Controversial Odontogenic Hamartomas- Review on Their Pathogenesis and Histopathology

Banerjee Abhishek, Tiwari V Tanu, Kanika Singroha, Singh Sakshi, Minu divakaran, Menon K Amrita, Wakhloo Tulika, Somashekhar Preethi

Banerjee Abhishek, Consultant Oral Pathologist, Lions Eye and Dental hospital, Durgapur, India
Tiwari V Tanu, Oral Pathologist, Nagpur, India
Singroha K, Post Graduate Student, Dr. Syamala Reddy Dental College hospital, Bengaluru, India
Singh Sakshi, Oral pathologist, Bangalore, India
Divakaran M, Senior lecturer, Oral Pathology, Anoor Dental College, Kerala, India
Menon K Amrita, Pediatric dentist, Gurgaon, India
Wakhloo Tulika, Pediatric dentist, Jammu, India
Somashekhar Preethi, Oral pathologist, Jeevika Hospital, Marathalli, Bangalore, India

Conflict-of-interest statement: The author(s) declare(s) that there is no conflict of interest regarding the publication of this paper.

Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http: //creativecommons.org/licenses/by-nc/4.0/

Correspondence to: Abhishek Banerjee, 5/17 Ambagan, Bhiringi- ambagan, Durgapur- 713213, West Bengal, India.
Email: abhishek.banerjee376@gmail.com
Telephone: +919886938095

Received: March 9, 2017
Revised: May 20, 2017
Accepted: May 23, 2017
Published online: July 26, 2017


Odontogenic tumour represents as growth and swellings of variedorigin. The histopathological features of hamartomatous odontogenic entities are not very distinct from neoplasms, but they exhibit different biological behavior. The pathobiology of these lesions is sometimes understated. There always lays a big controversy depicting an entity as hamartoma. Hamartomas are frequently encountered in major organs like liver, lung, pancreas etc. but the occurrence in oral cavity is rare. The lesions enlisted in this review may not be true hamartomas but depicts strong correlation to neoplasms. Understanding the hamartomatous nature of an odontogenic entity will help us understanding the outcome of the treatment and chances of fatality

Key words: Hamartoma; Odontogenic

© 2017 The Author(s). Published by ACT Publishing Group Ltd. All rights reserved.

Abhishek B, Tanu TV, Singroha K, Sakshi S, Divakaran M, Amrita MK, Tulika W, Preethi S. Controversial Odontogenic Hamartomas- Review on Their Pathogenesis and Histopathology. Journal of Tumor 2017; 5(3-4): 492-497 Available from: URL: http: //www.ghrnet.org/index.php/jt/article/view/2024


Hamartomas, which are dysmorphic or morphologically altered proliferation of cells native to the organ in which they arise, gain a certain size before ceasing their proliferation. This type of biologic behavior may be expansile and is locally resorptive of bone but does not invade adjacent tissue.

Odontogenic gingival epithelial hamartoma (OGEH)

There are two important sources that are responsible for the development of the odontogenic group of lesions; cell rests of Serres (remnants of dental lamina) and cell rests of Malassez (remnants of Hertwig epithelial root sheath). These cell rests are found as clusters which upon getting stimulus give rise to pathological entities. The terminology OGEH was initially suggested by Baden et al[1,2]. This lesion has a rare occurrence, prevalent mostly in the middle age group (3rd to 5th decade) and most commonly seen in females (M: F- 1: 7)[1,2,3]. The lesion present as a slowly growing, recurrent in occurrence in the soft tissues like gingiva and vestibule. Histopathologically it shows clusters of odontogenic epithelial which are bordered by a fibrous pseudocapsule. Each nodule is separated from each other by loose fibrous stroma containing thin lined blood vessels. The entire nodules are composed of numerous round nests of epithelial cells of odontogenic origin. The cells are usually polyhedral in shape with a basophilic rounded nucleus. Focal areas show clear cell changes without any involvement of inflammatory cells, which suggest an absence of inducing stimuli; hence they are derived from the dental lamina[4,5]. These lesions are essentially non neoplastic as they lack uncoordinated and abnormal growth features. The abnormal mixtures of cells are native to their part of origin. In rare cases, the odontogenic epithelial cells were found to be in direct continuity with the basal layer of the overlying stratified squamous epithelium. The unique presentation and the lack of invasiveness separate OGEH from peripheral ameloblastoma and WHO-type peripheral odontogenic fibroma[3].

