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Quick Review for Patients
Note: click on underlined words for more detail or photos. Inflammatory papillary hyperplasia, also known as papillary hyperplasia of the palate and erroneously as palatal papillomatosis, is almost always restricted to the mucosa under a denture base. First reported by Berry in 1851, it results from selective but severe edema and eventual inflammatory fibrosis of the connective tissue papillae between the rete processes of the palatal epithelium. It is found in three of every 1,000 adults (Table 1).
The great majority of cases are seen beneath ill-fitting dentures of long
use and in persons who do not take their dentures out overnight. The lesion
seems to result from a combination of chronic, mild trauma and low-grade
infection by bacteria or candida yeast. It is occasionally seen in patients
without dentures but with high palatal vaults or with the habit of breathing
through their mouths.
Clinical Features Papillary hyperplasia is seen in middle-aged
and older persons and there is a strong female predilection (2 females:1
male). The disease occurs on the bone-bound oral mucosa of
the hard palate and alveolar ridges. It presents as a cluster of individual
papules or nodules which may be erythematous, somewhat translucent or normal
in surface coloration (Figures 1 & 2). Often the entire vault of the hard palate
is involved, with alveolar mucosa being largely spared. White cottage cheese-like
colonies of candida may be seen in clefts between papules.
There is seldom pain, but a burning sensation may be produced by the yeast
infection. Early papules are more edematous while older ones are more fibrotic
and firm, being individually indistinguishable from irritation
fibroma. Pathology and Differential Diagnosis Connective tissue papillae are greatly enlarged by edematous connective tissue, granulation tissue, densely fibrotic tissue, or a combination thereof, depending on the duration of the lesion (Figures 3-5). Small to moderate numbers of chronic inflammatory cells are present, perhaps admixed with occasional polymorphonuclear leukocytes. Each enlarged papilla produces a surface nodule which may be pedunculated or sessile, with deep clefts between nodules. Covering epithelium is often atrophic but may be acanthotic, especially near the base of the inter-nodal troughs. Occasional lesions demonstrate extensive pseudoepitheliomatous hyperplasia. Basal cell hyperchromatism and basal layer hyperplasia often impart a false appearance of mild epithelial dysplasia. Surface ulceration is surprisingly rare and deeper tissues show few alterations beyond a mild chronic inflammatory cell infiltration.
While individual nodules may appear identical to pyogenic granuloma and
irritation fibroma, the palatal location and the multinodularity of the lesion
makes the diagnosis of papillary hyperplasia an easy one. Some of the more
edematous papules may mimic the mucus extravasation of mucocele,
but will be negative for mucus with the mucicarmine stain. A silver or periodic
acid-Schiff (PAS) stain will frequently identify candida spores and hyphae
in the superficial portions of the epithelium, especially in cases with severe
acanthosis or pseudoepitheliomatous hyperplasia. Treatment and Prognosis The old concern that papillary hyperplasia of the palate held increased risk for cancer is no longer accepted. Even extensive lesions will continue indefinitely, waxing and waning in the early years but remaining more constant as nodules become more and more fibrotic. Occasional proliferations are so exuberant that clefts between nodules may be more than a centimeter deep.
Early lesions may completely disappear with cessation of denture use for
2-4 weeks, perhaps aided by topical antibiotic or antifungal
therapies. Persistent lesions must be surgically removed or
laser ablated if a proper base is to be prepared for a new and better-fitting
denture.
References (Chronologic Order) Note: General references can be found by clicking on that topic to the left. Berry A. A partial set of teeth sustained by air chambers instead of clasps. Dent Reg West 1851; 9:114-116. Bhaskar SN, Beasley JD III, Cutright DE. Inflammatory papillary hyperplasia of the oral mucosa: report of 341 cases. J Am Dent Assoc 1970; 81:949-952. Priddy RW. Inflammatory hyperplasias of the oral mucosa. J Can Dent Assoc 1992; 58:311-315,319-321. Bouquot JE, Wrobleski. Papillary (pebbled) masses of the oral mucosa, so much more than simple papillomas. Pract Perio Anesth Dent 1996; 8:533-543.
Salonen MAM, Raustia AM, Oikarinen KS.
Effect of treatment of palatal inflammatory papillary hyperplasia with local
and systemic antifungal agents accompanied by renewal of complete dentures.
Acta Odont Scand 1996; 54:87-91. Table 1: Gender-specific
prevalence rates per 1,000 population for selected oral masses and surface
alterations in U.S. adults, ranked by total frequency. Modified from Bouquot
JE. Common oral lesions found during a mass screening examination. J Am
Dent Assoc 1986; 112:50-57, and Bouquot JE, Gundlach KKH. Oral exophytic
lesions in 23,616 white Americans over 35 years of age. Oral Surg Oral Med
Oral Pathol 1986; 62:284-291. Diagnosis Number of lesions per 1,000
population* Males Females Total Leukoplakia 43.2 20.9 28.9 Torus palatinus 13.2 21.7 18.7 Irritation fibroma 13.0 11.4 12.0 Fordyce granules 17.7 5.2 9.7 Hemangioma 8.4 4.1 5.5 Papilloma 5.3 4.2 4.6 Epulis fissuratum 3.5 4.4 4.1 Varicosities, lingual 3.5 3.4 3.5 Papillary hyperplasia 1.7 3.8 3.0 Mucocele 1.9 2.6 2.5 Enlarged lingual tonsil 2.4 1.2 1.6 Lichen planus 1.2 1.1 1.1 Buccal exostosis 0.9 0.9 0.9 Median rhomboid glossitis 0.8 0.5 0.6 Epidermoid cyst 0.7 0.4 0.5 Oral melanotic macule 0.5 0.3 0.4 Oral tonsils (except lingual) 0.5 0.3 0.4 Lipoma 0.2 0.1 0.2 Ranula 0.2 0.1 0.2 Buccinator node, hyperplastic 0.1 0.1 0.1 Pyogenic granuloma 0.0 0.07 0.04 Nasoalveolar cyst 0.0 0.07 0.04 Neurofibroma 0.0 0.07 0.04 * total examined population = 23,616 adults over 35 years of
age
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