title: The cytologic composition of dacryops: an immunohistochemical investigation of 15 lesions compared to the normal lacrimal gland.
abstract: OBJECTIVE
  To define the cytologic composition of the double-layered epithelial lining of dacryops (lacrimal duct cyst), improve histopathologic diagnosis, and better understand pathogenesis.
  
  
  METHODS
  Clinicopathologic retrospective study with immunohistochemical studies of 15 lesions compared with normal lacrimal gland.
  
  
  METHODS
  Clinical data from 14 patients were reviewed and microscopy was performed with routine stains and immunohistochemical probes for epithelial membrane antigen (EMA), gross cystic disease fluid protein-15 (GCDFP-15), cytokeratin 7 (CK7), and smooth muscle actin (SMA).
  
  
  RESULTS
  The major lacrimal gland was involved in 13 lesions; 2 lesions arose in an accessory gland of Krause. One case was bilateral; the average age of the patients was 50.7 years. Neither visual acuity nor motility was disturbed. No lesion was discovered to have recurred after excision. Microscopically, in all dacryops specimens goblet cells and luminal pseudoapocrine apical cytoplasmic projections were identified. Lacrimal acinar cells immunoreacted with GCDFP-15 and CK7, whereas the normal ducts and the epithelium of the dacryops lesions reacted diffusely only with CK7. SMA-positive myoepithelial cells were found in the acini but not in the normal ducts or dacryops epithelium.
  
  
  CONCLUSIONS
  Negative GCDFP-15 staining ruled out apocrine metaplasia in dacryops. Normal ducts and dacryops showed no immunohistochemical evidence for the presence of myoepithelial cells. Pathogenetic theories of dacryops that implicate a failure of ductular "neuromuscular" contractility must therefore be revised. A dysfunction of the rich neural plexus around the ductules may play a role in the development of dacryops in conjunction with periductular inflammation and induced scarring.
authors.affiliation: David G. Cogan Laboratory of Ophthalmic Pathology, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts 02114, USA. Fred_Jakobiec@meei.harvard.edu
authors.forename: Frederick A
authors.initials: FA
authors.lastname: Jakobiec
authors.forename: Fouad R
authors.initials: FR
authors.lastname: Zakka
authors.forename: Lynn P
authors.initials: LP
authors.lastname: Perry
mesh_terms: D000199:Actins / Q000378:metabolism; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000378:metabolism; D002352:Carrier Proteins / Q000378:metabolism; D002675:Child, Preschool; D003560:Cysts / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D007124:Immunoenzyme Techniques; D053552:Keratin-7 / Q000378:metabolism; D007765:Lacrimal Apparatus / Q000166:cytology* / Q000378:metabolism; D007766:Lacrimal Apparatus Diseases / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D026901:Membrane Transport Proteins; D008875:Middle Aged; D018396:Mucin-1 / Q000378:metabolism; D012189:Retrospective Studies; D014057:Tomography, X-Ray Computed
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D015415:Biomarkers; D002352:Carrier Proteins; D006023:Glycoproteins; D053552:Keratin-7; D026901:Membrane Transport Proteins; D018396:Mucin-1; C488892:PIP protein, human