|Year : 2018 | Volume
| Issue : 1 | Page : 7-10
Pyogenic granuloma: A clinicopathological analysis of fifty cases
Ujwala Rohan Newadkar1, Swapnil Khairnar1, Arun Dodamani2
1 Department of Oral Medicine and Radiology, ACPM Dental College, Dhule, Maharashtra, India
2 Department of Public Health Dentistry, ACPM Dental College, Dhule, Maharashtra, India
|Date of Web Publication||2-Feb-2018|
Ujwala Rohan Newadkar
Department of Oral Medicine and Radiology, ACPM Dental College, Dhule - 424 003, Maharashtra
Source of Support: None, Conflict of Interest: None
Aim: To evaluate the clinicopathological features including variations of fifty oral pyogenic granuloma cases reported to Department of Oral medicine and Radiology, Dhule.
Materials and Methods: A retrospective review for the fifty cases reported as PG was performed, and data for the following parameters were recorded: age, gender, history of trauma or any other etiology, site and clinical presentation, variation in histology, treatment mode, and recurrence.
Results: PG was most commonly seen in the second (36%) and third (46%) decade, with a female preponderance (male: female 1:4). Gingiva was more commonly involved (90%) followed by the lip (6%) and ventral surface of the tongue (4%). Classic clinical presentation of PG exhibited as a sessile or pedunculated, firm or soft, erythematous, exophytic, and/or painful papule or nodule with a smooth or lobulated surface that bleeds easily.
Conclusion: Although it is a benign lesion which is commonly encountered and excised in dental practice, it is important to recognize these variants to avoid misdiagnosis, it is always wise to subject it to histopathological confirmation owing to its close clinical resemblance to neoplastic condition.
Keywords: Epulis, pyogenic granuloma, swellings of lower/upper lip
|How to cite this article:|
Newadkar UR, Khairnar S, Dodamani A. Pyogenic granuloma: A clinicopathological analysis of fifty cases. J Oral Res Rev 2018;10:7-10
|How to cite this URL:|
Newadkar UR, Khairnar S, Dodamani A. Pyogenic granuloma: A clinicopathological analysis of fifty cases. J Oral Res Rev [serial online] 2018 [cited 2018 Oct 22];10:7-10. Available from: http://www.jorr.org/text.asp?2018/10/1/7/224536
| Introduction|| |
The term “pyogenic granuloma (PG)” is a misnomer because the lesion does not contain pus and does not represent a granuloma histologically. Over the years, various authors have suggested other names such as granuloma gravidarum/pregnancy tumors, Rocker and Hartzell's disease, vascular epulis, benign vascular tumors, epulis telangectium granulomatousa, and lobular capillary hemangioma (LCH). It is a kind of inflammatory hyperplasia. Hullihen's (1844) reported the first case of PG. The term “PG” or “granuloma pyogenicum” was introduced by Hartzell (1904). Hence, it was also called a Crocker and Hartzell's disease.
It is now universally agreed that this lesion is formed as a result of an exaggerated localized connective tissue reaction to a minor injury or any underlying irritation. The irritating factor can be calculus, poor oral hygiene, nonspecific infection, over hanging restorations, cheek biting, etc., Due to this irritation, the underlying fibrovascular connective tissue becomes hyperplastic, and there is a proliferation of granulation tissue which leads to the formation of a PG. Factors such as inducible nitric oxide synthase, vascular endothelial growth factor, or connective tissue growth factor are known to be involved in angiogenesis and rapid growth of PG.
Angelopoulos  histologically described it as “hemangiomatous granuloma” due to the presence of numerous blood vessels and the inflammatory nature of the lesion. Cawson et al., in dermatologic literature, have described it as “granuloma telangiectacticum” due to the presence of numerous blood vessels seen in histological sections. They described two forms of PGs, the LCH and the non-LCH.
| Materials and Methods|| |
A retrospective review for the fifty cases reported as PG was performed, which underwent biopsy during a 4-year period from 2012 to 2016 at the Department of Oral Medicine and Radiology, ACPM Dental college, Dhule. Data for the following parameters were recorded: age, gender, history of trauma or any other etiology, site and clinical presentation, variation in histology, treatment mode, and recurrence. Descriptive statistical methods were applied to data and analysis of variance test was employed to assess the mean difference. SPSS software, version 15.0 (SPSS, Chicago, IL, USA) was used for statistical analysis of collected data.
