(Antiprotozoal) Trichomoniasis Canker Treatment: (Spondias) Sineguela


Traditional Herbs

Spondias purpurea is a species of flowering plant in the cashew family, Anacardiaceae, that is native to tropical regions of the Americas. It is most commonly known as Jocote, which derives from the Nahuatl word xocotl, meaning “fruit.” Other common names include Red Mombin, Purple Mombin, Hog Plum, Sineguela, and Siriguela.

Sineguela, especially its resin, has antiprotozoal properties.

Traditionally, mild oral lesions in human babies are applied with “grated” stem of sineguela.

  • The green stem of sineguela is devoid of its bark.
  • The exposed stem is then “grated” or “scraped” to produce a fine pulp mash consistency with all the stem liquid resin or extract.
  • The sineguela stem fine pulp mash is then applied directly to the oral lesions.
  • Repeat everyday or twice a day.

Traditionally, canker in gamecock chickens must be treated with care. The worst canker is in the throat which affect both the respiratory system and the digestive system.

  • The yellow cheesy growth must be carefully removed without injuring the oral flesh.
  • Take extra precaution to not let the chicken swallow any of the yellow cheesy growth.
  • Give plain water (or saline water) to the chicken to wash (or to disinfect) the flesh where the yellow cheesy growth was removed.
  • Apply the sineguela stem fine pulp mash to the oral flesh where the yellow cheesy growth was removed.
  • Give broad spectrum antibiotic 250mg tablet or capsule for secondary infection.
  • Repeat everyday or twice a day.

Trichomoniasis in humans

Trichomoniasis in humans is caused by Trichomonas vaginalis. Trichomonas vaginalis is an anaerobic, flagellated protozoan, a form of microorganism. The parasitic microorganism is the causative agent of trichomoniasis, and is the most common pathogenic protozoan infection of humans in industrialized countries. Infection rates between men and women are the same with women showing symptoms while infections in men are usually asymptomatic. Transmission takes place directly because the trophozoite does not have a cyst. The WHO has estimated that 160 million cases of infection are acquired annually worldwide. The estimates for North America alone are between 5 and 8 million new infections each year, with an estimated rate of asymptomatic cases as high as 50%. Usually treatment consists of metronidazole and tinidazole.

Mechanism of Infection

Trichomonas vaginalis, a parasitic protozoan, is the etiologic agent of trichomoniasis, and is a sexually transmitted infection. More than 160 million people worldwide are annually infected by this protozoan.


Trichomoniasis, a sexually transmitted infection of the urogenital tract, is a common cause of vaginitis in women, while men with this infection can display symptoms of urethritis.


20% of women with the infection will have a “strawberry” cervix (colpitis macularis, an erythematous cervix with punctate areas of exudation) or vagina on examination. This is due to capillary dilation as a result of the inflammatory response.


Some of the complications of T. vaginalis in women include: preterm delivery, low birth weight, and increased mortality as well as predisposing to HIV infection, AIDS, and cervical cancer. T. vaginalis has also been reported in the urinary tract, fallopian tubes, and pelvis and can cause pneumonia, bronchitis, and oral lesions. Condoms are effective at reducing, but not wholly preventing, transmission.

Recent research also suggests a link between T. vaginalis infection in males and subsequent aggressive prostate cancer.


Classically, with a cervical smear, infected women have a transparent “halo” around their superficial cell nucleus. It is unreliably detected by studying a genital discharge or with a cervical smear because of their low sensitivity. T. vaginalis was traditionally diagnosed via a wet mount, in which “corkscrew” motility was observed. Currently, the most common method of diagnosis is via overnight culture, with a sensitivity range of 75-95%. Newer methods, such as rapid antigen testing and transcription-mediated amplification, have even greater sensitivity, but are not in widespread use. The presence of T. vaginalis can also be diagnosed by PCR, using primers specific for GENBANK/L23861.


Infection is treated and cured with metronidazole or tinidazole. Metronidazole would normally be prescribed for a 7 day period and Tinidazole as a two day course, which appears to have a higher success rate than the single dose option. Medication should be prescribed to any sexual partner(s) as well because they may be asymptomatic carriers.

Trichomoniasis in gamecocks or avian species

Trichomoniasis in gamecock or avian species is caused by Trichomonas gallinae. The protozoan Trichomonas gallinae is a cosmopolitan parasite of pigeons and doves. Other birds such as domestic and wild turkeys, chickens, raptors (hawks, golden eagle, etc.) may also become infected. The disease in pigeons is commonly called “canker”. A similar condition in falcons is called “frounce.” In 2005, Trichomonas gallinae was first recognized as a cause of disease in British finches, with Greenfinch and Chaffinch most affected, although a range of garden birds have been found to be susceptible to the parasite. Recent studies have shown that up to a third of adult wood pigeons in Spain may carry the disease. The protozoan has four anterior flagellae and an undulating membrane on one side. An important diagnostic feature is the lack of a free posterior flagellum.

Trichomoniasis is a disease of the upper digestive tract, seen in pigeons, doves, raptors, turkeys, chickens as well as many other wild birds.


Trichomoniasis (Trich. For short) occurs frequently in pigeons and doves, as well as raptors which feed upon them. The disease is called canker in pigeons and frounce in falcons. With the current improved management practices in the poultry industry trichomoniasis is not common in turkeys and chickens. Outbreaks usually occur in warm climates or during warm weather.


The etiological agent of trichomoniasis is Trichomonas gallinae (Tg). Tg is a pear-shaped flagellated protozoan with 4 anterior flagella and an undulating membrane to provide motility. The life cycle of Tg is very simple; it divides by longitudinal binary fission.


