You must be signed in to read the rest of this article.
Registration on CDEWorld is free. Sign up today!
Forgot your password? Click Here!
Oral allergy syndrome (OAS), also known as either pollen-food allergy syndrome (PFAS) or pollen-related food allergy, is a relatively common allergic/hypersensitivity reaction to fruits, spices, nuts, and vegetables and is strongly associated with allergic reactivity to pollen. The most common manifestation of this allergic condition is pruritus of the lips, throat, gingiva, mouth, and/or tongue. OAS can be suspected by dentists when diagnosing patients who report oral inflammation complaints immediately after eating specific fruits, spices, nuts, and vegetables, and as such, clinicians should be knowledgeable concerning this malady.
OAS is not a simple food allergy reaction because it requires prior sensitization to a cross-reaction of an inhalant allergen, typically pollen, rather than direct sensitization to a specific (food) protein. OAS occurs in 15% to 70% of allergic rhinitis pollen patients and tends to appear more frequently in children compared to adults.1-4 The prevalence of pollen-induced allergic rhinitis/hayfever is between 10% and 30%.5 Although OAS is typically benign, some clinicians have reported more severe symptoms, including angioedema, bronchial asthma, hives, and anaphylaxis. The condition is IgE-mediated mast cell degranulation. Symptoms typically occur within minutes of food ingestion. Cooking foods that produce OAS symptoms may result in the elimination of the reactive symptoms.1-4,6-13
Because the primary symptom is oral pruritus, it is expected that many patients experiencing OAS might consult with their dentists. A type I immediate hypersensitivity reaction, OAS occurs almost immediately after the ingestion of the offending fruit, vegetable, spice, or nut. With digestive enzymes being located within saliva, the initial digestive breakdown occurs in oral tissues and the oropharynx, where the release of the problematic antigens occurs.1
Caliskaner et al investigated risk factors of OAS in patients with seasonal allergic rhinitis/hayfever.2 They reported that OAS was more prevalent in females compared to males and also noted an association with age and asthma. The study examined 111 patients (78 male and 33 female) with seasonal allergic rhinitis, of which 16 (14.4%) were diagnosed with OAS. The authors reported such nasal symptoms as seasonal allergic rhinitis, nasal congestion, runny nose, nasal itching, sneezing, post-nasal drip, and smelling disorders. They described other rhinitis-related symptoms such as headache, itchy palate, itchy pharynx, itchy eyes, watery eyes, red eyes, gritty feeling in eyes, itchy auditory canals, and ear stuffiness. To confirm atopy, all patients underwent skin prick tests with common allergens, including house dust mites, grasses, molds, trees, weeds, feathers, and dander mixtures. Patients in the study population who described OAS symptoms were further evaluated with "prick by prick" testing with fresh fruits and vegetables used as allergens selected according to individual patient history. The authors further reported that with respect to nasal symptoms, only nasal itching was related to OAS.
Matsson and Möller reported on secondary gingivitis reactions to rhinoconjunctivitis to birch pollen in children.6 They investigated 34 children ranging in age from 8 to 17 years with rhinoconjunctivitis secondary to a reactivity to birch pollen and compared those children with sex- and age-matched healthy controls. The children with atopy to birch pollen demonstrated an enhanced degree of gingivitis during the pollen season compared to the children in the healthy control group.
Ausukua et al reported that although rare, anaphylaxis is a possible food-induced severe form of OAS.4
Etiology and History
OAS is within the category of "adverse reactions to food"1-3; it is a distinct pathological entity and is separate from "food allergy," which may or may not be mediated by IgE antibodies, or "contact allergy." All IgE-mediated food allergies are within the category of immediate gastrointestinal hypersensitivity and include type I hypersensitivity reactions, such as anaphylaxis and OAS. OAS is an IgE-mediated type I hypersensitivity sensitization to pollen connected with subsequent cross-reactivity to food allergens. The reaction is against specific proteins and involves the development of specific IgE antibodies. With respect to OAS, these specific allergen proteins are converted to "panallergens," and the IgE antibodies jointly recognize specific pollens and vegetable allergens. OAS typically does not manifest in patients without previous sensitivity to pollen. These vegetable panallergens, which are native to the vegetable, are involved in vegetable defense mechanisms against bacteria, parasites, and fungi, the most common of which are Bet v 1, profilms, and lipid transport proteins.1-4 The proposed issue of cross-reactivity is due to shared epitopes of the structures of both pollen and food allergens. The pollen-specific IgE antibodies may recognize the dietary allergens that share the same epitopes. The IgE allergen complexes bind to the surface of the mast cells (and basophils), which triggers the release of histamine, resulting in OAS symptomatology.1
Bohle et al evaluated major birch pollen allergens after cooking with respect to symptomatology and IgE- and T cell-mediated reactions, both in vitro and in vivo.14 They reported that in vivo the allergens did not cause OAS symptomatology after cooking, although they did report that atopic eczema tended to worsen. In vitro, they reported the loss of the ability to bind IgE and to induce mediator release but with the same activation of Bet v 1-specific T cells as native proteins in cooked food allergens.
