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 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 13  |  Issue : 2  |  Page : 107-113

Lobular capillary haemangioma of the gingiva: Clinical management and a review of the literature


1 Department Oral Diagnostic Sciences, Faculty of Dentistry, Bayero University; Department of Oral and Maxillofacial Surgery and Radiology, Aminu Kano Teaching Hospital, Kano, Nigeria
2 Department of Oral and Maxillofacial Surgery, Aminu Kano Teaching Hospital, Kano, Nigeria
3 Department of Histopathology, Aminu Kano Teaching Hospital, Kano, Nigeria
4 Department Oral Diagnostic Sciences, Faculty of Dentistry, Bayero University, Kano, Nigeria

Date of Web Publication1-Aug-2016

Correspondence Address:
Babatunde Olamide Bamgbose
Department Oral Diagnostic Sciences, Faculty of Dentistry, Bayero University, Kano
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0331-8540.181031

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  Abstract 

Introduction: Lobular capillary hemangioma, otherwise called pyogenic granuloma represents an exuberant connective tissue proliferation to a known stimulus or injury. The aim of this paper is to present a case in our clinical practice, discuss the differential diagnosis and review the literature. Materials and Methods: A narrative review of the literature was performed to evaluate recent information as regards etiopathogenesis, clinical presentation as well as management of pyogenic granuloma. A search of the literature was performed on PubMed using the following keys terms: lobular capillary hemangioma, pyogenic granuloma, etiopathognenesis, clinical features and management. The search criteria were filtered to include articles on human studies, which were published in English Language. Results: We present a clinical case of pyogenic granuloma demonstrating positivity for estrogen receptor and a narrative review of the English Literature and management of a large case of lobular capillary hemangioma of the gingiva. Conclusion: The conventional deep scaling and polishing and root plaining, in addition to surgical excision of the lesion is still the acceptable treatment option of lobular capillary hemangioma of the gingiva. However, there is need to consider other less aggressive and less morbid methods of treatment such as cryosurgery and laser therapy.

Keywords: Gingiva, lobular capillary haemangioma, pyogenic granuloma


How to cite this article:
Bamgbose BO, Kaura MA, Atanda AT, Ajayi OF. Lobular capillary haemangioma of the gingiva: Clinical management and a review of the literature. Niger J Basic Clin Sci 2016;13:107-13

How to cite this URL:
Bamgbose BO, Kaura MA, Atanda AT, Ajayi OF. Lobular capillary haemangioma of the gingiva: Clinical management and a review of the literature. Niger J Basic Clin Sci [serial online] 2016 [cited 2020 Sep 21];13:107-13. Available from: http://www.njbcs.net/text.asp?2016/13/2/107/181031


  Introduction Top


Lobular capillary haemangioma (LCH) of the oral mucosa represents inflamed fibrovascular tissues and has been given a myriad of names including fibrous inflammatory hyperplasia, palatal papillary hyperplasia, giant cell granuloma, pregnancy epulis and most famously, pyogenic granuloma (PG).[1],[2]

LCH is a common entity that causes soft tissue enlargement in the oral cavity or skin and is considered by many researchers to be non-neoplastic in nature.[3],[4],[5]

The term 'pyogenic granuloma' or 'granuloma pyogenicum' was coined by Hartzell in 1904.[6],[7] Whereas the term 'pyogenic granuloma' is suggestive of an infectious process, the lesion does not contain pus and it is, histologically, not granulomatous.[3],[6],[8],[9] Histologically, it was described as 'haemangiomatous granuloma' by Angelopoulos [10] due to the presence of numerous blood vessels and the inflammatory nature of the lesion. While this lesion is very common in the skin, it is extremely rare in the gastrointestinal tract except the oral cavity where it is commonly found on keratinised tissues.[11],[12] It mostly presents as a painless, pedunculated or sessile mass of gingival tissue. Lesions are more common on the maxillary gingiva than the mandibular gingiva, and anterior region of arches are more commonly affected than posterior regions. PG exists in two histological forms namely, LCH type and non-LCH type.[13],[14]


  Clinical Report Top


We share our experience of a case of LCH at the Aminu Kano Teaching Hospital, Kano, Nigeria. A 22-year-old female patient presented to the Oral Diagnostic Sciences Clinic with a complaint of gingival swelling on the facial surface of the upper left quadrant of 4 months duration. The swelling initially was millet-sized and progressively increased in size. There was no history of trauma or toothache before the swelling, and the patient was not pregnant. There was a history of intermittent pain and bleeding. There was no history of dysphagia or weight loss.