Nearly all pigeons are carriers of Tg. The pathogenicity of the different strains of Tg is very variable. Adult pigeons transfer the organism to squabs via the “pigeon milk”. Raptors often contract trichomoniasis by eating infected pigeons and doves. Turkeys and chickens contract the disease by drinking stagnant surface water containing T. gallinae . Pigeons are believed to be the most common vector by which the water supplies are contaminated.

Clinical signs

Affected birds may have difficulty closing their mouths and may drool and make repeated swallowing movements. Severely affected birds will stop eating, become depressed, ruffled in appearance, and emaciated before death.


Lesions are seen in the mouth, sinuses, pharynx, esophagus, crop, and proventriculus. Typical lesions are white to yellow plaques or raised masses.

  • Yellow plaques and raised cheesy masses in mouth, pharynx, oesophagus, crop and proventriculus.
  • Raptors may have liver lesions.


Gross lesions are very suggestive of trichomoniasis but are not unlike those seen with visceral pox, candidiasis, and hypovitaminosis A.

Histopathology of the lesions will help distinguish trichomoniasis from the above diseases. The presence of large numbers of trichomonads in the oral fluids is usually considered confirmatory. A wet mount of fresh oral fluids will reveal the motile trichomonads when examined microscopically.


Eliminate any carrier birds as they will contaminate the waterers with Tg. Provide clean fresh water and eliminate sources of stagnant water.

Avoid contact between pigeons and doves and susceptible poultry. A low preventative level of protozoacide can be fed in the ration or in the drinking water. Agents that have been used are dimetridazole (Emtryl), nithiazide (Hepzide) and Enheptin.


Several drugs have been used to treat trichomoniasis including Emtryl (dimetridazole), aminonitrothiazole, and Enheptin. These drugs are no longer available for use in the U.S.A. Back yard flocks or pigeons not used for food production may be effectively treated with dimetridazole by prescription of a veterinarian (1000 mg/L in drinking water for 5-7 days).

2-amino-5-nitrothiazole is currently widely used as it is efficient and there is as yet no resistance.

Antiprotozoal medications, such as dimetridazole and metronidazole, have also been used successfully to treat birds infected with T. gallinae. Treatment usually is successful after 1–2 days. A new culture system called InPouch has practical advantages over the usual in vitro system. If a bird is dyspneic or cannot swallow food, oral plaques can be removed with thumb forceps.

Previously approved products included dimetridazole, nithiazide, and enheptin. Organic arsenical compounds (where approved) and some herbal products may be of some benefit in managing this problem in food animals.

Damerow, G (1994) The Chicken Health Handbook. Storey Publishing, MA

Nitroimidazole antibiotic medications for canker


The common brand name here is Emtryl, available as a water-soluble powder. Dimetradazole was the first nitro imidazole available and is still an effective drug, although trichomonad resistance to it in some areas is a problem because it has been used for the longest. It must be used with care as it has a narrow safety margin. Overdose leads to a reversible loss of balance and coordination and, in high doses, death. The medication can interfere with sperm production in cocks, leading to a temporary infertility, and so is not recommended for use during breeding. The usual dose is 1 teaspoon (3 grams) to 4 ½ – 8 litres of water. Lower dose rates should be used in stock birds feeding youngsters and during hot weather when water intake increases and evaporation occurs from drinkers, increasing the concentration of the medication.


The common brand name here is Spartrix. It is only available in tablet form. It has a wide safety margin and is very useful for individual bird dosing, particularly youngsters in the nest. The dose is one 10-mg tablet daily.


The common brand name is Flagyl. This is available as a water-soluble syrup and as tablets in a variety of strengths. It is very economical, with the tablets being useful to dose individual birds. Individual birds are given ¼ of a 200-mg Flagyl tablet once daily. Flagyl syrup is water soluble and is given at the dose of 5 – 10 ml per litre but is very sugary and not very palatable to the birds.


This is available as a water-soluble powder under a number of brand names world-wide, including Ridsol-S, Turbosole, Tricho-Plus and Ronivet. The usual strength used is 10%. The dose at this strength is ½ teaspoon per litre. Weaker preparations are available but the birds need to be treated longer with these. The drug is very bitter so preparations stronger than 10% tend to be unpalatable to the birds. It has a very wide safety margin and is safe to use during breeding, racing and moulting. World-wide, ronidazole is the current medication of choice to treat canker. However, in some countries it is not available for use in pigeons, authorities being concerned that resistant organisms may develop. As the drug is used in food-producing animals such as pigs, its use is reserved for these.

In any canker-control program, it is often best to rotate between at least two of these medications in order to decrease the chance of a resistant trichomonad strain developing. Currently, ronidazole-based preparations are used as the primary treatment because of their effectiveness and wide safety margin, but it is a good idea to swap to one of the other available drugs every third or fourth treatment.

Related Diseases

Common Oral Lesions: Part I. Superficial Mucosal Lesions

WANDA C. GONSALVES, M.D., ANGELA C. CHI, D.M.D., and BRAD W. NEVILLE, D.D.S., Medical University of South Carolina, Charleston, South Carolina

Am Fam Physician. 2007 Feb 15;75(4):501-506.

  This is part I of a two-part article on oral lesions. Part II, “Masses and Neoplasia,” appears in this issue of AFP .

  Patient information: See related handout on canker sores.

