Dentistry and the Allergic Patient

The successful management of upper respiratory tract allergy is based on a triad of interdependent approaches that, with rare exceptions, must all be considered in every allergic patient. They consist of allergen avoidance with environmental control measures, pharmacotherapy with use of a step-care approach, and immunotherapy. Environmental control measures should be used to prevent events that trigger and sustain the condition. Once started, the allergic reaction includes the release of mediators of inflammation that produce well-known symptoms of allergic rhinitis. Treatment should consist of a step-wise, rational approach that includes site-based therapy with one or more drugs acting at different sites. The drugs used are antihistamines, decongestants, cromolyn sodium, and corticosteroids. Immunotherapy should be considered at any step, because it offers the only curative approach.

Download Full-text

Allergic Rhinitis

Pediatrics in Review ◽

10.1542/pir.13.9.323 ◽

1992 ◽

Vol 13 (9) ◽

pp. 323-328

Author(s):

Frank S. Virant

Keyword(s):

Allergic Rhinitis ◽

Clinical Signs ◽

Upper Airway ◽

Allergic Patient ◽

The United States ◽

Specific Ige ◽

Interferon Γ ◽

Interleukin 4 ◽

Primary Defect ◽

Primary Focus

Epidemiology Allergic rhinitis affects as many as 8% to 10% of children in the United States. Many of these children suffer significant morbidity, leading to millions of lost school days annually. Morbidity is amplified when these children concurrently suffer from complications of allergic rhinitis, such as recurrent otitis media or chronic sinus disease. Typically, children who have allergic rhinitis have a family history of atopic disorders. Upper airway allergy may become manifest at any age, but the appearance of symptoms is most common during childhood or young adulthood. Clinical signs of rhinitis may be perennial, seasonal, or episodic, and the primary focus of complaints may relate to secondary problems, including ear, sinus, or lung disease. Pathophysiology In the allergic patient, disease is mediated by the production of antigenspecific IgE by the patient's B lymphocytes. Current research suggests that the primary defect may be the excessive production of interleukin 4 (IL-4) or a deficient level of gamma interferon (γ-INF) when a T-cell is presented with an antigen. This constellation of immunomodulators directs the B-cell to produce IgE rather than the IgG response of the non-allergic patient. Clinical disease occurs when an allergen reacts with antigen-specific IgE on the patient's nasal mast cells. When these factors combine, the mast cell is activated to release a variety of preformed and newly produced mediators, including histamine, leukotrienes, and prostaglandins (Fig 1).

Download Full-text