The patient was otherwise in good health, and she presented no history of prior hospitalization, hypertension or diabetes mellitus. She was not pregnant. Intraoral examination revealed firm, inflamed and pedunculated swelling between the maxillary left lateral incisor and canine; protruding out of the oral cavity and measuring about 3 cm by 5 cm in diameter with intact overlying mucosa. There was hyperaemia of the adjacent attached gingiva [Figure 1].
Figure 1: Patient retracting upper lip to reveal a firm, pedunculated gingival mass in the region of the maxillary left lateral incisor and canine, measuring about 3 cm by 5 cm

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Mouth opening was adequate and oral hygiene was poor. Visual examination revealed heavy deposit of supragingival calculus ad plaque. Probing depth around the maxillary left lateral incisor and canine was >5.5 mm, with bleeding on probing and Grade III mobility of the maxillary left lateral incisor. The patient had all the complement of teeth, but the upper left lateral incisor was mobile (Grade III), and the lower central and lateral incisors were also mobile (Grade II). A clinical impression of PG was made with the differential diagnosis of peripheral giant cell granuloma and peripheral fibroma.

Anterior maxillary occlusal radiograph showed a gross horizontal bone loss in the region of the maxillary central incisors, maxillary left lateral incisor and canine. The crown-root ratio was grossly increased. There was also present, a radiopaque entity in the region of the maxillary left lateral incisor and canine. The appearance was suggestive of calculus [Figure 2].
Figure 2: Anterior maxillary occlusal radiograph showing gross horizontal bone loss in the region of the maxillary central incisors, maxillary left lateral incisor and canine. The crown-root ratio is grossly increased. There is also present, a radiopaque entity in the region of the maxillary left lateral incisor and canine. The appearance is suggestive of calculus

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A surgical excision was done under local anaesthesia (2% lignocaine 1:80,000 epinephrine). Extraction of maxillary left lateral incisor was carried out. The specimen was sent for histopathologic evaluation in 10% neutral buffered formalin solution. Patient, thereafter, had deep scaling and root planing of all the teeth in the quadrant [Figure 3].
Figure 3: Immediate postoperative photograph showing the extraction socket of the lateral incisor and the associated hyperemic gingiva

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Post-operative instructions were given, and the patient was placed on tablets doxycycline 100 mg 12 hourly for 5 days; tablets metronidazole 400 mg 8 hourly for 5 days; tablets ibuprofen 400 mg 8 hourly for 3 days. A review appointment was scheduled to discuss the histopathology report and possible need for follow-up. On review after 2 weeks, there was evidence of good healing [Figure 4].
Figure 4: Photograph showing presentation at two weeks following excisional biopsy and root planning. There is evidence of healing and resolution of the gingivitis

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The histopathology report confirmed PG and the lesion was reported as LCH. The histological section showed keratinised squamous epithelium overlying a stroma composed of lobules of small sized capillary blood vessels containing red blood cells lined by plump endothelial cells. The interstitium exhibited mild lymphocytic infiltrates [Figure 5] and [Figure 6]. Immunohistochemistry staining revealed positivity for oestrogen receptor [Figure 7].
Figure 5: Low power photomicrograph of the lesion. Shows keratinized epithelium overlying stroma composed of lobules of small sized capillary vessels containing red blood cells and lined by plump endothelial cells. There is mild lymphocytic infiltrate in the interstitium

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Figure 6: High power photomicrograph of the lesion

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Figure 7: Immunihistochemistry stain ×400 shows nuclei of the spindle cells demonstrating positivity for estrogen receptor