  Related Editorial

Common superficial oral lesions include candidiasis, recurrent herpes labialis, recurrent aphthous stomatitis, erythema migrans, hairy tongue, and lichen planus. Recognition and diagnosis require taking a thorough history and performing a complete oral examination. Knowledge of clinical characteristics such as size, location, surface morphology, color, pain, and duration is helpful in establishing a diagnosis. Oral candidiasis may present as pseudomembranous candidiasis, glossitis, or perlèche (angular cheilitis). Oral candidiasis is common in infants, but in adults it may signify immune deficiency or other illness. Herpes labialis typically is a mild, self-limited condition. Recurrent aphthous stomatitis most often is a mild condition; however, severe cases may be caused by nutritional deficiencies, autoimmune disorders, or human immunodeficiency virus infection. Erythema migrans is a waxing and waning disorder of unknown etiology. Hairy tongue represents elongation and hypertrophy of the filiform papillae and most often occurs in persons who smoke heavily. Oral lichen planus is a chronic inflammatory condition that may be reticular or erosive. Certain risk factors have been associated with each of these lesions, such as poor oral hygiene, age, tobacco use, and alcohol consumption, and some systemic conditions may have oral manifestations. Many recommended therapies for oral lesions are unsupported by randomized controlled trials.

The Surgeon General’s report on oral health highlights the relationship between oral and overall health, emphasizing that oral health involves more than dentition.1 Physicians regularly encounter oral health issues in practice. For recognition and diagnosis of common oral lesions, a thorough history and a complete oral examination are required; knowledge of clinical characteristics such as size, location, surface morphology, color, pain, and duration also is helpful.

Large-scale, population-based screening studies have identified the most common oral lesions as candidiasis, recurrent herpes labialis, recurrent aphthous stomatitis, mucocele, fibroma, mandibular and palatal tori, pyogenic granuloma, erythema migrans, hairy tongue, lichen planus, and leukoplakia.2,3  This article, part I of a two-part series, reviews superficial mucosal lesions: candidiasis, herpes labialis, aphthous stomatitis, erythema migrans, hairy tongue, and lichen planus (Table 1).4–22 Part II covers masses and neoplasia.23


Clinical recommendation Evidence rating References
When treating recurrent herpes labialis with systemic antivirals such as acyclovir (Zovirax) or valacyclovir (Valtrex), therapy should be initiated during the prodrome. Topical penciclovir (Denavir) may help speed healing and reduce pain even if started after the prodrome. B 10,12–14
Patients with severe recurrent aphthous stomatitis should be evaluated for possible underlying systemic diseases and vitamin deficiencies. B 16,34

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, see page 453 or http://www.aafp.org/afpsort.xml.

TABLE 1: Common Superficial Oral Lesions

Condition Clinical presentation Treatment Comments
Candidiasis4–9 Pseudomembranous: adherent white plaques that may be wiped off Topical antifungals (e.g., nystatin [Mycostatin] suspension or troches, clotrimazole [Mycelex] troches, fluconazole [Diflucan] suspension, or systemic antifungals (e.g., fluconazole, ketoconazole [Nizoral], itraconazole [Sporanox]) Can confirm diagnosis with oral exfoliative cytology (stained with periodic acid-Schiff or potassium hydroxide), biopsy, or culture
Erythematous: red macular lesions, often with a burning sensation
Perlèche (angular cheilitis): erythematous, scaling fissures at the corners of the mouth
Recurrent herpes labialis10–14 Prodrome (itching, burning, tingling) lasts approximately 12 to 36 hours, followed by eruption of clustered vesicles along the vermilion border that subsequently rupture, ulcerate, and crust Immunocompetent patients usually do not require treatment Reactivation triggers: ultraviolet light, trauma, fatigue, stress, menstruation
Topical agents include 1% penciclovir cream (Denavir)
Systemic agents (e.g., acyclovir [Zovirax], valacyclovir [Valtrex], famciclovir [Famvir]) are most effective if initiated during prodrome or as prophylaxis
Recurrent aphthous stomatitis15–17 Ulcers surfaced by a yellowish-white pseudomembrane surrounded by erythematous halo Mild cases do not require treatment
Fluocinonide gel (Lidex) or triamcinolone acetonide (Kenalog in Orabase), amlexanox paste (Aphthasol), chlorhexidine gluconate (Peridex) mouthwash
Erythema migrans18 Migrating lesions with central erythema surrounded by white-to-yellow elevated borders; typically on tongue Asymptomatic cases do not require treatment
Symptomatic cases may be treated with topical corticosteroids, zinc supplements, or topical anesthetic rinses
Hairy tongue19–21 Elongated filiform papillae Regular tongue brushing or scraping; avoidance of predisposing factors Predisposing factors include smoking and poor oral hygiene as well as antibiotics and psychotropics
Lichen planus22 Reticular: white, lacy striae Asymptomatic cases do not require treatment Buccal lesions typical in reticular form; other sites (e.g., tongue, gingiva) may be involved
Erosive: erythema and ulcers with peripheral radiating striae, erythematous and ulcerated gingiva Symptomatic cases may be treated with a topical corticosteroid gel or mouth rinse

Information from references 4 through 22.

Oral Candidiasis

As many as 60 percent of healthy adults carry Candida species as a component of their normal oral flora. However, certain local and systemic factors may favor overgrowth. These include use of dentures, use of a steroid inhaler, xerostomia, endocrine disorders, human immunodeficiency virus (HIV) infection, leukemia, malnutrition, reduced immunity based on age, radiation therapy, systemic chemotherapy, and use of broad-spectrum antibiotics or corticosteroids.4–6,24,25

Oral candidiasis typically is a localized infection; however, rarely it may progress to or occur in patients with systemic candidiasis. Clinical patterns of oral candidiasis are variable and include pseudomembranous candidiasis, or thrush (Figure 1); median rhomboid glossitis and other forms of erythematous candidiasis (Figure 2); and perlèche, or angular cheilitis (Figure 3). Risk factors for systemic infection include acquired immunodeficiency syndrome, diabetes, hospitalization, immunosuppressive therapy, malignancy, neutropenia, organ transplantation, and prematurity.26,27

Figure 1.

