Journal of Interdisciplinary Dentistry

: 2015  |  Volume : 5  |  Issue : 1  |  Page : 31--36

Diagnostic dilemma and management of odontogenic grooves by platelet-rich-fibrin

Raghavendra Shrishail Medikeri1, Pinal Mahendra Jain1, Manjushri Raghavendra Medikeri2,  
1 Department of Periodontics, Sinhgad Dental College and Hospital, Pune, Maharashtra, India
2 Department of Oral medicine and Radiology, Sinhgad Dental College and Hospital, Pune, Maharashtra, India

Correspondence Address:
Raghavendra Shrishail Medikeri
Department of Periodontics, Sinhgad Dental College and Hospital, Pune, Maharashtra


Palatal radicular grooves (PRGs) are developmental anomalies of maxillary incisors, when present can act as a site for plaque accumulation and periodontal infection. They are easily overlooked as etiologic factors, as these grooves are covered by periodontal tissues. The clinician has to be alert and check for variations in the anatomy of the tooth as a cause of pulp necrosis in the anterior segment of the tooth when other causes are ruled out. It is often associated with incorrect diagnosis, and subsequent treatment failure. This case report describes the diagnosis and management of two cases of Type II PRG of a maxillary lateral incisor with periapical and periodontal regeneration. Clinical Relevance to Interdisciplinary Dentistry
  • PRG presents with myriad symptoms.
  • Accurate diagnosis requires careful clinical and radiographic examination and advanced imaging, in doubt.
  • Early detection and an interdisciplinary approachs are required to improve the prognosis of the involved tooth.
  • Platelet-rich-fibrin acts as the promising material of choice for regeneration of lost structures and faster soft tissue wound healing.

  • How to cite this article:
    Medikeri RS, Jain PM, Medikeri MR. Diagnostic dilemma and management of odontogenic grooves by platelet-rich-fibrin.J Interdiscip Dentistry 2015;5:31-36

    How to cite this URL:
    Medikeri RS, Jain PM, Medikeri MR. Diagnostic dilemma and management of odontogenic grooves by platelet-rich-fibrin. J Interdiscip Dentistry [serial online] 2015 [cited 2023 May 29 ];5:31-36
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    Full Text


    Palatoradicular grooves (PRGs) are developmental deformities of the tooth that bears a significant threat to periodontal attachment and can cause pulpal infection. [1] Its overall prevalence ranges from 1.01% to 8.5% [2] with maxillary lateral incisors (93.8%) mostly affected. [3] They might act as a local etiological factor for bacterial plaque accumulation that can alter the response to periodontal treatment. They also serve as a pathway of communication between periodontal tissues and pulpal tissues other than vascular, lymphatic pathways, dentinal tubules, apical foramen, and lateral canals.

    PRG as a contributing factor adds to a diagnostic dilemma for the clinician. Because, it manifests with myriad symptoms either true periodontal or endodontic lesion or combined lesions or abscess or not at all. It requires thorough debridement and careful exploration to identify it. Occasionally, use of disclosing agents aids in identification from surrounding sound tooth structure. Rarely, it appears as a radiolucent line along with the root canal that mimics additional canal of the involved teeth called parapulpal line. [4] Advanced imaging techniques like cone beam computed tomography (CBCT) provides the extent, depth of the groove and the severity of localized destruction caused and can overcome the limitations of conventional radiographs. [4] Based on an extension of the groove on root surface a classification was proposed by Gu. [5] Accurate diagnosis and elimination of the inflammatory irritants and other contributory factors are extremely important in achieving the successful treatment outcome. Currently, platelet-rich-fibrin (PRF) which is the second generation platelet concentrate is a promising material for regenerative of lost osseous structures. [6]