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  Discussion Top


Lawoyin et al.[15] reported 38 cases of oral PG in a 10-year study with a male: female ratio of 1:1.2 with a preponderance of cases located on the gingiva (74%). PG was reported as 1.85% of all oral pathoses, excluding dental caries and gingivitis, treated at the US Army Institute of Dental Research.[6] PG was originally thought to be caused by pyogenic organisms. However, it is now believed to be unrelated to infection.[2],[3] Staphylococci and botryomycosis, foreign bodies and localisation of infection in walls of blood vessel have been reported as contributing factors in the development of the lesion.[15]

While it is generally believed that PG is unrelated to infection,[2],[3] some authors have demonstrated the presence of bacilli in oral PG, especially the superficial surface of the ulcerated lesion. This observation led to the conclusion that minor trauma to the PG causes tissue ulceration which, in turn, encourages colonisation of the surface of the ulcer by non-specific microorganisms that may represent contaminants from the oral flora.[6],[16],[17] The characteristic tissue reaction is the overzealous proliferation of a vascular type connective tissue. A common causative factor for extragingival PG is trauma. About 30% of the lesions will occur after trauma, chronic irritation, defective fillings in the region of the lesion, food impaction and tooth brushing and many patients will present with these findings.[3],[18],[19],[20],[21],[22],[23] Theories that have been postulated that trauma can cause the release of endogenous substances, including angiogenic factors, from the tumour cells and it may also cause disturbances in the vascular system of the affected area. It has been postulated that habitual tooth brushing may also be considered as a significant cause of micro-trauma and irritation to the gingiva.[23] In addition to trauma, poor oral hygiene, by way of heavy plaque and calculus, may aggravate the lesion.[1],[3],[8] PG represents an exuberant reactive or reparative connective tissue proliferation to a known stimulus or injury.[8] These stimuli may be calculus or foreign material within the gingival crevice.[3],[8]

PG is seen predominantly in the second decade of life in females. This is thought to be due to the vascular effects of female hormones.[1],[3],[8],[14] There continues to be no ground of agreement in the gender distribution and age of incidence. While some authors believe PG in more common in males, some believe otherwise.[14],[17] Female hormonal changes have remained a focus of investigation in the aetiology of pregnancy tumour, a type of PG that occurs during pregnancy. Pregnancy tumour arises from the gingiva and shares similar histologic characteristics with oral PG.[24] Pronounced vascularity of gingiva, hyperplastic gingivitis and PG are some of the oral changes associated with pregnancy. Similar changes are seen with the use of oral contraceptives.[25] Five percent of pregnant woman present with PG (pregnancy tumour or granuloma gravidarum) and is often attributed to the heightened tissue response to plaque and irritation due to hormonal imbalance.[1],[3],[26] In the first trimester of pregnancy, this heightened tissue response may present as hyperplastic gingivitis, which occasionally may become localised hyperplasia (pregnancy granuloma).[20] It is postulated that oestrogen and progesterone act directly on the gingiva causing enlargement during pregnancy and atrophy during menopause.[27] Such a role is due to the circulating hormones and exerts a great effect on the endothelium of PG.[28] On the contrary, Bhaskar and Jacoway conclude that since PG occur often in males as well as females, it is doubtful that it has any hormonal basis.[6]

Clinically, PG may present as a lobulated, exophytic, pedunculated or sessile mass. It is often haemorrhagic and compressible and may manifest as small, erythematous papules.[1],[3],[8] It occurs over a wide age range of 4.5–93 years with a slight female preponderance.[14] It commonly affects the gingiva, followed by lips, tongue, buccal mucosa and hard palate.[1] PGs generally are soft, painless and deep red to reddish purple in colour and haemorrhagic on slight irritation.[1] The colour may change from pink to red to purple depending on the stage of the lesion. Young PGs are highly vascular in appearance because they are composed predominantly of hyperplastic granulation tissue in which capillaries are prominent. Thus minor trauma to the lesion may cause considerable bleeding, whereas older lesions tend to become more collagenised and pink.[3] It was reported by Epivatianos et al.[13] that the two types of PG were clinically different. They found that the LCH PG occurred more frequently (66%) as sessile lesion, whereas non-LCH PG mostly occurred as pedunculated (77%).[13] In the clinic, the diagnosis will always be PG. The clinical behaviours of the two histological types are essentially the same. Further studies may needed to study the biology of the two histologic variants to determine the prognostic significance of the variants.

