Stillman's cleft is a mucogingival triangular-shaped defect on the buccal surface of a root with unknown etiology and pathogenesis. The aim of this study is to examine the Stillman's cleft obtained from excision during root coverage surgical procedures at an histopathological level

Cassini, MARIA ANTONIETTA

Cerroni, Loredana

Ferlosio, Amedeo

Orlandi, Augusto

Pilloni, Andrea

Annali di Stomatologia

English

CASSINI, MARIA ANTONIETTA

PILLONI, ANDREA

Archivio della ricerca- Università di Roma La Sapienza

Annali di Stomatologia 2015; VI (3-4): 100-103100The gingival Stillman’s clefts: histopathology and cellular characteristicsMaria Antonietta Cassini, DDS, MS1,2Loredana Cerroni, BSc, DDS, MS, PhD2Amedeo Ferlosio, MD3Augusto Orlandi, MD3Andrea Pilloni, MD, DDS, MS11 Department of Oral and Maxillofacial Sciences,Section of Periodontology “Sapienza”, University ofRome, Italy2 Department of Clinical Sciences and TranslationalMedicine, “Tor Vergata” University of Rome, Italy3 Department of Biomedicine and Prevention, Insti-tute of Anatomic Pathology, “Tor Vergata” Universi-ty of Rome, ItalyCorresponding author:Maria Antonietta CassiniDepartment of Oral and Maxillofacial Sciences“Sapienza” University of RomeVia Caserta 600161 Rome, ItalyE-mail: dr.cassini@libero.itSummaryAim of the study. Stillman’s cleft is a mucogingi-val triangular-shaped defect on the buccal surfaceof a root with unknown etiology and pathogene-sis. The aim of this study is to examine the Still-man’s cleft obtained from excision during rootcoverage surgical procedures at an histopatho-logical level.Materials and method. Harvesting of cleft was ob-tained from two periodontally healthy patientswith a scalpel and a bevel incision and thenplaced in a test tube with buffered solution to beprocessed for light microscopy.Results. Microscopic analysis has shown thatStillman’s cleft presented a lichenoid hand-like in-flammatory infiltration, while in the periodontalpatient an inflammatory fibrous hyperplasia wasidentified.Conclusion. Stillman’s cleft remains to be investi-gated as for the possible causes of such lesion ofthe gingival margin, although an inflammatory re-sponse seems to be evident and active from astrictly histopathological standpoint.Key words: Stillman’s cleft, recessions, gingivalmargin, histological analysis, inflammation.IntroductionStillman’s cleft is a mucogingival triangular-shaped de-fect predominantly seen on the buccal surface of a root,first described by Stillman as a recession related to oc-clusal trauma, either associated with marginal gingivitisor with mild periodontitis (1). It can be found as a de-pression or as a sharply defined fissure extending up to5-6 mm of length (Fig. 1). This particular type of ulcera-tive gingival recession occurs as single or multiple cleftand it can be classified as simple (one direction shape)or composed (multiple and differently directed shape)(2, 3). Other possible etiological factors are assumed tobe periodontal inflammation (2), which leads to prolifer-ation of the pocket epithelium into the gingival coriumand its subsequent anastomosis with the outer epitheli-um (4). In addition, the traumatic tooth-brushing andthe incorrect use of the interdental floss have been de-scribed among the possible causes (5, 6). A recent sys-tematic review concluded that although the majority ofthe observational studies confirmed a relationship be-tween tooth brushing and gingival recessions the datato support or question the association are inconclusive(7). To date, the etiology and pathogenesis of this de-fects remain unclear even though the assumptions arerelated to chronic factors that ulcerate the epitheliumand healing occurs through the anastomosis of the ex-ternal and internal epithelium in the gingival sulcus, cre-ating a triangular defect (8). When flossing trauma is in-volved, superficial gingival tissue clefts are ‘red’ be-cause the injury is confined within connective tissue. Inthis case the lesion is reversible: flossing procedureshave to be interrupted for at least 2 weeks and chemi-cal plaque control only (i.e. chlorexidine rinses) shouldbe performed. If the cleft appears ‘white’ the whole con-nective tissue thickness is involved and the root surfacebecomes evident; in this case the gingival lesion is irre-versible (9, 10).In case of Stillman’s clefts, home oral hygiene couldbecome very difficult to be performed and bacterial orReview articleFigure 1. Stillman’s cleft.viral infections may induce the formation of a buccalprobing pocket of sufficient depth to reach the peri-apical areas of the tooth. Sometimes a delayed diag-nosis is made only when an endodontic abscess oc-curs (10). The prognosis of the clefts is variable: theycan heal uneventfully or remain as superficial lesionscombined with deep periodontal pockets.In 2013 Pilloni showed how a laterally moved, coro-nally advanced technique could modify and eliminatethis kind of anatomical lesion. He demonstrated thatsuch surgical approach was effective in treating anisolated Stillman’s cleft and the result remained sta-ble over a 5-year period (11).Analysis of gingival clefts indicate an apically-directedspread of an inflammatory exudate through the gingi-val connective tissues, with concurrent epithelial re-sorptive and proliferative reactions, with collagen re-sorption being mediated by an hydrolytic enzymaticactivity (8).The aim of this study was to examine the Stillman’scleft histological features in two different patients andcompare them with the clinical aspects (healthy vsnon healthy periodontal tissues).Case reportTwo patients with in common the presence of anasymptomatic Stillman’s cleft on a vital and stable el-ement, without any restoration, were selected for thestudy. They presented with two different periodontalconditions: patient A was periodontally healthy,meanwhile patient B was healthy but previously treat-ed for mild periodontitis. Patient B showed a deeperlesion (5 mm) than patient A (2 mm).The surgical protocol consisted of the excision of thecleft, as indicated by previously validated techniques(12), in order to create a better manageable contourof the gingival recession for subsequent treatment.Preparation of the surgical site followed the samesurgical protocol of the treatment of a single gingivalrecession with a subepithelial connective tissue graft,that allows the coverage of the exposed root surface(11). Patients received ibuprofen twice daily for threedays and a 0.12% chlorhexidine rinse every 12 hoursfor 7 days. No systemic antibiotics were used.The tissue samples were fixed in 10% neutral bufferedformalin for 24 hours and than were oriented in orderto correctly identify the cleft and sectioned perpendic-ularly longitudinally by 2 mm cuts. The biopsies weresampled in toto in two histological biocasettes: therepresentative sample of cleft was placed within thefirst one (one or two samples) and the lateral part ofsurgical biopsies into the second one. Finally, theywere embedded in paraffin wax and 4 µm serial sec-tions were cut at different levels and stained withhaematoxylin and eosin for each block. The slideswere examined with a Nikon Eclipse E1200 light mi-croscope and pictures taken with a Nikon camerasystem.Patient A: at scanning magnification, a lichenoidband-like inflammatory infiltrate is observed with focalepithelial ulceration corresponding to cleft floor.At higher magnification, the epithelium shows reac-tive atypia with many mitoses, spongiosis, acantosisand occasional diskeratotic cells.The inflammatory infiltrate is mainly constituted bysmall lymphocytes with sligthly irregular nuclei andonly scarce plasma cells. The lamina propria showsfragmentation of elastic fibers (Fig. 2).Annali di Stomatologia 2015; VI (3-4): 100-103 101The gingival Stillman’s clefts: histopathology and cellular characteristicsFigure 2. Histological analysispatient A.

The gingival Stillman's clefts: histopathology and cellular characteristics

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The gingival Stillman's clefts: histopathology and cellular characteristics

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