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Aim of the study. 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.
Materials and method. Harvesting of cleft was obtained from two periodontally healthy patients with a scalpel and a bevel incision and then placed in a test tube with buffered solution to be processed for light microscopy.
Results. Microscopic analysis has shown that Stillman’s cleft presented a lichenoid hand-like inflammatory infiltration, while in the periodontal patient an inflammatory fibrous hyperplasia was identified.
Conclusion. Stillman’s cleft remains to be investigated as for the possible causes of such lesion of the gingival margin, although an inflammatory response seems to be evident and active from a strictly histopathological standpoint.
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1971-1441
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A. Pilloni
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Annali di stomatologia
inflammation
The gingival Stillman’s clefts: histopathology and cellular characteristics
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Case Report
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A. Pilloni
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Department of Oral and Maxillofacial Sciences, Section of Periodontology “Sapienza”, University of Rome, Italy
1971-1441
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inflammation
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The gingival Stillman’s clefts: histopathology and cellular characteristics
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                                                                                                             Case report



    The gingival Stillman’s clefts: histopathology
    and cellular characteristics




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    Maria Antonietta Cassini, DDS, MS1,2                      Introduction
    Loredana Cerroni, BSc, DDS, MS, PhD2
    Amedeo Ferlosio, MD3                                      Stillman’s cleft is a mucogingival triangular-shaped de-
    Augusto Orlandi, MD3                                      fect predominantly seen on the buccal surface of a root,
    Andrea Pilloni, MD, DDS, MS1                              first described by Stillman as a recession related to oc-




                                                                                            zi
                                                              clusal trauma, either associated with marginal gingivitis
                                                              or with mild periodontitis (1). It can be found as a de-
    1   Department of Oral and Maxillofacial Sciences,        pression or as a sharply defined fissure extending up to




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        Section of Periodontology “Sapienza”, University of   5-6 mm of length (Fig. 1). This particular type of ulcera-
        Rome, Italy                                           tive gingival recession occurs as single or multiple cleft
    2   Department of Clinical Sciences and Translational     and it can be classified as simple (one direction shape)
        Medicine, “Tor Vergata” University of Rome, Italy     or composed (multiple and differently directed shape)
    3




                                                                er
        Department of Biomedicine and Prevention, Insti-      (2, 3). Other possible etiological factors are assumed to
        tute of Anatomic Pathology, “Tor Vergata” Universi-   be periodontal inflammation (2), which leads to prolifer-
        ty of Rome, Italy                                     ation of the pocket epithelium into the gingival corium
                                                              and its subsequent anastomosis with the outer epitheli-



                                                        t     um (4). In addition, the traumatic tooth-brushing and
    Corresponding author:
    Maria Antonietta Cassini
                                                     In       the incorrect use of the interdental floss have been de-
                                                              scribed among the possible causes (5, 6). A recent sys-
    Department of Oral and Maxillofacial Sciences             tematic review concluded that although the majority of
    “Sapienza” University of Rome                             the observational studies confirmed a relationship be-
    Via Caserta 6                                             tween tooth brushing and gingival recessions the data
                                         ni
    00161 Rome, Italy                                         to support or question the association are inconclusive
    E-mail: dr.cassini@libero.it                              (7). To date, the etiology and pathogenesis of this de-
                                                              fects remain unclear even though the assumptions are
                                 io

                                                              related to chronic factors that ulcerate the epithelium
    Summary                                                   and healing occurs through the anastomosis of the ex-
                                                              ternal and internal epithelium in the gingival sulcus, cre-
    Aim of the study. Stillman’s cleft is a mucogingi-        ating a triangular defect (8). When flossing trauma is in-
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    val triangular-shaped defect on the buccal surface        volved, superficial gingival tissue clefts are ‘red’ be-
    of a root with unknown etiology and pathogene-            cause the injury is confined within connective tissue. In
    sis. The aim of this study is to examine the Still-       this case the lesion is reversible: flossing procedures
           Ed




    man’s cleft obtained from excision during root            have to be interrupted for at least 2 weeks and chemi-
    coverage surgical procedures at an histopatho-            cal plaque control only (i.e. chlorexidine rinses) should
    logical level.                                            be performed. If the cleft appears ‘white’ the whole con-
    Materials and method. Harvesting of cleft was ob-         nective tissue thickness is involved and the root surface
    tained from two periodontally healthy patients            becomes evident; in this case the gingival lesion is irre-
    with a scalpel and a bevel incision and then              versible (9, 10).
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    placed in a test tube with buffered solution to be        In case of Stillman’s clefts, home oral hygiene could
    processed for light microscopy.                           become very difficult to be performed and bacterial or
    Results. Microscopic analysis has shown that
    Stillman’s cleft presented a lichenoid hand-like in-
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    flammatory infiltration, while in the periodontal
    patient an inflammatory fibrous hyperplasia was
    identified.
    Conclusion. Stillman’s cleft remains to be investi-
©




    gated as for the possible causes of such lesion of
    the gingival margin, although an inflammatory re-
    sponse seems to be evident and active from a
    strictly histopathological standpoint.