The size varies in diameter from a few millimetres to several centimetres.[1],[3] PG reaches its full size within weeks or months and rarely exceeds 2.5 cm in diameter. It is not unusual to maintain a constant size over the course of the lesion.[9] The lesion may grow rapidly, but the common clinical course is slow asymptomatic and painless.[3],[29] The surface is characteristically ulcerated and friable which may be covered by a yellow, fibrinous membrane.[3],[8] In very rare circumstances, PG has been reported to be associated with significant bone loss and calculus formation in the crypt of the lesion.[1],[30] In our clinical experience, there was a significant horizontal bone loss with a crown root ratio of 5:1 and a heavy deposit of calculus in the resultant periodontal pocket. The crown-root ratio is a radiographic measure of bone loss and it represents the quantity of tooth structure suprabony or infrabony. A crown-root ratio of 5:1 shows that the bone loss is near the tip of the tooth root, and the radiographic crown is quite long.

The histologic features of PG include granulation tissues with high vascular proliferation in the stroma.[3] Vascular channels which are engorged with red blood cells and lined by flat or plum endothelial cells that may be mitotically active.[1],[3],[17] These blood vessels often show a clustered or medullary pattern separated by less vascular fibrotic septa. PG has, therefore, been considered a polypoid form of capillary haemangioma.[9] The blood vessels are sometimes arranged in lobular aggregates. Therefore, the basis of the diagnosis of LCH.[3],[8]

Polymorphs, micro-abscesses and chronic inflammatory cells consistently feature in the stroma of PG.[2] As the lesion ages, fewer and more mature cells, fibrocytes, are seen. Occasionally, a preponderance of plasma cells is encountered. Some pathologists have, therefore, called the lesion plasma cell granuloma. It is controversial calling PG plasma cell granuloma because of the possible confusion with mucosal solitary plasmacytoma or multiple myeloma.[2],[8],[31]

At low magnification, the lobular arrangement of thin capillaries is often seen at the periphery of the lesion. The lobules are surrounded by a thin collagen layer. Larger, irregularly shaped vascular channels are seen at the base. These larger channels communicate with the lobulated peripheral vascular channels. A higher magnification, the thin, small capillary endothelial-lined spaces are surrounded by a perithelial or pericytic layer of cells.[31] This is an important feature in the classification of PG as a benign vascular lesion.[31]

The surface of the lesion is often ulcerated and lined by a thick fibrin purulent membrane. A mixed inflammatory cell infiltrates of neutrophils is mostly prevalent near the ulcerated surface while chronic inflammatory cells are found deeper in the lesion.[3],[8],[32]

The lesion follows three classic phases of evolution, viz., cellular phase, capillary phase and involutionary phase.[31]

Two histological types of PG have been reported.[13] They are LCH type and non-LCH. The LCH type is characterised by proliferating blood vessels that are organised in lobular aggregates. Whereas the second type (non-LCH type) consists of highly vascular proliferation that resembles granulation tissue.[3],[13] The lobular area of the LCH type PG contains a greater number of blood vessels with small luminal diameter than does the central area of non-LCH PG. It is possible that these differences may suggest that two histological types of PG may represent biologic behaviours.[13] The presence of blood vessels with different luminal diameter in the lobular area of LCH PG and in the central area of non-LCH PG may be because different pathogenic factors influencing their development.[3],[13] It was further observed that foci of fibrous maturation were present in 15% of non-LCH PG but were totally absent in LCH PG.[13]