Pericoronal hamartomatous lesions (PHLs)

This group of lesion is frequently associated with the dental follicle and hence has a close link to the dental follicle hamartomas. The association is seen with the opercula of the unerupted or delayed erupted second and third molars[6,7]. Previous literature has reported lesions like odontogenic giant cell fibromatosis (OGCF) and peripheral myxofibrous hyperplasia (PMH)[8]. OGCF was described by Philipsen et al[8], the histopathology of the tissue shows no encapsulation with dense fibrous connective tissue containing large multinucleated giant cells, proliferating odontogenic islands with occasional squamous metaplasia. PMH shows hyperplasia of the myxomatous connective tissue (resembles odontogenic ectomesenchyme), giant cells and flecks of calcifications[9,10]. PHLs have strong histopathological similarities to peripheral odontogenic fibromas. The etiology of the peripheral odontogenic fibroma whether reactive or hamartomatous is always debatable. The significant recurrence of the lesion suggests its neoplastic character and the lack of giant cells in the histopathology suggest that PHLs are unique as an entity[7].


It accounts for less than 1% of the entire odontogenic tumour. The initial case was reported by Norberg in 1930. It is considered as a hamartomatous proliferation of cementoblasts forming dysmorphic and disorganized cementum around the apical half of the root. It usually present as a hard expansion in the jaw mostly reported in the mandibular molars and in the young adults[11]. Histopathologically it shows hypocellular masses of cementum embedded in fibrovascular connective tissue surrounded by a thin fibrous capsule continuous with the periodontal ligament. The cemental mass is in association with the root of the tooth. The proliferating cemental mass is lined by numerous plump cementoblasts. Prominent basophilic reversal lines can also appreciated in the cemental mass which gives a pagetoid appearance. The fibrous connective tissue stroma is loose, may contain multinucleated giant cells (cementoclasts) and numerous dilated small blood vessels which is the hallmark of the lesion[11,12] ( Figure 1).

Figure 1 Cementoblastoma. A: Areas of cementum like masses formation with active cells entrapped, these cemental masses are surrounded by loose stroma X40. B: Dilated blood vessels with thick cemental mass containing cementocytes. C: Irregularly formed cemental matrix with entrapped cells.

Ameloblastic fibroma-

A debatable entity till date even after WHO has enlisted ameloblastic fibroma in the neoplastic group of lesions. It is rare odontogenic tumour exhibiting the proliferation of both the odontogenic epithelial component and the Mesenchymal component. The tumour mostly occurs in the children and young adults, though seen in other age groups too. The tumour is mostly seen in posterior mandible than in maxilla. This lesion is usually associated to impacted or unerupted teeth in majority of the cases, sometimes it is also seen associated to missing teeth[13,14]. The histopathology of the mixed odontogenic group of lesions resembles the stages of odontogenesis[15]. Ameloblastic fibroma also included in the category of mixed odontogenic lesions. The identity of the ameloblastic fibroma has always been a source of debate where one school of oral pathologists considers it to be a hamartoma; as if the ameloblastic fibroma is allowed to progress or left undisturbed it may progress further to ameloblastic fibro-odontoma and then to odontoma while the other group of oral pathologist considers it as neoplastic because of its recurrence of the tumour (16.3%), occurrence even after 22 years when there should be no odontogenesis and the malignant transformation of ameloblastic fibroma to ameloblastic fibrosarcoma (6.4%)[13,14]. As per Trodahl et al, ameloblastic fibroma histopathologically resembles two entities; early odontome and the other is true neoplasm lacking inductive potential[16].

Histopathologically, the proliferating odontogenic epithelium is arranged in form of strands, cords and islands. The strand often exhibits double or triple layer of cuboidal cells which has a close resemblance to dental lamina. The odontogenic islands resemble ameloblastic islands which show peripheral arrangement of columnar to tall cuboidal cells. Stellate reticulum like cells are also displayed in the centre of those islands. The ectomesenchymal cells resembling primitive dental papilla are seen surrounding the islands and strands (Figure 2). There is usually a juxta epithelial hyalinization around those islands signifying the process of epithelial mesenchymal interaction[17]. Immunohistochemical markers like proliferating cell nuclear antigen (PCNA) and MIB-1 has been studied where it was found that MIB-1 has been expressed in the mesenchymal component suggesting the higher labeling indices in the Mesenchymal component rather than the epithelial component[18,19]. The role of these markers helped in understanding the growth and aggressive potential of the tumours.