Pseudomembranous candidiasis. The typical adherent white plaques may be removed by wiping firmly with a tongue blade or gauze.

Figure 2.

Median rhomboid glossitis (a form of erythematous candidiasis): a roughly symmetric, asymptomatic red lesion involving the midline of the posterior dorsal tongue.

Figure 3.

Perlèche (angular cheilitis): scaling, erythematous fissures at the corners of the mouth associated with infection by Candida albicans or Staphylococcus aureus.

Oral candidiasis is common in infants, affecting 1 to 37 percent of newborns.28 Candidiasis in otherwise healthy infants manifests as a minor infection of the oral cavity, oropharynx, or skin (e.g., candidal diaper dermatitis).29 In contrast, candidiasis among preterm or hospitalized critically ill infants can, in rare instances, become systemic and potentially fatal.27 Chronic mucocutaneous candidiasis in infancy or early childhood can be associated with the development of autoimmune endocrine disorders, such as hypoparathyroidism, hypoadrenalism, hypothyroidism, and diabetes mellitus.5

Treatment involves topical or systemic antifungals. Commonly used topical regimens include nystatin (Mycostatin; not absorbed), clotrimazole (Mycelex troche), and systemic fluconazole (Diflucan). Randomized controlled trials have demonstrated fluconazole suspension to be more effective than nystatin in normal and immunocompromised children.7 Systemic agents such as fluconazole, ketoconazole (Nizoral), and itraconazole (Sporanox) may be used for patients who have candidiasis refractory to topical therapy, are intolerant of topical agents, or are at high risk of developing systemic infection.8,9

Herpes Labialis

Primary oral infection with the herpes simplex virus (HSV) typically occurs at a young age, is asymptomatic, and is not associated with significant morbidity. A minority of persons develop a symptomatic primary infection, presenting with an acute outbreak of oral vesicles that rapidly collapse to form zones of erythema and ulceration. In all cases, the gingiva is involved; in addition, other oral mucosal sites and the perioral skin may be affected. Concomitant cervical lymphadenopathy, fever, chills, anorexia, and irritability are common findings.

After primary oral infection, HSV may persist in a latent state in the trigeminal ganglion and later reactivate as the more common herpes labialis, or “cold sores.” Common triggers for reactivation are well known and include ultraviolet light, trauma, fatigue, stress, and menstruation. These lesions affect approximately 15 to 45 percent of the U.S. population.10 They classically manifest as a well-localized cluster of small vesicles along the vermilion border of the lip or adjacent skin(Figure 4). The vesicles subsequently rupture, ulcerate, and crust within 24 to 48 hours. Spontaneous healing occurs over seven to 10 days.

Figure 4.

Herpes labialis with a cluster of vesicles involving the vermilion border of the lip and adjacent skin.

In immunocompetent patients, herpes labialis usually is mild and self-limited. However, pain, swelling, and cosmetic concerns may prompt physician consultation. Orally administered antiviral agents, such as acyclovir (Zovirax) or valacyclovir (Valtrex), have a modest clinical benefit if initiated during the prodrome.10,11,30 Topical treatment with 1% penciclovir cream (Denavir) may reduce healing time and pain slightly, even if initiated after the prodrome.12,30 Reduction in healing time with systemic or topical agents is modest—approximately one day or less. Use of systemic antivirals for herpes labialis generally should be reserved for immunocompromised patients. Prophylactic treatment with oral antiviral medications may help patients who experience frequent recurrences, anticipate unavoidable exposure to a known trigger, or suffer from frequent episodes of postherpetic erythema multiforme.13,14,31,32 Recurrent herpetic infections should not be treated with corticosteroids.

Recurrent Aphthous Stomatitis

Recurrent aphthous stomatitis, or “canker sores,” is an oral ulcerative condition with a prevalence ranging from 5 to 21 percent.33 Although a variety of host and environmental factors have been implicated, the precise pathogenesis remains unknown. Smoking is associated with a lower prevalence, but other associations, such as nutritional deficiencies (e.g., vitamin B12, folate, iron), remain unclear.33 Severe cases may be related to underlying systemic conditions such as inflammatory bowel disease, celiac disease, Behçet’s syndrome, and HIV infection.34,35

Recurrent aphthous stomatitis is characterized by recurring, painful, solitary or multiple ulcers, typically covered by a white-to-yellow pseudomembrane and surrounded by an erythematous halo(Figure 5). Recurrent aphthous stomatitis usually involves nonkeratinizing mucosa (e.g., labial mucosa, buccal mucosa, ventral tongue). There are three clinical forms: minor, major, and herpetiform. The minor form is the most common and appears as rounded, well-demarcated, single or multiple ulcers less than 1 cm in diameter that usually heal in 10 to 14 days without scarring.

Figure 5.

Recurrent aphthous stomatitis: ulcer with a yellow pseudomembranous covering and surrounding erythematous halo.

