Pleomorphic adenoma of the nasal cavity is a very rare benign tumor more predominant in female patients in forth to sixth decade of life and could sometimes be found in teenagers [1,2,3]. No reports on occupational exposition to inhaled toxics are related to it .
Pleomorphic adenoma of the nasal septum is thought to originate from a remanence of the vomeronasal organ, from a misplaced ectodermal tissue, or from a viral infection [1, 4].
Stevenson et al. have stated that it is due to vomeronasal organ epithelial duct on cartilaginous nasal septum . While Ersner and Satzman stipulate that during the migration of nasal buds, ectopic embryonic epithelialized cells that migrate are precursors for pleomorphic adenomas .
Generally, it is present ether in nasal septum or lateral wall: Since it is a slow growing tumor, symptoms only appear after a long silent period [2, 3]. Most frequently found symptoms are unilateral nasal obstruction, occasional bleeding, external deformity of nasal pyramids, and nasal swelling and pain [1,2,3, 5].
Endoscopic aspect: Clinically polypoid unilateral sessile and translucid, gray and pink polyp with regular surface and soft consistency [2, 4, 8].
CT scan and MRI are important before surgery: While CT scan allows to define the tumors as well as signs of aggressive local extension , MRI shows a heterogeneous lesion that could also be isointense to brain tissue in T1 weighted sections, curvilinear enhancement with unenhanced small foci in fat-suppressed contrast enhanced T2 (cystic or myxoid component of tumor) [2, 7, 9].
Pleomorphic adenomas are differential diagnosis to malignant mixed tumors  (Table 1).
Nasal pleomorphic adenoma differs from other localization in regard to its structure: They contain little cellularity with epithelial component, associated with high stromal component. Besides, they generally lack a capsule. Tumors are generally between 0.5 and 7 cm [1, 2, 4, 7, 8, 10].
Immunohistochemical: Various cytokeratins, glial fibrillary acidic protein (GFAP), S100 protein, alpha smooth muscle actin, vimentin, and Ki67 proliferation marker [1, 2, 7].
Main treatment is surgery; complete excision with clear margins is mandatory as it lowers the risk of recurrence [2, 10] (Table 2). Approach depends. Methods depend on size of the tumor and its location [1, 2, 7].
Two main risks are associated with pleomorphic adenomas: recurrence and malignant transformation [1,2,3, 7].
Recurrence and risk of malignant transformation
Recurrences rate is of 7.5 to 8% [2, 3]. Potential risk of malignant transformation of pleomorphic adenomas is of 6% with a predilection to female patients . This risk increases with delay in diagnosis. Most malignant tumors found in malignant transformations are squamous cell carcinoma and adenoid cystic carcinoma  as well as undifferentiated carcinoma and mucoepidermoid carcinoma .
Mechanisms of transformation are poorly understood; there is no consensus to predictive histological criteria. Immunohistochemical studies are shedding light: MUC1 is linked as a predictive factor to recurrence of pleomorphic adenoma. Besides, HMG1 and MDM2 may be genetic factors for malignant transformation .
As a result of incomplete excision, one case of metastasis was found after 17 years of follow-up [2, 7]. Spread through hematogeneous and or lymphatic routes are the most suspected etiologies .
Risk factors of recurrence are an irregular or invaded capsule, as well as multi-nodularity . Multiple recurrences also increase the risk for malignant transformation .
Long-term follow-up is essential for diagnosis of loco-regional recurrences; CT scan and MRI are the best diagnostic tools after clinical suspicion of recurrence in endoscopic exam [3, 7].