although periodontal flap surgery may be indicated when

osseous recontouring is needed, if there are mucogingival

considerations, or in pediatric patients in whom tooth
eruption is affected. Laser ablation gingivectomy may offer
an advantage over conventional surgery since procedures
are faster and there is improved hemostasis and more rapid
healing.29
Hereditary Gingival Fibromatosis
Both autosomal dominant and autosomal recessive patterns
of inheritance are recognized. Genetic heterogeneity and
variable expressivity contribute to the difculty encountered
in assigning this diagnosis to a specifc syndrome. Gingival
fbromatosis without other syndrome-associated physical
or mental abnormalities is not rare (Figure 7-13). A putative inherited mutation is in the sos1
gene.27 Enlargement
may be present at birth or may become apparent only with
the eruption of the deciduous or permanent dentitions. Te
most common problems associated with hereditary gingival fbromatosis are tooth migration,
prolonged retention
of the primary dentition, and diastemata. Enlargement may
completely cover the crowns of the teeth, resulting in difculty masticating or speaking and
poor esthetics. Histologic features include proliferative fbrous overgrowth with a
highly collagenized connective tissue stroma sparsely populated with fbroblasts and blood
vessels.
Other Causes of Gingival Enlargement
Patients with acute myelogenous leukemia (principally
acute monocytic [M4] or acute myelomonocytic [M5]
leukemia) may present with gingival leukemic infltrates
(Figure 7-14).31 Others include von Recklinghausen’s neurofbromatosis (neurofbromatosis 1),
Wegener’s granulomatosis, sarcoidosis, Crohn’s disease, primary amyloidosis,
Kaposi’s sarcoma, acromegaly, and lymphoma.

Benign Soft Tissue Tumors

Oral mucosal benign tumors comprise lesions that form from
fbrous tissue, adipose tissue, nerve, and muscle. Benign proliferations of blood vessels and
lymphatic vessels resemble
neoplasms but do not have unlimited growth potential and
therefore are more appropriately considered hamartomatous
proliferations.
Epithelial Tumors
Tere are several benign oral epithelial virus–induced
growths, principally those caused by the human papillomavirus (HPV). 32,33 Molecular biologic
techniques
(e.g., in situ hybridization, polymerase chain reaction)
used to detect HPV34,35 reveal that viral deoxyribonucleic
acid (DNA) can be found in these lesions but may also
be present in normal oral mucosa. Tere are more than
120 HPV strains, of which at least 25 have been detected
in oral lesions. Much attention has been focused on the
relationship between HPV and oropharyngeal carcinogenesis (see Chapter 8, “Oral and
Oropharyngeal Cancer”). High-risk oncogenic HPV subtypes (predominantly
HPV 16) are far more likely to be detected in cancers
involving the oropharynx and tonsils compared with the
oral cavity.36,37
Of the benign oral epithelial HPV–induced growths
(Figure 7-15), viral papilloma (also called squamous papilloma) is relatively common. It
usually occurs in the third to
ffth decades, most commonly as an isolated small growth
(<1 cm diameter) on the palate, ranging in color from pink
to white, rugose (ridged or wrinkled), exophytic, and pedunculated. When these lesions
occur on the surface of the
lips, alveolar gingivae, or palate, they are well keratinized,
and on nonkeratinized mucosal surfaces, they appear soft
and pink/red. HPV DNA is detected in approximately 50%
of squamous papillomas, predominantly HPV 6, followed by
HPV 11.33
Figure 7-13 Hereditary gingival fbromatosis. Note the
severity, with almost complete coverage of teeth in some locations.