Whenever a swelling is found in the oral cavity, it is imperative to formulate a differential diagnosis as this would facilitate further evaluation of the condition and management of the patient. In making a diagnosis, it is important to exhaust all the possible clinical differentials consequent upon the history and clinical examination. Even though histopathology is the ultimate diagnostic modality, it is, none the less, invasive. Other diagnostic modalities such as imaging, cytology and hormonal analysis are non-invasive and should be exhausted before doing a biopsy. The differential diagnosis of PG includes peripheral giant cell granuloma, peripheral ossifying fibroma, metastatic cancer, haemangioma, pregnancy tumour, conventional granulation tissue, hyperplastic gingival inflammation, Kaposi's sarcoma, bacillary angiomatosis, angiosarcoma and non-Hodgkin's lymphoma.[1],[3],[13],[17],[31],[33],[34]

It is important to be able to differentiate PG from oral haemangioma. Haemangioma is a developmental disorder, and small lesions may be difficult to distinguish from PG.[1],[2] Diascopy is a technique used in confirming that, indeed, a lesion is vascular. When pressure is applied to a suspected case of haemangioma, an evacuation of the coloration is visualised, and this supports the impression that patent blood-filled spaces constitute the lesion. PG is not a developmental disorder, and the lesion is not composed of patent, blood-filled spaces. Most oral haemangiomas are located on the tongue and are multinodular and bluish red.[2] Histologically, haemangiomas have plump, histiocytoid endothelial cell proliferation without an acute inflammatory cell infiltrate.[32]

The difference between PG and peripheral giant cell granuloma is minimal, and the lesions may be clinically indistinguishable. Peripheral giant cell granuloma is a reactive hyperplasia presenting as an exophytic lesion involving the gingiva exclusively.[2] The lesion may present clinically similar features as PG, but it is often more bluish-purple compared to the bright red colour of PG.[3],[8] Histologically, peripheral giant cell granuloma presents with multinucleated giant cells. This is absent in PG.[8] PG may be suggestive of a fibroma because it may be soft or firm to touch depending on the duration of the lesion.[1],[8] Whereas metastatic tumours in the gingiva may resemble PG clinically, they are often seen in patients in the fifth to seventh decades of life.[35],[36],[37] This is different from PG, which is often seen in younger patients.[35]

The increased prevalence of pregnancy epulis during pregnancy and the tendency to shrink after delivery has learn to the conclusion that hormones have a role in the aetiology of pregnancy tumour.[2] Even though Ojanotko-Harri et al.[37] reported no clinical or histopathological difference between PG and pregnancy tumour, some authors believe that unlike PG, pregnancy tumour is usually confined to the interdental papilla.[38]

Hyperplastic gingival inflammation may be very difficult to differentiate from PG, both clinically and histopathologically.[9]

In considering conventional granulation tissue as a differential diagnosis of PG, the clinical behaviour of the latter is distinct. PG presents rapid growth, multiple occurrence and recurrence.[33] Kaposi's sarcoma of acquired immunodeficiency syndrome shows proliferation of dysplastic spindle cells, vascular clefts, extravasated erythrocytes and intracellular hyaline globules, none of which are features of PG.[9] The initial diagnosis of Kaposi's sarcoma requires microscopic evaluation of biopsy material because this disease can mimic a number of intraoral lesions such as PG, bacillary angiomatosis, haemangioma and lymphoma.[39]

Another important differential is non-Hodgkin's Lymphoma. This presents in primary sites in the head and neck such as the Waldeyer's ring, paranasal sinuses, salivary glands, the oral cavity and larynx. The clinical appearance of gingival non-Hodgkin's lymphoma varies but is usually found to be an asymptomatic gingival enlargement or mass resembling a PG.[34]

The choice of a particular treatment option for PG may depend on many factors such as severity of symptoms, accessibility of the lesion, proximity to dental hard tissues and available resources. In many instances, combination of different treatment modalities is recommended.[1],[2],[3],[4]

Surgical excision is indicated for the treatment of PG except when the procedure would produce marked deformity.[2] The excision should extend down to the periosteum and combined with the removal of causative irritants such as plaque, calculus, foreign material and sources of trauma.[1],[3] A conservative management by clinical observation and follow-up is often sufficient when the lesion is small, painless and free of bleeding. In this case, deep scaling and root planning will be recommended.[26]

Other treatment protocols have been proposed apart from the conventional surgical excision mentioned above. Powell et al.[40] reported the use of neodymium-doped yttrium aluminium garnet (Nd: YAG) laser for excision of PG because of the lower risk of bleeding compared to other surgical techniques. They chose the Nd: YAG laser over the carbon dioxide (CO2) laser because of its superior coagulation characteristics. However, Fekrazad et al.[41] have recommended the use of erbium-doped YAG laser for treatment of PG that is very close to the dental hard tissues due to its minimal thermal effects.

