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By far, the most common of the oral fibromatoses involves the gingiva, usually affecting all gingival surfaces of both arches. Even so, it is seen in only 1/9,000 adults (Table 1). The term fibrous gingival hyperplasia is often used for this phenomenon when it is induced by one of a variety of drugs (Table 2), while gingival fibromatosis is used for those cased which have an hereditary pattern, are part of a more extensive syndrome (Table 3), or are idiopathic. Hereditary gingival fibromatosis and idiopathic gingival fibromatosis first present in childhood, while drug-induced gingival hyperplasia first becomes noticeable three or more months after the onset of drug use. Some cases occur years after drug use is initiated.
As the fibrous hyperplasia is significantly enhanced by poor oral hygiene, gingivitis and periodontitis may be associated with the fibrosis. This entity was first reported in 1856 by Goddard and Gross under the rather descriptive term, "fungus excrescence of the gingiva."
Occasional adults develop a large, smooth, fleshy hyperplasia of the soft
tissues overlying the bone of the maxillary tuberosity. This symmetrical
fibromatosis of the tuberosity is a localized variant of gingival
fibromatosis and appears to be a developmental type of phenomenon, although
its true etiology is unknown. This form of hyperplasia may actually
be more common than generalized gingival fibromatosis.
Gingival fibromatosis presents as a generalized but often irregular enlargement of the facial and lingual aspects of the attached and marginal gingiva (Figure 4a). A portion of one quadrant may be involved, or all four quadrants of the gingival tissues may be involved. Enlargement is painless, slowly progressive and dependent to a great extent on the oral hygiene of the individual. While the hyperplastic tissues are usually firm to palpation, inflammation and edema may make some surface areas (facing the teeth) spongy, erythematous and easily bleeding. It is not unusual for the fibromatosis to completely cover the teeth.
Symmetrical fibromatosis of the tuberosity is typically bilateral and presents
as a generalized, soft, smooth-surfaced, painless enlargement of the tissues
overlying the posterior maxillary alveolus. Slow growth may eventuate
in lesions so large as to actually touch one another across the arch of the
hard palate, or to become traumatized by contact with mandibular teeth. Most
cases, however, remain much smaller.
Pathology and Differential Diagnosis
Gingival fibromatosis and drug-induced fibrous hyperplasia are comprised of dense or moderately dense, rather avascular, bland collagenic connective tissue with scattered chronic inflammatory cells, especially beneath the surface epithelium (Figure 4b). The attached gingival epithelium may have extreme elongation of rete processes. The crevicular epithelium facing the tooth surfaces usually shows considerable degeneration, subepithelial edema, and more extensive inflammatory cell infiltration because of the gingivitis or periodontitis so often present.
When evaluating the inflammatory cell infiltrate, the pathologist must be careful to differentiate the polyclonal, mixed infiltrate from a diffuse submucosal infiltration of atypical leukocytes in leukemia or diffuse lymphoma (MALT lymphoma). Both chronic and acute leukemic patients may develop a generalized gingival hyperplasia secondary to massive infiltration of neoplastic leukocytes, presumably because these cells retain a certain amount of normal chemotactic ability and are drawn to an area of inflammation, such as gingivitis. The clinical presentation is often called leukemic gingivitis or leukemic gingival hyperplasia. The criteria used for the determination of leukemia or lymphoid malignancy are the same as those used for leukemic or extranodal (MALT) lymphoma infiltrations anywhere in the body.
Some cases of generalized gingival hyperplasia show focal collections of histiocytes intermixed with lymphocytes and foreign-body type multinucleated giant cells. This granulomatous gingivitis may be a foreign body reaction to toothpaste or may be indicative of a more systemic chronic granulomatous disease, such as sarcoidosis, Crohn's disease, or Wegener's granulomatosis. Other gingival hyperplasias have large numbers of plasma cells scattered throughout the subepithelial stroma. This plasma cell gingivitis is presumed to be an unusual allergic reaction.