Most patients with mild aphthae require no treatment or only periodic topical therapy. Commonly used therapies include topical corticosteroids, such as fluocinonide gel (Lidex) and triamcinolone acetonide with carboxymethylcellulose paste (Kenalog in Orabase). However, much of the evidence in support of these treatments is from small, incompletely blinded trials, and thus their effectiveness is uncertain.36,37 Chlorhexidine gluconate (Peridex) mouthwash decreases the severity of an episode but does not reduce the incidence of ulcers.15 Amlexanox 5% paste (Aphthasol) may promote healing and lessen pain.16 In severe or constantly recurring cases, systemic therapy with agents such as thalidomide (Thalomid) may be necessary. Because of the risk of serious adverse effects and its off-label status, thalidomide generally is reserved for severe cases such as those associated with HIV infection.17

Erythema Migrans

Erythema migrans, which should not be confused with the characteristic rash of early Lyme disease, also is known as geographic tongue or benign migratory glossitis. A common oral inflammatory condition of unknown etiology, it has an estimated prevalence of 1 to 3 percent. The most commonly suggested associations are atopy and psoriasis.18 It usually affects the tongue, although other oral sites may be involved.

Erythema migrans may occur in children and adults and exhibits a female predilection. Tongue lesions exhibit central erythema caused by atrophy of the filiform papillae and usually are surrounded by slightly elevated, curving, white-to-yellow borders (Figure 6). The condition typically waxes and wanes, and the lesions demonstrate a migrating pattern. Some patients may complain of pain or burning, especially when eating spicy foods. However, most individuals are asymptomatic and do not require treatment for this benign condition. For symptomatic cases, several treatments have been proposed, including topical steroids, zinc supplements, and topical anesthetic rinses. None of these treatments has been proven to be uniformly effective.18

Figure 6.

Erythema migrans of the dorsal tongue.

Hairy Tongue

Hairy tongue is characterized by elongation and hypertrophy of the filiform papillae on the dorsal tongue, causing a hair-like appearance (Figure 7). This condition results from inadequate desquamation or increased keratinization of the papillae. These papillae, which normally are about 1 mm in length, may become as long as 12 mm. It occurs most often in persons who smoke heavily and it also may be associated with poor oral hygiene, oxidizing mouthwashes, Candida albicans, and certain medications.19–21

Figure 7.

Hairy tongue showing elongated papillae with brown discoloration.

Although often called “black” hairy tongue, the condition may cause black, brown, or yellow discoloration depending on the foods ingested, tobacco use, and the amount of coffee or tea consumed. Rarely, patients may complain of gagging or of a metallic taste. Debris between elongated papillae can result in halitosis. Most cases improve with avoidance of predisposing factors and regular tongue brushing using a soft toothbrush or tongue scraper. Hairy tongue should not be confused with oral hairy leukoplakia, a condition characterized by vertical white striations typically affecting the lateral tongue bilaterally.

Lichen Planus

Oral lichen planus is a chronic waxing and waning inflammatory condition that affects an estimated 1 to 2 percent of adults. Although the etiology is uncertain, evidence suggests an immune-mediated mechanism involving CD8+ cytotoxic T-cell–induced apoptosis of epithelial cells.38 All age groups may be affected, but it predominates in adults older than 40 years, with a female-to-male ratio of 1.4:1.39

Two major clinical forms of oral lichen planus exist: reticular and erosive. The reticular form can appear as bilateral asymptomatic, white, lacy striations (Wickham’s striae) or papules on the posterior buccal mucosa (Figure 8). The erosive form manifests as zones of tender erythema and painful ulcers surrounded by peripheral white, radiating striae (Figure 9A). It may also manifest as generalized erythema and ulceration of the gingiva, known as desquamative gingivitis (Figure 9B).

Figure 8.

Reticular oral lichen planus. White, lace-like striations on the buccal mucosa are known as Wickham’s striae.

Figure 9.

Erosive lichen planus. (A) Central ulceration with peripheral radiating Wickham’s striae on the buccal mucosa.(B) Generalized gingival erythema and erosions (desquamative gingivitis).

Classic lesions of reticular form often are readily identified clinically. However, lesions that do not exhibit classic features may require biopsy for diagnosis. Asymptomatic patients do not require treatment. For symptomatic patients, topical corticosteroid gels, such as fluocinonide and corticosteroid mouth rinses, may be prescribed.22 There is debate about whether oral lichen planus is associated with an increased risk of oral cancer.40 Therefore, periodic follow-up of patients is appropriate.

The Authors

WANDA C. GONSALVES, M.D., is assistant professor of family medicine at the Medical University of South Carolina, Charleston. Dr. Gonsalves received her degree in dental hygiene from the University of Louisville, Ky., and her medical degree and residency training in family medicine from the University of Kentucky, Lexington.

ANGELA C. CHI, D.M.D., is assistant professor of oral pathology at the Medical University of South Carolina College of Dental Medicine. Dr. Chi received her dental degree from Harvard School of Dental Medicine, Boston, Mass., and completed a residency in oral, head, and neck pathology at Emory University, Atlanta, Ga.

BRAD W. NEVILLE, D.D.S., is professor and director of the Division of Oral Pathology at the Medical University of South Carolina College of Dental Medicine. Dr. Neville received his dental degree from West Virginia University School of Dentistry, Morgantown, and completed a residency in oral, head, and neck pathology at Emory University.

Address correspondence to Wanda C. Gonsalves, M.D., Department of Family Medicine, 295 Calhoun St., P.O. Box 250192, Charleston, SC 29425 (e-mail: gonsalvw@musc.edu). Reprints are not available from the authors.

Author disclosure: Nothing to disclose.

Photographs provided by the authors.


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15. Porter  S, Scully  C.  Aphthous ulcers (recurrent).  Clin Evid.  2005;13:1687–94.

