rash, including TEN
Drug combination used to treat bacteria resistant to beta-lactam antibiotics.
In children >3 mo, base dosing protocol on amoxicillin content. Due to different amoxicillin/clavulanic acid ratios in 250-mg tab (250/125) vs 250-mg chewable tab (250/62.5), do not use 250-mg tab until child weighs >40 kg.
250-500 mg PO q8h or 875 mg PO q12h
<3 months: 30 mg/kg/d PO divided q12h; use 125 mg/5 mL susp
>3 months and <40 kg: 20-40 mg/kg/d PO in divided doses q8h or 45 mg/kg PO in divided doses q12h; dose based on amoxicillin content
>3 months and >40 kg: Administer as in adults
Probenecid decreases renal elimination of amoxicillin; coadministration with warfarin or heparin increases risk of bleeding
Documented hypersensitivity; associated jaundice/hepatic dysfunction
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May cause jaundice/hepatic dysfunction; use with caution if history of hepatic dysfunction; some products contain phenylalanine; may cause diarrhea; use for a minimum of 10 d to eliminate organisms and prevent sequelae (eg, endocarditis, rheumatic fever); after treatment, obtain cultures to confirm eradication of streptococci
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half of total daily dose may be administered q12h. For more severe infections, double the dose.
Stearate or estolate formulations: 250 mg PO q6h or 500 mg PO q12h; administer in fasting state or immediately before meals; not to exceed 4 g/d
Ethyl succinate formulation: 4 g/d PO divided bid/tid
Stearate and estolate formulations: 30-50 mg/kg/d PO divided tid/qid
Ethyl succinate formulation: 50-80 mg/kg/d (15-25 mg/lb/d) PO divided q6-8h; double dose for severe infection
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and medications (eg, cyclosporin) metabolized by CYP (P-450) 3A4; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects common (administer doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of parent compound lincomycin.
Serious infections: 150-300 mg PO q6h
Severe infections: 300-450 mg PO q6h
Serious infections: 8-16 mg/kg/d (4-8 mg/lb/d) PO divided tid/qid
Severe infections: 16-20 mg/kg/d (8-10 mg/lb/d) PO divided tid/qid
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption
Documented hypersensitivity, including hypersensitivity to tartrazine (if 75- or 150-mg tabs are used) or lincomycin
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution with history of regional enteritis, ulcerative colitis, hepatic impairment, antibiotic-associated colitis, or allergic reaction to aspirin; adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile
Oral synthetic antiprotozoal and antibacterial agent, 1-(beta-hydroxyethyl)-2-methyl-5-nitroimidazole. Active in vitro against most obligate anaerobes but does not appear to possess clinically relevant activity against facultative anaerobes or obligate aerobes.
7.5 mg/kg PO q6h (approximately 500 mg for 70-kg adult) for 7-10 d; bone, joint, lower respiratory tract, and endocardium infections may require longer treatment; not to exceed 4 g/d
36-50 mg/kg/d PO divided tid
May increase toxicity of anticoagulants (coumarin) and lithium; phenytoin may increase metabolism and decrease efficacy; cimetidine may increase toxicity; disulfiram reaction may occur with orally ingested ethanol (psychosis reported if used within 2 wk of disulfiram)
Documented hypersensitivity; first trimester of pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in hepatic disease; caution in patients with a history of CNS disease or blood dyscrasia; monitor for seizures and peripheral neuropathy (discontinue if noted); patient should avoid alcohol during use
The possibility of a neoplastic cause may require biopsy and further treatment. If the biopsy specimen is positive for malignancy, a complete medical workup including MRI, positron emission tomography, and/or CT scanning is needed.
With any cutaneous fistula or sinus tract, careful follow-up is mandatory. The potential for infection with swelling and pain is always present. Fistulas provide natural pockets in which infection can start.
The patient may require supportive care. Fistulas are unsightly and cause patient distress. Severe persistent infections, especially actinomycosis and osteomyelitis, can be distressing and frustrating for the patient.
The early detection of dental problems and preventative dentistry are the best deterrents of oral cutaneous fistula formation. Because poor oral hygiene and trauma cause most dental infections, good hygiene and the prevention of trauma may prevent oral cutaneous fistula formation.
With oral antral fistulas, if a cleft or fistula from the oral cavity to the sinus is too large for surgical closure, prosthetic devices such as dentures and obturators can be used to prevent nasal speech and the aspiration of liquids and food.