    Key words: Stillman’s cleft, recessions, gingival
    margin, histological analysis, inflammation.              Figure 1. Stillman’s cleft.

    100                                                                         Annali di Stomatologia 2015; VI (3-4): 100-103
    The gingival Stillman’s clefts: histopathology and cellular characteristics


    viral infections may induce the formation of a buccal            The surgical protocol consisted of the excision of the
    probing pocket of sufficient depth to reach the peri-            cleft, as indicated by previously validated techniques
    apical areas of the tooth. Sometimes a delayed diag-             (12), in order to create a better manageable contour
    nosis is made only when an endodontic abscess oc-                of the gingival recession for subsequent treatment.
    curs (10). The prognosis of the clefts is variable: they         Preparation of the surgical site followed the same




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    can heal uneventfully or remain as superficial lesions           surgical protocol of the treatment of a single gingival




                                                                                                          al
    combined with deep periodontal pockets.                          recession with a subepithelial connective tissue graft,
    In 2013 Pilloni showed how a laterally moved, coro-              that allows the coverage of the exposed root surface
    nally advanced technique could modify and eliminate              (11). Patients received ibuprofen twice daily for three




                                                                                                       on
    this kind of anatomical lesion. He demonstrated that             days and a 0.12% chlorhexidine rinse every 12 hours
    such surgical approach was effective in treating an              for 7 days. No systemic antibiotics were used.
    isolated Stillman’s cleft and the result remained sta-           The tissue samples were fixed in 10% neutral buffered
    ble over a 5-year period (11).                                   formalin for 24 hours and than were oriented in order
                                                                     to correctly identify the cleft and sectioned perpendic-




                                                                                              zi
    Analysis of gingival clefts indicate an apically-directed
    spread of an inflammatory exudate through the gingi-             ularly longitudinally by 2 mm cuts. The biopsies were
    val connective tissues, with concurrent epithelial re-           sampled in toto in two histological biocasettes: the
                                                                     representative sample of cleft was placed within the




                                                                                  na
    sorptive and proliferative reactions, with collagen re-
    sorption being mediated by an hydrolytic enzymatic               first one (one or two samples) and the lateral part of
    activity (8).                                                    surgical biopsies into the second one. Finally, they
    The aim of this study was to examine the Stillman’s              were embedded in paraffin wax and 4 µm serial sec-
    cleft histological features in two different patients and        tions were cut at different levels and stained with




                                                                       er
    compare them with the clinical aspects (healthy vs               haematoxylin and eosin for each block. The slides
    non healthy periodontal tissues).                                were examined with a Nikon Eclipse E1200 light mi-
                                                                     croscope and pictures taken with a Nikon camera
                                                                     system.
    Case report

                                                            t        Patient A: at scanning magnification, a lichenoid
                                                         In          band-like inflammatory infiltrate is observed with focal
    Two patients with in common the presence of an                   epithelial ulceration corresponding to cleft floor.
    asymptomatic Stillman’s cleft on a vital and stable el-          At higher magnification, the epithelium shows reac-
    ement, without any restoration, were selected for the            tive atypia with many mitoses, spongiosis, acantosis
    study. They presented with two different periodontal             and occasional diskeratotic cells.
                                               ni
    conditions: patient A was periodontally healthy,                 The inflammatory infiltrate is mainly constituted by
    meanwhile patient B was healthy but previously treat-            small lymphocytes with sligthly irregular nuclei and
    ed for mild periodontitis. Patient B showed a deeper             only scarce plasma cells. The lamina propria shows
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    lesion (5 mm) than patient A (2 mm).                             fragmentation of elastic fibers (Fig. 2).

                                                                                                Figure 2. Histological analysis
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                                                                                                patient A.
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    Annali di Stomatologia 2015; VI (3-4): 100-103                                                                         101
    M. A. Cassini et al.


                                                                                              Figure 3. Histological analysis
                                                                                              patient B.