The most common OAS pollen allergen is birch pollen, which is implicated in such OAS fruit allergens as kiwi, apple, pear, plum, peach, melon, avocado, tomato, and cherry, and such vegetable allergens as celery, lentils, and peas, and such nut allergens as hazelnut, walnut, and almond (Table 1).3,4,11,15 Other OAS problematic pollens include common weeds, grasses, ragweed, wormwood, and parietaria.1,3,4,6-13
Kondo and Urisu reported initial controversy regarding the definition of OAS,16 in that in 1987 Almot et al first described this phenomenon as allergic symptomology induced by foods with a positive skin test, which mainly produced oral mucosal symptoms.17 Almot et al did not infer any initial association with pollen allergy. In 1988, Ortolani et al further promoted the term OAS and noted an association with birch pollen allergy.18 Valenta and Kraft and Ma et al further defined the term OAS as PFAS so as to avoid confusion between OAS and other food allergies.19,20 OAS was defined as a class 2 food allergy (noting cross-reactivity with a pollen antigen) as compared to a class 1 food allergy (caused by direct intestinal sensitization).6-10 Although OAS clearly is not syndromic, the term OAS has remained the primary descriptive terminology for this condition.1
OAS should be suspected in patients with a known pollen allergy history and in whom oral itching/tingling occurs immediately after eating fresh fruits, vegetables, or nuts. Further confirmation may be attained if the patient has a history of the symptoms being eliminated when eating the offending food(s) cooked, since cooking the particular causative food(s) typically results in the elimination of symptomatology.1,3,4 Such symptoms include tingling, irritation, burning, and/or swelling of the oropharynx, lips, tongue, and palate. The maximum timeframe for symptoms is 1 hour. Symptoms typically are not severe, although some patients may present with more acute local and possibly even systemic symptoms. Although rare, such systemic symptoms include nausea, vomiting, stomach aches, diarrhea, eczema, asthma, hives, and laryngeal edema, and, even more unlikely, anaphylactic shock.
The diagnostic process may be enhanced by use of highly controlled double-blind provocation with a placebo. It is important to use only fresh foods, and it may be difficult to disguise the associated taste. If the patient has a history of more severe symptomatology, there is also risk to such a diagnostic strategy. Immediate hypersensitivity skin assays such as a skin prick test to evaluate for pollen and food hypersensitivities may also be helpful. Further tests such as complete blood count, total IgE, and IgE serum antibodies may be considered as well. Problems with such tests/assays include interpretation issues, added expense, and false positives.
Differential diagnoses include oral viral infections, recurrent aphthae, erythema multiforme, burns, and contact allergies to other substances.1-4,6-13 Patients reporting a history positive for food allergy with the symptom of oral pruritus, and yet reporting the absence of food allergy symptoms after eating the same allergy-producing food(s) after cooking, would lend suspicion to a possible diagnosis of OAS.15 Management by dentists for severe symptoms such as anaphylaxis would be the same as for any other allergenic manifestation of anaphylaxis,4 although an anaphylactic reaction related to OAS would be extremely rare and the authors have no knowledge of any reported cases in the literature.
Five patients presented to a private practice oral medicine clinician with histories significant for an OAS diagnosis. All five patients noted a history positive for seasonal allergic rhinitis, and all of them reported that cooking of the offending foods eliminated the symptomatology. The age range of these patients was from 32 to 61; their age range when the symptoms first occurred was from 12 to approximately 41 (Table 2). (All but one of the patients remembered only the approximate time of first occurrence of symptoms.) The age of the initiation of symptoms of these five patients was considerably older than that reported in most of the literature.1-4
Because OAS is a benign condition, these patients were not referred for allergy patch testing. Furthermore, it did not appear necessary to order a metabolic workup for these patients, including routine blood studies or other laboratory evaluations; only taking a thorough history, checking vital signs, and performing a clinical examination seemed to be required. The history of seasonal allergies and itchy (or irritated) tongue, mouth, and/or throat, and possibly minor oral swelling, along with the absence of clinical findings, are usually sufficient to make the diagnosis. Also, a history that notes eating the fruit or vegetable cooked does not cause the reaction aids in defining the diagnosis.
Avoidance of foods producing OAS symptoms is the first-line management strategy for this condition. Referral to the patient's primary care physician or an allergy and immunology physician should be considered, both with respect to diagnosis and management. The necessary degree of management is dependent on the severity of the patient's symptoms. Only the specific "trigger" foods that have a history of producing symptoms need to be avoided.
Prescription of pollen-specific immunotherapy has demonstrated success with some but not all OAS patients.3,4 Because atopic patients may outgrow pollen allergies, it is possible that they may also develop greater tolerance to OAS-associated foods, with diminished allergy symptoms or even the absence of such symptoms. However, such a situation is not always reliable. Furthermore, because many of the immunogenic proteins in fruits and vegetables are unstable (heat-labile), cooking of some OAS-associated foods may eliminate OAS symptomatology to those foods. The clinician may or may not consider prescribing a self-injected epinephrine device.1,4,6-13,15
To reiterate, suggesting the avoidance of the particular food causing the OAS symptoms is a reasonable first choice in managing patients with an OAS diagnosis. Secondary management consists of cooking the problematic foods and/or a referral to the patient's primary care physician or such specialists as dermatologists, pulmonologists, and allergy and immunology physicians.