Flash lamp pulsed dye laser was used by Meffert et al.[42] on a mass of granulation tissue which did not respond to the usual treatment methods and concluded that previously resolute tissue responded well to a series of treatment with the pulsed dye laser.[42] Cryosurgery is a very useful technique for treatment of PG. Yasin et al.[43] have reported success in the treatment of PG involving the lower lip after some days of cryosurgery using CO2 snow in a 14-year-old child. The CO2 snow is placed in contact with the lesion for 1 min, then the lesion is allowed to warm up again, and the same procedure is repeated for another minute. This cycle will be repeated every day till the lesion completely disappears.

When all conventional surgical and non-surgical treatment proves ineffective, a favourable response may be achieved by combination of cryosurgery, intra-lesional triamcinolone injection, and topical application of timolol.[44] Other procedures of benefit include injection of absolute ethanol,[45] use of sclerosing agents such as sodium tetradecyl sulphate.[46]

The conventional deep scaling and root planing, in addition to surgical excision of the lesion is still the acceptable treatment option for PG and its histologic variants of LCH and non-LCH. However, there is a need to consider other less aggressive and less morbid methods of treatment such as cryosurgery and laser therapy.

Financial support and sponsorship

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Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Eversole LR. Clinical Outline of Oral Pathology: Diagnosis and Treatment. 3rd ed. Hamilton: BC Decker; 2002. p. 113-4.  Back to cited text no. 1
    
2.
Greenberg MS, Glick M. Burket's Oral Medicine: Diagnosis and Treatment. 10th ed. Hamilton: BC Decker; 2003. p. 141-2.  Back to cited text no. 2
    
3.
Nevile BW, Damm DD, Allen CM, Bouquot JE. Oral & Maxillofacial Pathology. 2nd ed. Philadelphia: WB Saunders; 2002. p. 437-95.  Back to cited text no. 3
    
4.
Vilmann A, Vilmann P, Vilmann H. Pyogenic granuloma: Evaluation of oral conditions. Br J Oral Maxillofac Surg 1986;24:376-82.  Back to cited text no. 4
    
5.
Kamal R, Dahiya P, Puri A. Oral pyogenic granuloma: Various concepts of etiopathogenesis. J Oral Maxillofac Pathol 2012;16:79-82.  Back to cited text no. 5
[PUBMED]  Medknow Journal  
6.
Bhaskar SN, Jacoway JR. Pyogenic granuloma – Clinical features, incidence, histology, and result of treatment: Report of 242 cases. J Oral Surg 1966;24:391-8.  Back to cited text no. 6
    
7.
Hartzell MB. Granuloma pyogenicum. J Cutan Dis Syph 1904;22:520-5.  Back to cited text no. 7
    
8.
Regezi JA, Sciubba JJ, Jordon RC. Oral Pathology: Clinical Pathological Considerations. 4th ed. Philadelphia, PA, USA: WB Saunders; 2003. p. 115-6.  Back to cited text no. 8
    
9.
Bouquot JE, Nikai H. Lesions of the oral cavity. In: Gnepp DR, editor. Diagnostic Surgical Pathology of Head and Neck. Philadelphia, PA, USA: WB Saunders; 2001. p. 141-233.  Back to cited text no. 9
    
10.
Angelopoulos AP. Pyogenic granuloma of the oral cavity: Statistical analysis of its clinical features. J Oral Surg 1971;29:840-7.  Back to cited text no. 10
    
11.
Yao T, Nagai E, Utsunomiya T, Tsuneyoshi M. An intestinal counterpart of pyogenic granuloma of the skin. A newly proposed entity. Am J Surg Pathol 1995;19:1054-60.  Back to cited text no. 11
    