Figure 2 Ameloblastic fibroma, Cords of odontogenic epithelium scattered throughout the immature connective tissue stroma x40.

Ameloblastic fibro-odontoma

Ameloblastic fibro-odontoma (ABFO) is considered to be a hamartomatous tumour which holds similarity to ameloblastic fibroma but show inductive changes (formation of hard structures of tooth)[13,20]. It represents 1-3 % of the occurrence of the total odontogenic tumours[21,22]. Chau et al suggested ameloblastic fibroma as a distinct entity from ameloblastic fibroodontome with neoplastic potential[23]. It was suggested by Buchner and Vered that ameloblastic fibro odontoma can occur as a recurrent lesion of previously occurred ameloblastic fibroma (age before 22 years)[14]. Philpsen and Slootweg have suggested ABFO as a hamartomatous lesion, though histologically indistinguishable from complex odontoma[24,25]. ABFO is more prevalent in the young age group, Philipsen reported the mean age of occurrence to be 9 years[24]. The posterior mandible is most common site of occurrence followed by the posterior maxilla. This tumour is usually associated to the unerupted tooth and radiographically present as a well circumscribed radiolucent lesion which may or may not contain radio-opaque foci.

Histopathologically the tumour presents in forms of odontogenic epithelial strands, cords and islands distributed in the ectomesenchymal stroma. There is a formation of the dentinoid or osteodentin material with an occasional presence of enamel (fibrillar and key hole patterns). Ameloblastic layer can be seen attached to the formed enamel like matrix. All of these features resemble an early tooth or a combination of the tooth structures (Figure 3). Few studies have even reported that ABFO represents histological combination of ameloblastic fibroma and complex odontoma[13,26]. ABFO can be also distinguished from ameloblastic fibro-dentinoma by the additional presence of disorganized enamel like material which the later does not exhibit. The definite arrangement of the soft tissues and the overall presentation of tooth structures development can give a clue to reach diagnosis. ABFO is not an aggressive tumour hence treated with extensive curettage or by block resection to prevent recurrence of the lesion.

Figure 3 Ameloblastic fibroodontoma. A: Odontogenic ameloblasts like cells and adjoining matrix formation x40. B: Numerous cords of odontogenic epithelium and attempts of hard tissue formation. X10.

Adenomatoid Odontogenic Tumour (AOT): - It is a relatively rare neoplasm constituting about 2-7% of odontogenic cysts and tumours combined. The current terminology used for AOT has had a history of frequent changes with adenoameloblastoma ameloblastic adenomatoid tumour, epithelioma adamantinum, pseudoadenoma adamantinum by Dreybladt, and glandular adamantinoma to name a few[27].

AOT is traditionally being believed to be derived from the odontogenic apparatus due to its close association with impacted tooth as well as tooth bearing areas of the jaw and it cytological resemblance to the remnants of enamel organ epithelium, reduced enamel epithelium and rests of Malassez have been postulated as possible sources[28,29].

In a recent article by Ferreira et al[30] described in detail both the gubernacular cord and the gubernacular canal assessed the possible contribution of these structures in the process of tooth eruption. Philpsen et al[8] in their article further went ahead to state that regarding origin and pathogenesis of the AOT, it would seem that this lesion is derived from odontogenic epithelium of the dental lamina complex or its cellular remnants located in the gubernacular cord[30].

AOT is also a unique lesion that presents in a fairly consistent manner, as a result of which it has come to be regarded as a “tumor of two-thirds,” i.e., two-thirds occur in female patients, two-thirds occur in the second decade of life, two-thirds develop in the anterior sextant of the maxilla, two-thirds are superimposed on dentigerous cysts, and two-thirds of associated unerupted teeth are permanent canines. In addition, two-thirds of cases show scattered dot-like (snowflake) opacities within the unilocular radiolucency[31]. There have been reported cases of root resorption associated with AOT[32].