    Case 1

    A 28 years male patient presented with gingival bleeding on provocation in maxillary anterior teeth since 3-4 months. On examination, pocket depth and clinical attachment loss (CAL) of 6 mm was present on the palatal surface of #12 [Figure 1]. A "funnel-shaped" notch and groove on the palatal aspect was observed. The tooth was nonvital on pulp testing. Medical history was nonsignificant. Intra-oral periapical (IOPA) radiograph revealed angular bony defect extending upto middle third of root and parapulpal line [Figure 2]. On CBCT image, the groove was shallow and extended from cingulum to the middle third of root associated with a periodontal bony crater like a defect on palatal aspect up to the level of groove [Figure 3]. Based on the above findings, the case was diagnosed as chronic localized periodontitis associated with PRG in respect to #12.{Figure 1}{Figure 2}{Figure 3}

    Probing depth was persistent after 1-month of phase-1 therapy. Hence, periodontal flap surgery was planned with the elimination of PRG. After obtaining informed consent, under aseptic condition, local anesthesia (LA) (2% Lignox) was administered. Upon full thickness flap reflection and degranulation of #12, a shallow "well-shaped" bony defect and PRG was clearly evident [Figure 4]. Saucerization of PRG was done with a round bur to eliminate the groove and restored with glass inomer cement (Fuji II, Japan) [Figure 5]. Surgical hemostasis was achieved by using a hemostatic gelatin sponge (Abgel) during restoration. Patient's venous blood (10 ml) was collected and centrifuged to separate PRF. Immediately, it was placed over the bone defect [Figure 6] and the flap was approximated with 3-0 silk interrupted sutures [Figure 7]. The surgical field was protected by periodontal dressing (Coe-Pak, USA).{Figure 4}{Figure 5}{Figure 6}{Figure 7}

    Postsurgical instructions were given. Antibiotics and nonsteroidal anti-inflammatory drugs for 7 days and 0.2% chlorhexidine gluconate mouthwash (twice a day for 2 weeks) were advised. The sutures were removed after 10 days. The postoperative healing was uneventful. There was a gain in clinical attachment level by 3 mm after 1-year with evidence of bone fill observed on radiograph [Figure 8].{Figure 8}

    Case 2

    A 38 years female patient complained of mobility of #22. On clinical examination, #22 exhibited Grade II tooth mobility with CAL of 6 mm on the palatal surface [Figure 9]. There was no history of trauma or caries, and medical history was nonsignificant. A groove was noted on the cingulum of #22. The tooth did not respond to electric and thermal pulp testing. IOPA radiograph revealed widening of periodontal ligament space and large periapical radiolucency with periapical index (PAI) score [6] of 4 and the presence of horizontal bone loss up to middle third of root, but no parapulpal line [Figure 10]. CBCT revealed the extension of the PRG upto the middle third of root and periapical bone loss about #22 [Figure 11]. Based on the clinical and radiographic findings, the case was diagnosed as a primary periodontal secondary endodontic lesion in respect to #22 associated with PRG.{Figure 9}{Figure 10}{Figure 11}

    Phase I periodontal therapy and endodontic treatment was performed. At 3 months recall, the probing depth and tooth mobility persisted. Under LA after reflection of the flap, on the labial surface, a large bony fenestration in the periapical area of #22 was evident. On the palatal side, the shallow PRG emerged from the cingulum distopalatally extending upto middle one-third of the root. The lesion was curetted thoroughly [Figure 12]. The groove was saucerized and sealed with glass ionomer cement [Figure 13]. The defect was filled with xenograft (Osseograft, Encoll, USA) [Figure 14] and PRF membrane was placed and flaps sutured. Later splinting was done with fiber-reinforced composite splinting (Interlig).{Figure 12}{Figure 13}{Figure 14}

    Postoperative care was similar to Case 1. At 1-year follow-up, the tooth was asymptomatic, and radiograph revealed bone fill of the periapical defect with PAI score [6] reduced to 1 [Figure 15].{Figure 15}


    PRG is considered one of the important contributing factors to the development of localized chronic periodontitis and/or apical periodontitis. The diagnosis of PRG is depended on signs and symptoms of the lesion, careful examination of anatomical sites and investigations such as tooth vitality tests, radiographic examinations. Very often, anatomical sites are covered with organic debris and calculus, which make it difficult to identify the anatomical defect.