Dental clinicians should be familiar with OAS, a condition that is relatively common and known to manifest itself primarily with oral mucosal symptoms. In addition to being knowledgeable concerning the incidence, diagnosis, etiology, and management of OAS, dental clinicians should know when to consider physician referral and when to suggest the avoidance of trigger foods.
About the Authors
Heba Hussein, BDS, PhD
Lecturer, Department of Oral Medicine, Diagnosis, and Periodontology, Faculty of Dentistry, Cairo University, Cairo, Egypt
Robert K. Mensah, DDS
Private Practice limited to Orthodontics, Largo, Maryland
Ronald S. Brown, DDS, MS
Clinical Associate Professor, Department of Otolaryngology, Georgetown University Medical Center, Washington, DC; Professor Emeritus, Department of Oral Diagnosis and Radiology, Howard University College of Dentistry, Washington, DC
Queries to the author regarding this course may be submitted to firstname.lastname@example.org.
1. Price A, Ramachandran S, Smith GP, et al. Oral allergy syndrome (pollen-food allergy syndrome). Dermatitis. 2015;26(2):78-88.
2. Caliskaner Z, Naiboglu B, Kutlu A, et al. Risk factors for oral allergy syndrome in patients with seasonal allergic rhinitis. Med Oral Patol Oral Cir Bucal. 2011:16(3):e312-e316.
3. Vieths S, Scheurer S, Ballmer-Weber B. Current understanding of cross-reactivity of food allergens and pollen. Ann NY Acad Sci. 2002;964:47-68.
4. Ausukua M, Dublin I, Echebarria MA, Aguirre JM. Oral allergy syndrome (OAS), general and stomatological aspects. Med Oral Patol Oral Cir Buccal. 2009;14(11):e568-e572.
5. Schramm A, Jasiewicz-Honkisz B, Osmenda G, et al. Th17 responses are not altered by natural exposure to seasonal allergens in pollen-sensitive patients. Allergy Asthma Clin Immunol. 2016;12:55.
6. Matsson L, Möller C. Gingival inflammatory reactions in children with rhinoconjunctivitis due to birch pollinosis. Scand J Dent Res. 1990;98(6):504-509.
7. Breuer K, Wulf A, Constien A, et al. Birch pollen-related food as a provocation factor of allergic symptoms in children with atopic eczema/dermatitis syndrome. Allergy. 2004;59(9):988-994.
8. Reekers R, Busche M, Wittmann M, et al. Birch pollen-related foods trigger atopic dermatitis in patients with specific cutaneous T-cell responses to birch pollen antigens. J Allergy Clin Immunol. 1999;104(2 Pt 1):466-472.
9. Ozcelik O, Haytac MC. Oral challenge test for the diagnosis of gingival hypersensitivity to apple: a case report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006;101(3):317-321.
10. Blanco C. Latex-fruit syndrome. Curr Allergy Asthma Rep. 2003;3
11. Fernández-Rivas M, Benito C, González-Mancebo E, de Durana DA. Allergies to fruits and vegetables. Pediatr Allergy Immunol. 2008;19(8):675-681.
12. Ortolani C, Pastorello EA, Farioli L, et al. IgE-mediated allergy from vegetable allergens. Ann Allergy. 1993;71(5):470-476.
13. Lucas JS, Lewis SA, Hourihane JO. Kiwi fruit allergy: a review. Pediatr Allergy Immunol. 2003;14(6):420-428.
14. Bohle B, Zwölfer B, Heratizadeh A, et al. Cooking birch pollen-related food: divergent consequences for IgE- and T cell-mediated reactivity in vitro and in vivo. J Allergy Clin Immunol. 2006;118(1):242-249.
15. Kondo Y, Urisu A. Oral allergy syndrome. Allergol Int. 2009;58(4):485-491.
16. Amlot PL, Kemeny DM, Zachary C, et al. Oral allergy syndrome (OAS): symptoms of IgE-mediated hypersensitivity to foods. Clin Allergy. 1987;17(1):33-42.
17. Ortolani C, Ispano M, Pastorello E, et al. The oral allergy syndrome. Ann Allergy. 1988;61(6 Pt 2):47-52.
18. Valenta R, Kraft D. Type 1 allergic reactions to plant-derived food: a consequence of primary sensitization to pollen allergens. J Allergy Clin Immunol. 1996;97(4):893-895.
19. Ma S, Sicherer SH, Nowak-Wegrzyn A. A survey on the management of pollen-food allergy syndrome in allergy practices. J Allergy Clin Immunol. 2003;112(4):784-788.
20. Sussman G, Sussman A, Sussman D. Oral allergy syndrome. CMAJ. 2010;182(11):1210-1211.