16. Greer  RO  Jr, Lindenmuth  JE, Juarez  T, Khandwala  A.  A double-blind study of topically applied 5% amlexanox in the treatment of aphthous ulcers.  J Oral Maxillofac Surg.  1993;51:243–8.

17. Ramirez-Amador  VA, Esquivel-Pedraza  L, Ponce-de-Leon  S, Reyes-Teran  G, Gonzalez-Guevara  M, Ponce-de-Leon  S, et al.  Thalidomide as therapy for human immunodeficiency virus-related oral ulcers: a double-blind placebo-controlled clinical trial.  Clin Infect Dis.  1999;28:892–4.

18. Assimakopoulos  D, Patrikakos  G, Fotika  C, Elisaf  M.  Benign migratory glossitis or geographic tongue: an enigmatic oral lesion.  Am J Med.  2002;113(9):751–5.

19. Harada  Y, Gaafar  H.  Black hairy tongue. A scanning electron microscopic study.  J Laryngol Otol.  1977;91:91–6.

20. Heymann  WR.  Psychotropic agent-induced black hairy tongue.  Cutis.  2000;66:25–6.

21. Sarti  GM, Haddy  RI, Schaffer  D, Kihm  J.  Black hairy tongue.  Am Fam Physician.  1990;41:1751–5.

22. Chan  ES, Thornhill  M, Zakrzewska  J.  Interventions for treating oral lichen planus.  Cochrane Database Syst Rev.  1999;(2):CD001168.

23. Gonsalves  WC, Chi  AC, Neville  BW.  Common oral lesions. Part II: Masses and neoplasia.  Am Fam Physician.  2007;75:509–12.

24. Ghannoum  MA, Abu-Elteen  KH.  Pathogenicity determinants of Candida.  Mycoses.  1990;33:265–82.

25. Abu-Elteen  KH, Abu-Elteen  RM.  The prevalence of Candida albicans populations in the mouths of complete denture wearers.  New Microbiol.  1998;21:41–8.

26. Hajjeh  RA, Sofair  AN, Harrison  LH, Lyon  GM, Arthington-Skaggs  BA, Mirza  SA, et al.  Incidence of bloodstream infections due to Candida species and in vitro susceptibilities of isolates collected from 1998 to 2000 in a population-based active surveillance program.  J Clin Microbiol.  2004;42:1519–27.

27. Shetty  SS, Harrison  LH, Hajjeh  RA, Taylor  T, Mirza  SA, Schmidt  AB, et al.  Determining risk factors for candidemia among newborn infants from population-based surveillance: Baltimore, Maryland, 1998–2000.  Pediatr Infect Dis J.  2005;24:601–4.

28. Goins  RA, Ascher  D, Waecker  N, Arnold  J, Moorefield  E.  Comparison of fluconazole and nystatin oral suspensions for treatments of oral candidiasis in infants.  Pediatr Infect Dis J.  2002;21:1165–7.

29. Hoppe  JE.  Treatment of oropharyngeal candidiasis and candidal diaper dermatitis in neonates and infants: review and reappraisal.  Pediatr Infect Dis J.  1997;16:885–94.

30. Worrall  G.  Herpes labialis.  Clin Evid.  2004;12:2312–20.

31. Weston  WL, Morelli  JG.  Herpes simplex virus-associated erythema multiforme in prepubertal children.  Arch Pediatr Adolesc Med.  1997;151:1014–6.

32. Tatnall  FM, Schofield  JK, Leigh  IM.  A double-blind, placebo-controlled trial of continuous acyclovir therapy in recurrent erythema multiforme.  Br J Dermatol.  1995;132:267–70.

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34. Neville BW. Recurrent aphthous stomatitis (recurrent aphthous ulcerations; canker sores). In: Oral and Maxillofacial Pathology. Philadelphia, Pa.: Saunders, 2002: 285–90.

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Common Oral Lesions: Part II. Masses and Neoplasia


Medical University of South Carolina, Charleston, South Carolina

Am Fam Physician. 2007 Feb 15;75(4):509-512.

  This is part II of a two-part article on oral lesions. Part I, “Superficial Mucosal Lesions,” appears in this issue ofAFP on page 501.

  Related Editorial

Certain common oral lesions appear as masses, prompting concern about oral carcinoma. Many are benign, although some (e.g., leukoplakia) may represent neoplasia or cancer. Palatal and mandibular tori are bony protuberances and are benign anomalies. Oral pyogenic granulomas may appear in response to local irritation, trauma, or hormonal changes of pregnancy. Mucoceles represent mucin spillage into the oral soft tissues resulting from rupture of a salivary gland duct. Oral fibromas form as a result of irritation or masticatory trauma, especially along the buccal occlusal line. Oral cancer may appear clinically as a subtle mucosal change or as an obvious mass. Oral leukoplakia is the most common premalignant oral lesion. For persistent white or erythematous oral lesions, biopsy should be performed to rule out neoplastic change or cancer. Most oral cancers are squamous cell carcinomas. Tobacco and heavy alcohol use are the principal risk factors for oral cancer. Family physicians should be able to recognize these lesions and make appropriate referrals for biopsy and treatment.

Physicians regularly encounter oral health issues in practice. Part I of this two-part series discusses superficial mucosal lesions such as candidiasis and herpes labialis.1  This article reviews common oral lesions that may appear as masses or represent neoplastic change (Table 1).2–8 Many of these are benign conditions. Neoplastic or cancerous oral lesions may appear as white or erythematous patches, ulcerated lesions, or masses. Family physicians should be able to recognize these lesions and make appropriate referrals for biopsy and treatment. Differentiating benign from worrisome lesions and providing appropriate counseling regarding risk factors (e.g., tobacco use) is central to achieving national oral health goals.9


Clinical recommendation Evidence rating References
Observation is appropriate for pregnancy-related oral pyogenic granulomas because they have a high recurrence rate with excision and often resolve after parturition. C 4,13
For persistent erythematous or white oral lesions, biopsy should be performed. C 7

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, see page 453 or http://www.aafp.org/afpsort.xml.