Juvenile hyaline fibromatosis, a hereditary condition which may involve the gingiva, can be distinguished from gingival fibromatosis by its prominent PAS-positive background matrix of chondroitin sulfate. Amyloid infiltration of the gingival tissues is not uncommon in primary or secondary amyloidosis. It can be identified via Congo red stain under fluorescent or polarized light, thioflavine T stain under fluorescent light, or immunoreactivity with antibodies for immunoglobulin light chains.
Symmetrical fibromatosis of the tuberosity is composed of a moderately dense
fibrous stroma with a more myxoid appearance than is found in generalized
gingival fibromatosis. Focal areas may demonstrate edema or dense fibrosis,
and inflammatory cells are quite sparse. Stromal cells are inactive bipolar
and stellate mesenchymal cells lacking in mitotic activity or variation in
size. The surface epithelium is usually atrophic but may be acanthotic with
narrow, elongated rete ridges.
Treatment and Prognosis
Gingival fibromatosis is removed by gingivectomy, with recurrences being treated in the same fashion or by more conservative removal of local areas of hyperplasia. Improved oral hygiene will greatly diminish the risk of recurrence. Drug-induced gingival hyperplasia may also be treated by gingivectomy and plaque control. Discontinuation of drug use often results in cessation and even regression of the gingival enlargement.
Symmetrical fibromatosis of the tuberosity usually requires no
treatment. Large lesions or those which interfere with function
or denture placement may be removed with conservative surgical excision.
Recurrence has not been reported. Granulomatous gingivitis and
gingivitis are treated by addressing the underlying
References (Chronologic Order)
Note: General references can be found by clicking on that topic to the left.
Goddard WH, Gross L. Case of hypertrophy of the gums. Dent Regist West 1856; 9:276-282.
Jorgenson RJ, Cocker ME. Variation in the inheritance and expression of gingival fibromatosis. J Periodontol 1974; 45:472-477.
Butler RT, Kalkwarf KL, Kaldahl WB. Drug-induced gingival hyperplasia: phenytoin, cyclosporine, and nifedipine. J Am Dent Assoc 1987; 114:56-60.
Carranza FA. Glickman's Clinical periodontology, 7th edition. Philadelphia; W.B. Saunders, 1990.
Daley TD, Wysocki GP. Foreign body gingivitis: an iatrogenic disease? Oral Surg Oral Med Oral Pathol 1990; 69:708-712.
Miller CS, Damm DD. Incidence of verapamil-induced gingival hyperplasia in a dental population. J Periodontol 1990; 63:453-456.
Oikarinen K, et al. Hereditary gingival fibromatosis associated with growth hormone deficiency. Br J Oral Maxillofac Surg 1990; 28:335-339.
Takagi M, Yamamoto H, Mega H, et al. Heterogeneity in the gingival fibromatoses. Cancer 1991; 2202.
Sollecito TP, Greenberg MS. Plasma cell gingivitis: report of two cases. Oral Surg Oral Med Oral Pathol 1992; 73:690-693.
Dongari A, McDonnell HT, Langlais RP. Drug-induced gingival overgrowth. Oral Surg Oral Med Oral Pathol 1993; 76:543-548.
Wynne SE, Aldred MJ, Bartold PM. Hereditary gingival fibromatosis associated with hearing loss and supernumerary teeth - a new syndrome. J Periodontol 1995; 66:75-79.
Piattelli A, Scarano A, Dibellucci A, Matarasso S. Juvenile hyaline fibromatosis of gingiva - a case report. J Periodont 1996; 67;451-453.
Ramer M, Marrone J, Stahl B, Burakoff B.
Hereditary gingival fibromatosis -identification, treatment, control. J Amer
Dent Assoc 1996; 127:493-495.
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
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.
Number of lesions per 1,000 population*
Enlarged lingual tonsil
Median rhomboid glossitis
Oral melanotic macule
Oral tonsils (except lingual)
Buccinator node, hyperplastic
* total examined population = 23,616 adults over 35 years of age
With Papular Gingival Fibromatosis (Papulosis):
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