    It is usually diagnosed at much later stage unless any symptoms are present at initial stages. The difficulty in diagnosis is also related to the interpretation of clinical signs such as, periodontal disease and/or endodontic impairment and failing to relate these conditions to PRG. It may have symptoms of a periodontal or acute dentoalveolar abscess. Frequently a lesion related to a groove is characterized by recurrent symptomatic episodes. [7] The majority of cases found in the literature show complications arising from the presence of PRG. [8],[9] Friedman and Goultschin have suggested that pulpal necrosis followed by apical periodontitis is often the earliest manifestation of PRG. [10]

    The extent of depth and direction are most important in deciding treatment and prognosis. Frequently, the prognosis of these elements are compromised because of the missed diagnosis or because of the complex therapeutic approach that is necessary to cure associated pathologies. [11] CBCT has the advantage of estimating depth and extent of groove, with/without pulpal communication including severity of tissue destruction. Deep PRGs have fair to poor prognosis compared to a shallow groove.

    The inherent difficulty in treating the PRG makes its diagnostic complexes for practitioners. Odontoplasty or saucerization, restoration of the defect, endodontic therapy and osseous regeneration are choices of treatment, all are aimed at reduction of microbial population and restoration of lost structures. The prognosis of a tooth with a PRG depends mainly on location of the groove, severity of the periodontal problem, accessibility of the defect and the type of groove. Majority of diagnosed cases require an interdisciplinary approach for successful management of this pathology.

    Flap surgery aimed at pocket reduction results in long junctional healing instead of regeneration of lost periodontal structures. Choukroun et al. First described PRF as a second-generation platelet concentrate which contains platelets and multiple growth factors. [12] PRF has a dense fibrin network with leukocytes, cytokines, structural glycoproteins and contains multiple growth factors such as transforming growth factor-β1 (TGF-β1), platelet-derived growth factor (PDGF), vascular endothelial growth factor and glycoproteins during 7 days. [ 6],[13] It regulates both collagenous and noncollagenous proteins, and proteoglycan in the extracellular matrix of PRF. [14] The slow polymerization mode of PRF and cicatricial capacity creates a physiologic architecture favorable for wound healing. [15] Ease of preparation and application, minimal expense and lack of biochemical modification are other advantages of PRF over platelet-rich plasma.

    PRF enhances wound healing and regeneration and several studies show rapid and accelerated wound healing with the use of PRF than without it. [16],[17] PRF aids in healing of osseous defects by multiple mechanisms. [18],[19] It has inherent osteoconductive and/or osteoinductive property. The production of osteoprotegerin is enhanced which inturn causes proliferation of osteoblasts. Cell proliferation of osteoblasts, periodontal ligament cells, and growth factors are induced during a 3-day culture period and suppressed oral epithelial cell growth. PRF also releases growth factors such as PDGF and TGF which promote periodontal regeneration. It upregulates osteoprotegerin and alkaline phosphatase expression thereby stimulating ostegenic differentiation of human dental pulp cells. [20] PRF as a sole grafting material in infrabony defects acts both as graft and scaffold. [21]

    The second case required an interdisciplinary approach. The success of treatment depended on the regeneration of the periapical tissues and periodontal defects. The postsurgical results obtained in two cases, both clinically and radiographically, showed the predictable clinical outcome. As PRG hampers the prognosis, it is necessary that clinician should be aware of such grooves and detect them as early as possible, treat them adequately so that they will not cause further tissue destruction and ultimately tooth loss.