TABLE 1: Common Oral Lesions That Appear as Masses

Condition Clinical presentation Treatment Comment
Palatal and mandibular tori2,3 Bony protuberances of the palate or lingual aspect of the mandible Removal required only if interferes with function or denture fabrication, or is subject to recurrent trauma Developmental anomaly
Pyogenic granuloma4 Rapidly growing, red, lobulated mass Refer for surgical excision; observe in pregnancy unless excision warranted (e.g., excessive bleeding) Possible postpartum regression
Mucocele5 Bluish, fluctuant mucosal swelling, often with a history of periodic rupture Excision of lesion and adjacent “feeder” minor salivary glands Pathologic examination of specimen required
Fibroma6 Firm, pink, smooth-surfaced nodule Excision Pathologic examination required
Leukoplakia7 White patch that does not wipe off Refer for biopsy and surgical excision No evidence that surgical excision prevents malignant transformation
Erythroplakia7 Red patch without obvious cause Refer for biopsy and surgical excision No evidence that surgical excision prevents malignant transformation
Squamous cell carcinoma8 Nonhealing ulcer or mass Refer for biopsy, staging, surgery, and treatment

Information from references 2 through 8.

Palatal and Mandibular Tori

Tori are benign, nonneoplastic, bony protuberances that arise from the cortical plate. They sometimes are mistaken for malignancies. These exostoses are considered developmental anomalies, although they usually do not appear until adulthood. A torus located along the midline of the hard palate is called a palatal torus, or torus palatinus (Figure 1), and a torus located along the lingual aspect of the mandible is called a mandibular torus, or torus mandibularis (Figure 2). Palatal tori are reported in 20 to 35 percent of the U.S. population, whereas mandibular tori are reported in 7 to 10 percent.2,3 Removal is required only if a torus interferes with function or denture fabrication, or is subject to recurrent traumatic surface ulceration.10

Figure 1.

Palatal torus.

Figure 2.

Mandibular tori: bilaterally symmetric bony protuberances on the lingual aspect of the mandible.

Pyogenic Granuloma

A pyogenic granuloma is a rapidly growing lesion that develops as a response to local irritation (e.g., poor hygiene, overhanging dental fillings), trauma, or increased hormone levels in pregnancy.11 It is an erythematous, non-painful, smooth or lobulated mass that often bleeds easily when touched (Figure 3). Oral pyogenic granulomas most often develop on the gingiva, but less common locations include the lip, tongue, and buccal mucosa.12 They may vary in diameter from a few millimeters to several centimeters. Surgical excision usually is adequate because recurrence is uncommon unless the lesion or local sources of irritation are inadequately removed. Observation is more appropriate in pregnant women because many pyogenic granulomas resolve after the birth.13 Excessive bleeding or other considerations may prompt excision. However, lesions excised during pregnancy are more likely to recur (because of the hormone effect).4

Figure 3.

Pyogenic granuloma: erythematous gingival nodule.


A mucocele is an area of mucin spillage in soft tissue resulting from rupture of a salivary gland duct. Children and young adults are most commonly affected, although this lesion may occur at any age. There is often a history of local trauma (e.g., biting). Many patients describe episodes of recurrent swelling with periodic rupture. The typical clinical presentation is a bluish, dome-shaped, fluctuant mucosal swelling (Figure 4). However, if the area of mucin spillage is deeper, the overlying mucosa may be normal in color.5 Long-standing lesions may become fibrotic and therefore be firm rather than fluctuant upon palpation. The lower labial mucosa is the most common location, although any oral site with salivary gland tissue may be affected.14

Figure 4.

Mucocele: nodule involving the lower labial mucosa.

Appropriate treatment consists of local surgical excision, including the removal of adjacent minor salivary glands. Pathologic examination of the excised tissue is needed to rule out neoplasia.5


A fibroma is a focus of hyperplastic fibrous connective tissue representing a reactive response to local irritation or masticatory trauma.6 Fibromas occur in approximately 1.2 percent of adults.10 The most common location is along the occlusal line of the buccal mucosa—an area subject to masticatory trauma—although other locations, such as the tongue, labial mucosa, and gingiva, are possible. Fibromas manifest as asymptomatic, moderately firm, smooth-surfaced, pink, sessile or pedunculated nodules (Figure 5).6 They are treated by surgical excision, and recurrence is rare.10 The removed tissue should undergo pathologic examination to rule out the possibility of neoplasms that may have a similar appearance.6

Figure 5.

Fibroma: a firm nodule of the anterior buccal mucosa at the level of the occlusal plane.

Leukoplakia, Erythroplakia, and Oral Cancer

Precancer and early oral cancer can be subtle and asymptomatic. A lesion may begin as a white(Figure 6) or red patch, progress to an ulceration, and later become an endophytic or exophytic mass (Figure 7).

Figure 6.

Leukoplakia: white plaque involving the lateral tongue.

Figure 7.

Squamous cell carcinoma on the ventrolateral tongue.