Cavernous sinus thrombosis
Cavernous sinus thrombosis is a serious sequela of infection, but one that is rarely life threatening. This condition can originate from an infection of the anterior maxillary teeth, which is usually confined to the anterior maxillary vestibule; however, if it hematogenously spreads above the levator anguli oris muscle, it can involve the floor of the nose; the facial, angular, or ophthalmic veins; and the cavernous sinus. If the hematogenous spread does not extend beyond the facial vein, periorbital swelling and fistula formation can occur. Infection spread because of continuity through the tissue can produce the same result.
Cavernous sinus thrombosis can also develop from an infection of the maxillary third molars that hematogenously spreads through the pterygoid plexus of veins to the angular vein, ophthalmic vein, and cavernous sinus. This process may be more subtle than that of a maxillary cuspid infection that spreads through the periorbital region because the spread of infection is not as rapid.
Periocular facial swelling is a sign of infection and thrombosis of the cutaneous sinus, which is a life-threatening condition.
Infection of the periorbital region can extend through hematogenous spread via the ophthalmic vein to the cavernous sinus. Spreading via the facial or external route is rapid because of the large open system of veins that directly leads to the cavernous sinus. Once infection reaches this sinus, the abducens nerve, which causes abduction of the eye and is closest to the sinus, is often affected. Other structures in the wall of the cavernous sinus include the internal carotid artery, trochlear nerve, oculomotor nerve, maxillary vein, and ophthalmic vein. Paralysis of the external ocular muscles, vision impairment, headache, nausea, and fever can occur. The cavernous sinus is located at the base of the brain, from where infection can spread to the meninges and brain. Brain abscesses and meningitis were invariably fatal until the advent of antibiotics, and they remain serious complications.
Ludwig angina
Ludwig angina occurs when septic cellulitis is present in the bilateral submental, submandibular, and sublingual spaces, with elevation of the tongue. The most common sources of this infection are infections in the dental apices or an impaction of the mandibular second and third molars. Ludwig angina is a life-threatening cellulitis that can close the airway. Patients with Ludwig angina often require a tracheotomy (see Media File 1). In addition, infection can spread to the masticator space and, in rare instances, to the lateral pterygoid space.
Trismus is present with cavernous sinus thrombosis and Ludwig angina, and immediate intervention by means of incision and drainage and antibiotic therapy is imperative to prevent its spread to the mediastinum. From the lateral pterygoid space, infection can spread to the posterior pharyngeal space and mediastinum. Once the infection spreads to the mediastinum, treatment is difficult, and death may occur. If the infection spreads to the carotid space, erosion of the carotid artery may occur and create a great potential for hemorrhage.
With mucoceles, removal of the fluid-filled sac and surrounding minor salivary glands results in an excellent prognosis for cure.
For excellent patient education resources, visit eMedicine's Teeth and Mouth Center. Additionally, see eMedicine's patient education articles Dental Abscess and Toothache.
Proper diagnosis of the cause and correct treatment can avoid legal pitfalls (see Treatment). Fistulas often take a long time to heal. Rule out neoplasia if a fistula does not respond to antibiotic therapy or surgical closure.
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orofacial fistulas, sinus tract, intraoral fistulas, dentoalveolar abscesses, periapical infections, periapical granulomas, parulis, maxillary dental infections, trismus, mandibular space infections, osteomyelitis, lymphadenopathy, sialolith, dental implants, dens invaginatus, taurodontism, endodontics, maxillary sinusitis, Garre's osteomyelitis, dermoid cyst, Garre osteomyelitis
James Cade, DDS, Clinical Dentist, Honeycutt Family Dentistry
James Cade, DDS is a member of the following medical societies: American Academy of Oral and Maxillofacial Pathology, American Academy of Oral Medicine, and American Dental Association
Disclosure: Nothing to disclose.
Maureen B Poh-Fitzpatrick, MD, Professor Emerita of Dermatology and Special Lecturer, Columbia University; Professor of Medicine (Dermatology), University of Tennessee
Maureen B Poh-Fitzpatrick, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and New York Academy of Medicine
Disclosure: Nothing to disclose.
Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.
Drore Eisen, MD, DDS, Consulting Staff, Department of Dermatology, Dermatology Research Associates of Cincinnati
Drore Eisen, MD, DDS is a member of the following medical societies: American Academy of Dermatology, American Academy of Oral Medicine, and American Dental Association
Disclosure: Nothing to disclose.
Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.