    1Novak JM. Classification of diseases and conditions affecting the periodontium. In: Newman MG, Takei HH, Carranza FA, editors. Clinical Periodontology. 9 th ed. Philadelphia: W. B Saunders and Co.; 2002. p. 64-73.
    2Kogon SL. The prevalence, location and conformation of palato-radicular grooves in maxillary incisors. J Periodontol 1986;57:231-4.
    3Atkinson SR. The permanent maxillary lateral incisor. Am J Orthod 1943;29:685-8.
    4Rachana D. The palatal groove: Application of computed tomography in its detection - A case report. J Conserv Dent 2007;10:83-8.
    5Gu YC. A micro-computed tomographic analysis of maxillary lateral incisors with radicular grooves. J Endod 2011;37:789-92.
    6Dohan Ehrenfest DM, Diss A, Odin G, Doglioli P, Hippolyte MP, Charrier JB. In vitro effects of Choukroun's PRF (platelet-rich fibrin) on human gingival fibroblasts, dermal prekeratinocytes, preadipocytes, and maxillofacial osteoblasts in primary cultures. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009;108:341-52.
    7Robison SF, Cooley RL. Palatogingival groove lesions: Recognition and treatment. Gen Dent 1988;36:340-2.
    8Hungund S, Kumar M. Palato-radicular groove and localized periodontitis: A series of case reports. J Contemp Dent Pract 2010;11:056-62.
    9Hans MK, Srinivas RS, Shetty SB. Management of lateral incisor with palatal radicular groove. Indian J Dent Res 2010;21:306-8.
    10Friedman S, Goultschin J. The radicular palatal groove - A therapeutic modality. Endod Dent Traumatol 1988;4:282-6.
    11Mauro S, Orlando L, Panzoni R, Orlando PF. Groove associated periodontitis: Classification proposal and clinical. Case report. Minerva Stomatol 2005;54:79-89.
    12Choukroun J, Adda F, Schoeffer C, Vervelle A. PRF: An opportunity in perio-implantology. Implantodontie 2000;42:55-62.
    13Dohan Ehrenfest DM, de Peppo GM, Doglioli P, Sammartino G. Slow release of growth factors and thrombospondin-1 in Choukroun's platelet-rich fibrin (PRF): A gold standard to achieve for all surgical platelet concentrates technologies. Growth Factors 2009;27:63-9.
    14Grzesik WJ, Narayanan AS. Cementum and periodontal wound healing and regeneration. Crit Rev Oral Biol Med 2002;13:474-84.
    15Anitua E, Andia I, Ardanza B, Nurden P, Nurden AT. Autologous platelets as a source of proteins for healing and tissue regeneration. Thromb Haemost 2004;91:4-15.
    16Sharma A, Pradeep AR. Treatment of 3-wall intrabony defects in patients with chronic periodontitis with autologous platelet-rich fibrin: A randomized controlled clinical trial. J Periodontol 2011;82:1705-12.
    17Thorat M, Pradeep AR, Pallavi B. Clinical effect of autologous platelet-rich fibrin in the treatment of intra-bony defects: A controlled clinical trial. J Clin Periodontol 2011;38:925-32.
    18Naik B, Karunakar P, Jayadev M, Marshal VR. Role of Platelet rich fibrin in wound healing: A critical review. J Conserv Dent 2013;16:284-93.
    19Shah M, Deshpande N, Bharwani A, Nadig P, Doshi V, Dave D. Effectiveness of autologous platelet-rich fibrin in the treatment of intra-bony defects: A systematic review and meta-analysis. J Indian Soc Periodontol 2014;18:698-704.
    20Huang FM, Yang SF, Zhao JH, Chang YC. Platelet-rich fibrin increases proliferation and differentiation of human dental pulp cells. J Endod 2010;36:1628-32.
    21Yu-Chao C, Kuo-Chin W, Jing-Huei Z. Clinical application of platelet-rich fibrin as the sole grafting material in periodontal intrabony defects. J Dent Sci 2011;6:181-8.