12.
Fowler EB, Cuenin MF, Thompson SH, Kudryk VL, Billman MA. Pyogenic granuloma associated with guided tissue regeneration: A case report. J Periodontol 1996;67:1011-5.  Back to cited text no. 12
    
13.
Epivatianos A, Antoniades D, Zaraboukas T, Zairi E, Poulopoulos A, Kiziridou A, et al. Pyogenic granuloma of the oral cavity: Comparative study of its clinicopathological and immunohistochemical features. Pathol Int 2005;55:391-7.  Back to cited text no. 13
    
14.
Lawoyin JO, Arotiba JT, Dosumu OO. Oral pyogenic granuloma: A review of 38 cases from Ibadan, Nigeria. Br J Oral Maxillofac Surg 1997;35:185-9.  Back to cited text no. 14
    
15.
Kerr DA. Granuloma pyogenicum. Oral Surg 1951;4:158.  Back to cited text no. 15
    
16.
Shafer WG, Hane MK, Levy BM. Shafer's Textbook of Oral Pathology. 5th ed. Amsterdam: Elsevier Health Sciences; 2006. p. 459-61.  Back to cited text no. 16
    
17.
Reichart PA, Philipsen HP. Color Atlas of Dental Medicine Oral Pathology. Stuttgart: Thieme; 2000. p. 163.  Back to cited text no. 17
    
18.
Pilch BZ. Head and Neck Surgical Pathology. Philadelphia: Lippincott Williams & Wilkins; 2001. p. 389-90.  Back to cited text no. 18
    
19.
Macleod RI, Soames JV. Epulides: A clinicopathological study of a series of 200 consecutive lesions. Br Dent J 1987;163:51-3.  Back to cited text no. 19
    
20.
Jafarzadeh H, Sanatkhani M, Mohtasham N. Oral pyogenic granuloma: A review. J Oral Sci 2006;48:167-75.  Back to cited text no. 20
    
21.
Mussalli NG, Hopps RM, Johnson NW. Oral pyogenic granuloma as a complication of pregnancy and the use of hormonal contraceptives. Int J Gynaecol Obstet 1976;14:187-91.  Back to cited text no. 21
    
22.
Miller RA, Ross JB, Martin J. Multiple granulation tissue lesions occurring in isotretinoin treatment of acne vulgaris – Successful response to topical corticosteroid therapy. J Am Acad Dermatol 1985;12(5 Pt 1):888-9.  Back to cited text no. 22
    
23.
Ainamo J. The effect of habitual toothcleansing on the occurrence of periodontal disease and dental caries. Suom Hammaslaak Toim 1971;67:63-70.  Back to cited text no. 23
    
24.
Yih WY, Richardson L, Kratochvil FJ, Avera SP, Zieper MB. Expression of estrogen receptors in desquamative gingivitis. J Periodontol 2000;71:482-7.  Back to cited text no. 24
    
25.
Brooks JK. The effects of hormonal oral contraceptives on the female human periodontium and experimental animal models, a review of the literature. J Baltimore Coll Dent Surg 1980;33:12-6.  Back to cited text no. 25
    
26.
Sills ES, Zegarelli DJ, Hoschander MM, Strider WE. Clinical diagnosis and management of hormonally responsive oral pregnancy tumor (pyogenic granuloma). J Reprod Med 1996;41:467-70.  Back to cited text no. 26
    
27.
Hosseini FH, Tirgari F, Shaigan S. Immunohistochemical analysis of estrogen and progesterone receptor expression in gingival lesions. Iran J Public Health 2006;35:38-41.  Back to cited text no. 27
    
28.
Whitaker SB, Bouquot JE, Alimario AE, Whitaker TJ Jr. Identification and semiquantification of estrogen and progesterone receptors in pyogenic granulomas of pregnancy. Oral Surg Oral Med Oral Pathol 1994;78:755-60.  Back to cited text no. 28
    
29.
Parisi E, Glick PH, Glick M. Recurrent intraoral pyogenic granuloma with satellitosis treated with corticosteroids. Oral Dis 2006;12:70-2.  Back to cited text no. 29
    