Microscopically, the histopathologic features of this lesion are very distinctive to be separated from any other odontogenic tumor. The tumor exhibits population of spindle-shaped epithelial cells that form sheets, strands, or whorled masses of cells in a scant fibrous stroma. The epithelial cells show a variety of patterns in form rosettes which appear to be formed around a central space or lumen, which may be empty or contain small amounts of eosinophilic material showing positive staining for amyloid like material[33].

The tubular or duct-like structures may be predominant, scanty, or even absent in a given section. These tubular structures consist of a central space surrounded by a layer of columnar or cuboidal epithelial cell with their nuclei polarized away from the central lumen[6]. The lumina are frequently lined by eosinophilic rim of varying thickness popularly known as hyaline ring[3]. The mechanism of formation of these tubular structures is not entirely clear but is likely the result of the secretory activity of the tumor cells, which appear to be preameloblasts in nature[29]. In any event, these structures are not true ducts, and no glandular elements are present in the tumour. Small foci of calcification may also be scattered throughout the tumor[32]. These have been interpreted as abortive enamel formation (Figure 4). Some adenomatoid odontogenic tumors contain larger areas of matrix material or calcification which has been traditionally interpreted as dysplastic dentin, dentinoid, osteodentin or cementum like material. Irregular to round concentric layered calcified bodies exhibiting a Leisegang ring pattern may also be evident[29]. At the periphery few of the tumors may show narrow, often anastomosing cords of epithelium in an eosinophilic, loosely arranged matrix adjacent to the capsular area. The supporting stroma is loose hypocellular and fibrovascular and may show presence of prominent vascular component[17,34].

Recent advances in molecular mechanism have revealed that the mean values for Ki-67 when compared in solid ameloblastomas and AOTs were found to be 4% and 1%, respectively. Enamel proteins including amelogenin, ameloblastin, and amelotin, as well as TGF-β/SMADs, are more intensely expressed in AOTs than in ameloblastomas. Thus resulting in lesser aggressive biological behavior and increased cytodifferentiation and apoptosis in AOT than ameloblastomas[35,36]. Philipsen et al[4] in their study have suggested to continue reporting of unusual or rare histomorphological features, immunohistochemical findings and applications of molecular biological techniques for better understanding of this unusual odontogenic tumour[27].

Figure 4 Adenomatoid odontogenic tumour. A: Ductal structures of varying size surrounded by columnar palisading epithelial cells, darkly stained columnar cells arranged in form of whorls and sheets of throughout the fibrous connective tissue stroma. B: Odontogenic epithelial lining arranged in a rosette and whorling pattern. Focal areas showing calcifications.


Baden E, Splayer T. Odontogenic gingival epithelial hamartoma: report of a case. J Oral Surg 1973; 31: 932-5. [PMID: 4518454]

2. Philipsen HP, Reichart PA. An odontogenic gingival epithelial hamartoma (OGEH) possibly derived from remnants of the dental lamina (“dental laminoma”). Oral Oncology Extra. 2004 May 31; 40(4): 63-7. [DOI: 10.1016/j.ooe.2004.02.001]

3. Kitano M, Landini G, Urago A, Okubo A, Mukai H, Yamashita S. Odontogenic epithelial hamartoma of the gingiva: a case report. Journal of periodontology. 1991 Jul; 62(7): 452-7. [DOI: 10.1902/jop.1991.62.7.452]

4. Sciubba JJ, Zola MB. Odontogenic epithelial hamartoma. Oral Surg Oral Med Oral Pathol 1978; 45: 261-5. [PMID: 272607]

5. Nikitakis NG, Parashar P, Terezides A, Sarlani E. Dental follicular hamartomas in the operculum of teeth delayed in eruption: A case report and review of the literature. Oral Oncology Extra. 2006 Mar 31; 42(3): 129-32. [DOI: 10.1016/j.ooe.2005.10.005]

6. Yonemochi H, Noda T, Saku T. Pericoronal hamartomatous lesions in the opercula of teeth delayed in eruption: an immunohistochemical study of the extracellular matrix. Journal of oral pathology & medicine. 1998 Oct 1; 27(9): 441-52. [PMID: 979009]; [DOI: 10.1111/j.1600-0714.1998.tb01982.x]