Oral leukoplakia, the best-known pre-malignant oral lesion, is defined by the World Health Organization as “a white patch or plaque that cannot be characterized clinically or pathologically as any other disease.”15 Analogous red lesions are called erythroplakia, and combined red and white lesions are known as speckled leukoplakia or erythroleukoplakia. Erythroplakia and speckled leukoplakia are more likely than leukoplakia to exhibit dysplasia or carcinoma microscopically.16

In the United States, cancers of the oral cavity and oropharynx are the ninth most common cancer, accounting for approximately 3 percent of malignancies among men and 2 percent of malignancies among women.17 Prevalence increases with age. Approximately 90 percent of oral cancers are squamous cell carcinomas. They occur most commonly on the tongue, floor of the mouth, and vermilion border of the lower lip. Sixty percent of oral carcinomas are advanced by the time they are detected, and about 15 percent of patients have another cancer in a nearby area such as the larynx, esophagus, or lungs. Tobacco use and heavy alcohol consumption are the two principal risk factors, accounting for 75 percent of oral carcinomas.18

The evidence regarding the sensitivity, specificity, and impact of screening on morbidity and mortality is limited. Pending better evidence to guide clinical screening and intervention, a prudent course of action would be to refer patients with unclassified red or white lesions persisting longer than two weeks to an oral and maxillofacial surgeon or pathologist, or to an otolaryngologist, for evaluation, biopsy, and treatment.7

Precancerous lesions should be surgically removed, if possible. Cryotherapy and laser ablation have been used, although these methods do not allow for tissue preservation or microscopic examination. Treatment of oral squamous cell carcinoma is guided by clinical staging.8 The overall five-year survival rate for oral cancer is 50 to 55 percent.19 Long-term follow-up is advised because of the potential for recurrence or additional lesions.

Photographs provided by the authors.


1. Gonsalves  WC, Chi  AC, Neville  BW.  Common oral lesions. Part I: Superficial mucosal lesions.  Am Fam Physician.  2007;75:501–7.

2. Neville BW, Damm DD, Allen CM, Bouqout JE. Torus mandibularis. In: Oral and Maxillofacial Pathology. Philadelphia, Pa.: Saunders, 2002:21–2.

3. Neville BW, Damm DD, Allen CM, Bouqout JE. Torus palatinus. In: Oral and Maxillofacial Pathology. Philadelphia, Pa.: Saunders; 2002:20.

4. Sills  ES, Zegarelli  DJ, Hoschander  MM, Strider  WE.  Clinical diagnosis and management of hormonally responsive oral pregnancy tumor (pyogenic granuloma).  J Reprod Med.  1996;41:467–70.

5. Neville BW, Damm DD, Allen CM, Bouqout JE. Mucocele (mucus extravasation phenomenon; mucus escape reaction). In: Oral and Maxillofacial Pathology. Philadelphia, Pa.: Saunders, 2002:389–91.

6. Neville BW, Damm DD, Allen CM, Bouqout JE. Fibroma. In: Oral and Maxillofacial Pathology. Philadelphia, Pa.: Saunders, 2002:438–9.

7. Truman  BI, Gooch  BF, Sulemana  I, Gift  HC, Horowitz  AM, Evans  CA, et al.  Reviews of evidence on interventions to prevent dental caries, oral and pharyngeal cancers, and sports-related craniofacial injuries.  Am J Prev Med.  2002;23(1 suppl):21–54.

8. National Cancer Institute. Lip and oral cavity cancer (PDQ): treatment. Accessed July 28, 2006, at: http://www.cancer.gov/cancertopics/pdq/treatment/lip-and-oral-cavity/healthprofessional.

9. Evans  CA, Kleinman  DV.  The Surgeon General’s report on America’s oral health: opportunities for the dental profession [Published correction appears in J Am Dent Assoc 2001;132:444].  J Am Dent Assoc.  2000;131:1721–8.

10. Bouqout JE, Nikai H. Lesions of the oral cavity. In: Gnepp DR, ed. Diagnostic Surgical Pathology of the Head and Neck. Philadelphia, Pa.: Saunders, 2001:141–238.

11. Demir  Y, Demir  S, Aktepe  F.  Cutaneous lobular capillary hemangioma induced by pregnancy.  J Cutan Pathol.  2004;31:77–80.

12. Angelopoulos  AP.  Pyogenic granuloma of the oral cavity: statistical analysis of its clinical features.  J Oral Surg.  1971;29:840–7.

13. Kroumpouzos  G, Cohen  LM.  Dermatoses of pregnancy.  J Am Acad Dermatol.  2001;45:1–19.

14. Gnepp DR, Brandwein MS, Henley JD. Salivary and lacrimal glands. In: Gnepp DR, ed. Diagnostic Surgical Pathology of the Head and Neck. Philadelphia, Pa.: Saunders, 2001:325–430.

15. Kramer  IR, Lucas  RB, Pindborg  JJ, Sobin  LH.  Definition of leukoplakia and related lesions: an aid to studies on oral precancer.  Oral Surg Oral Med Oral Pathol.  1978;46:518–39.

16. Mashberg  A, Samit  A.  Early diagnosis of asymptomatic oral and oropharyngeal squamous cancers.  CA Cancer J Clin.  1995;45:328–51.

17. Jemal  A, Murray  T, Ward  E, Samuels  A, Tiwari  RC, Ghafoor  A, et al.  Cancer statistics, 2005 [Published correction appears in CA Cancer J Clin 2005;55:259].  CA Cancer J Clin.  2005;55:10–30.

18. Weinberg  MA, Estefan  DJ.  Assessing oral malignancies.  Am Fam Physician.  2002;65:1379–84.

19. Silverman  S  Jr.  Demographics and occurrence of oral and pharyngeal cancers. The outcomes, the trends, the challenge  J Am Dent Assoc.  2001;(132 suppl):7S–11S.

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