30.
Goodman-Topper ED, Bimstein E. Pyogenic granuloma as a cause of bone loss in a twelve-year-old child: Report of case. ASDC J Dent Child 1994;61:65-7.  Back to cited text no. 30
    
31.
Sternberg SS, Antonioli DA, Carter D, Mills SE, Oberman H. Diagnostic Surgical Pathology. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 69, 174.  Back to cited text no. 31
    
32.
Enzinger FM, Weiss SW. Soft Tissue Tumors. 3rd ed. St. Louis: Mosby; 1995. p. 600.  Back to cited text no. 32
    
33.
Calonje E, Wilson-Jones E. Vascular tumors: Tumors and tumor-like conditions of blood vessels and lymphatics. In: Elder D, Elenitsas R, Jaworsky C, Johnson BJ, editors. Lever's Histopathology of the Skin. 8th ed. Philadelphia: Lippincott-Raven; 1997. p. 895.  Back to cited text no. 33
    
34.
Raut A, Huryn J, Pollack A, Zlotolow I. Unusual gingival presentation of post-transplantation lymphoproliferative disorder: A case report and review of the literature. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;90:436-41.  Back to cited text no. 34
    
35.
Hirshberg A, Leibovich P, Buchner A. Metastases to the oral mucosa: Analysis of 157 cases. J Oral Pathol Med 1993;22:385-90.  Back to cited text no. 35
    
36.
Daley TD, Nartey NO, Wysocki GP. Pregnancy tumor: An analysis. Oral Surg Oral Med Oral Pathol 1991;72:196-9.  Back to cited text no. 36
    
37.
Ojanotko-Harri AO, Harri MP, Hurttia HM, Sewón LA. Altered tissue metabolism of progesterone in pregnancy gingivitis and granuloma. J Clin Periodontol 1991;18:262-6.  Back to cited text no. 37
    
38.
Sonis ST, Fazio RC, Fang LS. Principles and Practice of Oral Medicine. 2nd ed. Philadelphia: WB Saunders; 1995. p. 416.  Back to cited text no. 38
    
39.
Flaitz CM, Nichols CM, Hicks MJ. An overview of the oral manifestations of AIDS-related Kaposi's sarcoma. Compend Contin Educ Dent 1995;16:136-8, 140, 142.  Back to cited text no. 39
    
40.
Powell JL, Bailey CL, Coopland AT, Otis CN, Frank JL, Meyer I, Nd: YAG laser excision of a giant gingival pyogenic granuloma of pregnancy. Lasers Med Surg, 1994;14:178-183.  Back to cited text no. 40
    
41.
Fekrazad R, Nokhbatolfoghahaei H, Khoei F, Kalhori KA. Pyogenic granuloma: Surgical treatment with Er: YAG laser. J Lasers Med Sci 2014;5:199-205.  Back to cited text no. 41
    
42.
Meffert JJ, Cagna DR, Meffert RM. Treatment of oral granulation tissue with the flashlamp pulsed dye laser. Dermatol Surg 1998;24:845-8.  Back to cited text no. 42
    
43.
Yasin A, Edmund JJ, Robert AS, Pyogenic Granuloma of the Lip – Treatment with Carbondioxide slush cryosurgery as an approach in a resource poor country, AdvClinExp Med 2014;23:5-7.  Back to cited text no. 43
    
44.
Millsop JW, Trinh N, Winterfield L, Berrios R, Hutchens KA, Tung R. Resolution of recalcitrant pyogenic granuloma with laser, corticosteroid, and timolol therapy. Dermatol Online J 2014;20. pii: Doj_21726.  Back to cited text no. 44
    
45.
Ichimiya M, Yoshikawa Y, Hamamoto Y, Muto M. Successful treatment of pyogenic granuloma with injection of absolute ethanol. J Dermatol 2004;31:342-4.  Back to cited text no. 45
    
46.
Moon SE, Hwang EJ, Cho KH. Treatment of pyogenic granuloma by sodium tetradecyl sulfate sclerotherapy. Arch Dermatol 2005;141:644-6.  Back to cited text no. 46
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]



 

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