7. Philipsen HP, Thosaporn W, Reichart P, Grundt G. Odontogenic lesions in opercula of permanent molars delayed in eruption. J Oral Pathol Med 1992; 21(1): 38-41. [PMID: 1593494]; [DOI: 10.1111/j.1600-0714.1992.tb00967.x]

8. Flaitz CM. Gingival enlargement associated with a partially erupted mandibular molar. Pediatr Dent 2001; 23(5): 435-7. [PMID: 11699171]

9. Kim J, Ellis GL. Dental follicular tissue: misinterpretation as odontogenic tumors. J Oral Maxillofac Surg 1993; 51(7): 762–7.[PMID: 8509916]; [DOI: 10.1016/S0278-2391(10)80417-3]

10. Sankari LS, Ramakrishnan K. Benign cementoblastoma. Journal of Oral and Maxillofacial Pathology. 2011 Sep 1; 15(3): 358. [DOI: 10.4103/0973-029X.86725]; [PMID: 22144847]

11. Huber AR, Folk GS. Cementoblastoma. Head and neck pathology. 2009 Jun 1; 3(2): 133-5. [PMID: 19644548]; [DOI: 10.1007/s12105-008-0099-5]

12. Cohen DM, Bhattacharyya I. Ameloblastic fibroma, ameloblastic fibro-odontoma, and odontoma. Oral and Maxillofacial Surgery Clinics. 2004 Jan 8; 16(3): 375-84. [PMID: 18088738]; [DOI: 10.1016/j.coms.2004.03.005]

13. Buchner A, Vered M. Ameloblastic fibroma: a stage in the development of a hamartomatous odontoma or a true neoplasm? Critical analysis of 162 previously reported cases plus 10 new cases. Oral surgery, oral medicine, oral pathology and oral radiology. 2013 Nov 30; 116(5): 598-606. [PMID: 24055148]; [DOI: 10.1016/j.oooo.2013.06.039]

14. Jindal C, Bhola RS. Ameloblastic fibroma in six-year-old male: Hamartoma or a true neoplasm. Journal of Oral and Maxillofacial Pathology. 2011 Sep 1; 15(3): 303. [PMCID: 3227258]; [DOI: 10.4103/0973-029X.86695]

15. Trodahl JN. Ameloblastic fibroma. A survey of cases from the Armed Forces Institute of Pathology. Oral Surg Oral Med Oral Pathol. 1972; 33: 547-558. [PMID: 4502230]

16. Reichart PA, Philipsen HP. Ameloblastic fibroma. Odontogenic Tumors and Allied Lesions. 2004; 121.

17. Yamamoto K, Yoneda K, Yamamoto T, Ueta E, Osaki T. An immunohistochemical study of odontogenic mixed tumors. Oral Oncol 1995; 31: 122-8. [PMID: 7543314]; [DOI: 10.1016/0964-1955(94)00046-7]

18. Sano K, Yoshida S, Ninomiya H, Ikeda H, Ueno K, Sekine J, et al. Assessment of growth potential by MIB-1 immunohistochemistry in ameloblastic fibroma and related lesions of the jaws compared with ameloblastic fibrosarcoma. J Oral Pathol Med 1998; 27(2): 59-63. [PMID: 9526730]; [DOI: 10.1111/j.1600-0714.1998.tb02094.x]

19. Kumar LS, Manuel S, Khalam SA, Venugopal K, Sivakumar TT, Issac J. Ameloblastic fibro-odontoma. International journal of surgery case reports. 2014 Dec 31; 5(12): 1142-4 [PMID: 25437658]; [PMCID: PMC4276268]; [DOI: 10.1016/j.ijscr.2014.11.025]

20. Chang H, Precious DS, Shimizu MS. Ameloblastic fibro-odontoma: a case report. J Can Dent Assoc 2002; 68: 243-6.

21. Silva GC, Jham BC, Silva EC, Horta MC, Godinho SH, Gomez RS. Ameloblastic fibro- odontoma. Oral Oncology Extra. 2006 May 31; 42(5): 217-20. [DOI: 10.1016/j.ooe.2005.12.005]