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    Patient B: a different aspect resembling inflammatory      cells response with only few plasma cells and chronic
    fibrous hyperplasia could be seen. In fact, at scan-       scarring of lamina propria.
    ning electron microscopy, a pseudoepitheliomatous          This preliminary study aimed at also defining a pre-
    hyperplasia overlying sclerotic lamina propria has         dictable methodology to obtain proper amount of soft
                                         ni
    been observed.                                             tissue from the lesion to then fully obtain comprehen-
    At higher magnification, far from the lymphocyte-rich      sive histological evaluation. The future perspectives
    inflammation, mainly plasma cells could be seen            are to analyze the cleft sample also on an ultrastruc-
    around small vessels (Fig. 3).                             tural level by transmission electron microscopy to
                                io


                                                               better describe the presence and amount of both col-
                                                               lagen and other matrix components. Moreover, an im-
    Discussion and conclusion                                  munohistochemical study should be carried out in or-
                           iz



                                                               der to understand the cellular composition and the
    To date, only a few cases have been published on           expression of inflammatory mediators within the le-
    the etiology and pathogenesis of Stillman’s clefts and     sion. For these reasons, a larger sample is needed to
          Ed




    with the aim of explaining their histological features.    reach a better understanding of the pathogenesis of
    This may depend both on the rarity of such lesion and      this common lesion.
    on patient’s agreement in accepting surgical proce-
    dures to modify it, particularly in asymptomatic cases.
    Moreover, in recent years, literature has focused pri-     References
    marily on different surgical techniques aimed at the
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    resolution of esthetics with primarily the aim of seek-     1. Stillman PR. Early clinical evidences of diseases in the gin-
                                                                   gival and pericementum. J Dent Res. 1921;3:25-31.
    ing at the maintenance of the health of periodontal
                                                                2. Box HK. Gingival cleft and associated tracts. N Y State Dent
    tissues. For this reasons, we decided to investigate           J. 1950 Jan;16(1):3-10.
    the histological characteristics of two different Still-    3. Tishler B. Gingival clefts and their significance. Dent Cosm.
C




    man’s clefts and correlate them with their clinical pre-       1927;69:1003.
    sentation. According to our preliminary results, the        4. Goldman HM, Schluger S, Fox L, Cohen DW. Periodontal
    case A (cleft from healthy periodontal tissues)                Therapy. ed 3, St. Louis, C. V. Mosby Co, 1964.
    showed histological features resembling acute and           5. Hirschefeld I. Traumatization of soft tissues by tooth-brush.
                                                                   Dent Items Int.1933;55:329.
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    mild gingivitis. The first one with predominantly T
                                                                6. Greggianin BF, Oliveira SC, Haas AN, Oppermann RV. The
    small lymphocytes was sided in correspondence of
                                                                   incidence of gingival fissures associated with tooth brush-
    the cleft and the mild type with few plasmacells
                                                                   ing: crossover 28-day randomized trial. J Clin Periodontol.
    around the cleft in apparent clinically healthy gingiva.       2013;40:319-326.
    Case B (periodontal disease-treated associated cleft)       7. Rajapakse PS, McCracken GI, Gwynnett E, Steen ND,
    showed histological features similar to chronic gin-           Guentsch A, Heasman PA. Does tooth brushing influence
    givitis or mild periodontitis with a predominantly B           the development and progression of non-inflammatory gin-


    102                                                                         Annali di Stomatologia 2015; VI (3-4): 100-103
    The gingival Stillman’s clefts: histopathology and cellular characteristics


        gival recession? A systematic review. J Clin Periodontol.          riodontology. 2000;68:10.1111/prd.2015.68.issue-1:333-
        2007;34:1046-1061.                                                 368.
     8. Novaes AB, Ruben MP, Kon S, Goldman HM, Novaes AB Jr.          11. Pilloni A, Dominici F, Rossi R. Laterally moved, coronally ad-
        The development of the periodontal cleft. A clinical and           vanced flap for the treatment of a single Stillman’s cleft. A
        histopathologic study. J Periodontol. 1975 Dec;46(12):701-9.       5-year follow-up. Eur J Esthet Dent. 2013;8(3):390-396.




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     9. Zucchelli G. Chirurgia estetica mucogengivale. Quintessenza    12. Hallmon W, Waldrop T, Houston G, Hawkins B. Flossing




                                                                                                                  al
        Edizioni, 2012.                                                    clefts. Clinical and histologic observations. J Periodontol.
    10. Zucchelli G, Mounssif I. Periodontal plastic surgery. Pe-          1986;57:501-504.




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    Annali di Stomatologia 2015; VI (3-4): 100-103                                                                                  103