22. Chau E, Daley T, Darling MR, Hamilton D. The expression and immunohistochemical localization of periostin in odontogenic tumors of mixed epithelial/mesenchymal origin. Oral Surg Oral Med Oral Pathol Oral Radiol.2013; 116: 214-20. [PMID: 23849375]; [DOI: 10.1016/j.oooo.2013.05]

23. Philipsen HP, Reichart PA. Mixed odontogenic tumours and odontomas. Considerations on interrelationship. Review of the literature and presentation of 134 new cases of odontomas. Oral oncology. 1997 Mar 31; 33(2): 86-99. [PMID: 9231165]

24. Slootweg PJ. An analysis of the interrelationship of the mixed odontogenic tumors— ameloblastic fibroma, ameloblastic fibro-odontoma, and the odontomas. Oral Surgery, Oral Medicine, Oral Pathology. 1981 Mar 1; 51(3): 266-76.[PMID: 6938886]; [DOI: 10.1016/0030-4220(81)90056-6]

25. Tolentino ED, Centurion BS, Lima MC, Freitas-Faria P, Consolaro A, Sant’ana E. Ameloblastic fibro-odontoma: a diagnostic challenge. International journal of dentistry. 2010; 201: 1-4. [DOI: 10.1155/2010/104630]

26. Philipsen HP, Reichart PA, Siar CH, et al. An updated clinical and epidemiological profile of the adenomatoid odontogenic tumour: a collaborative retrospective study. J Oral Pathol Med 2007; 36: 383-93.[PMID: 17617830]; [DOI: 10.1111/j.1600-0714.2007.00536.x]

27. Rajendran R and Sivapathasundharam B, editors. Shafer’s Textbook of Oral Pathology. 7th ed. Noida (India) Elsevier Inc; 2012.

28. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and Maxillofacial pathology. 2nd ed. Philadelphia W B Saunders. Philadelphia. 2002.

29. Ferreira DCA, Fumes AC, Consolaro A, et al. Gubernacular cord and canal – do these anatomical structures play a role in dental eruption? RSBO (Online) 2013; 10: 167–71.

30. Ide F, Muramatsu T, Ito Y, et al. An expanded and revised early history of the adenomatoid odontogenic tumor. Oral Surg Oral Med Oral Pathol Oral Radiol 2013; 115: 646-51. [PMID: 23601219]; [DOI: 10.1016/j.oooo.2013.01.023]

31. Kundoor VK, Maloth KN, Guguloth NN, Kesidi S. ExtrafollicularAdenomatoid Odontogenic Tumor: An Unusual Case Presentation. Journal of Dentistry. 2016 Dec; 17(4): 370. [PMCID: 5136418]

32. Lee SK, Kim SY. Current concepts and occurrence of epithelial odontogenic tumours-I. Ameloblastoma and Adenomatoid Odontogenic Tumour. Korean Jour of Pathol 2013; 47: 191-202 [PMCID: PMC3701814]; [DOI: 10.4132/KoreanJPathol.2013.47.3.191]

33. Narayan VK, Girish HC, Murgod S, Kavya MS, Nishanthi L. Adenomatoid odontogenic tumor: A fluctuating tumor entity. J Adv Clin Res Insights 2016; 3: 170-172. [DOI: 10.15713/ins.jcri.131]

34. Crivelini MM, Felipini RC, Miyahara GI, de Sousa SC. Expression of odontogenic ameloblast-associated protein, amelotin, ameloblas¬tin, and amelogenin in odontogenic tumors: immunohistochemical analysis and pathogenetic considerations. J Oral Pathol Med 2012; 41: 272-80. [PMID: 21936873]; [DOI: 10.1111/j.1600-0714.2011.01079.x]

35. Karathanasi V, Tosios KI, Nikitakis NG, Piperi E,Koutlas L,Trimis G,Sklavounou A. TGF-beta1, Smad-2/-3, Smad-1/-5/-8, and Smad-4 signaling factors are expressed in amelo¬blastomas, adenomatoid odontogenic tumors, and calcifying cystic odontogenic tumors: an immunohistochemical study. J Oral Pathol Med 2013; 42: 415-23. [PMID: 23157422]; [DOI: 10.1111/jop.12016]

Peer reviewers: Drago Jelovac; Mohammed Grawish; Gokul Sridharan


  • There are currently no refbacks.