| Results|| |
A total of fifty cases of PGs were retrieved. Females showed a distinct predominance, the male: female ratio being 1:4. Age of the patient ranged from 4 to 55 years (26.4 ± 16.2). Maximum cases were seen in the second (36%) and third decades (46%) [Table 1]. Localized reactive hyperplastic lesions of gingiva are relatively common in biopsy services of oral pathology department. Most commonly gingiva was involved (90%) followed by the lip (6%) and ventral surface of the tongue (4%). Facial surface of gingiva involvement was more than that of the lingual or palatal surface [Table 2]. The duration of the lesions reported from 3 to 48 weeks and the maximum diameter of the lesion ranged from 0.1 to 2.5 cm and most of them were being pedunculated (80%) and sessile (20%). Lesions manifested as inflammatory overgrowths which were nontender and nonfluctuant (60%), nodular swellings with normal mucosal color (36%), and ulceration (4%) [Table 3]. The reactive lesions are common in the oral cavity because of the frequency with which the tissues are injured. History of trauma or chronic irritation was present in 86% of the cases, hormonal factors (pregnancy tumor) in 8%, and miscellaneous reasons in 6% cases [Table 4]. Histopathologically, there was almost similar reporting in all cases, consisting of marked vascular proliferation among immature fibroblastic connective tissue, granulation tissue, and chronic inflammatory infiltrate.
|Table 3: Distribution of size, base attachment surface, and color of the lesions|
Click here to view
| Discussion|| |
Regezi et al. suggested that PG is caused by a known stimulant or injury such as calculus or foreign material within the gingival crevice resulting in exuberant proliferation of connective tissue. In our study, we found that 43 cases had etiology of trauma or local irritation due to calculus. Age at presentation is an important clinical factor that should be considered for an accurate diagnosis of a lesion. In the current study, the majority of PG lesions occurred in the second and third decades of life. This age distribution is in support with findings in previous reports., Oral PGs occur in all age groups, children to older adult, but are more frequently encountered in females in their second decade due to the increased levels of circulating hormones estrogen and progesterone. In the present study, females showed a distinct predominance, the male: female ratio being 1:4. Maximum cases were seen in the second (36%) and third decades (46%). PG of the oral cavity appears as an elevated, smooth or exophytic, sessile, or pedunculated growth covered with red hemorrhagic and compressible erythematous papules, which appear lobulated and warty showing ulcerations and covered by yellow fibrinous membrane., The color varies from red, reddish purple to pink depending on the vascularity of the growth. Most of the cases in our study present with the same features.
In the previous series, gingiva is the most common affected intraoral region followed by the lips, tongue, palate, and buccal mucosa., Our study showed that gingiva was involved (90%) followed by the lip (6%) and ventral surface of the tongue (4%). Facial surface of gingiva involvement was more than that of the lingual or palatal surface. Interdental and marginal gingival involvement was marked. This finding was consistent with the results shown by Vilmann et al. They concluded that majority of the PGs are found on the marginal gingival with only 15% of the tumors on the alveolar part. The size varies from a few millimeters to several centimeters and it is usually slow growing, asymptomatic, painless growth,, but at times it grows rapidly. In our study on average, the lesion ranged from 0.1 to 2.5 cm. Few cases reported that the growth involved the attached gingiva and the marginal gingiva extending beyond the occlusal plane, thereby interfering with mastication.
Four pregnant patients reported with the same lesion. Daley et al. found that pregnancy epulides accounted for only 42 of the 757 epulides of all types. Hosseini et al. stated that there are clinical observations that gingiva may be enlarged during pregnancy and may atrophy during menopause. On the basis of these observations, gingiva can be regarded as another “target organ” for direct action of estrogen and progesterone. In Whitaker et al.'s study, it was suggested that the quantity of estrogen or progesterone receptors in oral PG is not the determining factor in its pathogenesis of. Rather, such a role could be attributed to the levels of circulating hormones. The levels of estrogen and progesterone are markedly elevated in pregnancy and could, therefore, exert a greater effect on the endothelium of oral PG.
Radiographic findings are usually absent. However, Angelopoulos  concluded that, in some cases, long-standing gingival PGs caused localized alveolar bone resorption. In 38 cases, there was a mild-to-moderate bone loss was present interdentally seen on intraoral periapical radiographs.
Histologically, PGs are classified as the LCH type and the non-LCH type., The LCH type has proliferating blood vessels organized in lobular aggregates, no specific changes such as edema, capillary dilation, or inflammatory granulation were noted. Forty-three (86%) biopsy reports in our study showed that the bulk of the lesion shows angiomatous tissue with endothelial cell proliferation, inflammatory cell infiltrate is seen in the form of few neutrophils, lymphocytes, and plasma cells covered by parakeratinized epithelium and confirmed the diagnosis of oral PG of the LCH type [Figure 1] and [Figure 2]. Histopathologically, foci of fibrous maturation were present in non-LCH type of two cases. This finding was similar observed by Epivationas et al.
|Figure 1: Histopathological section showing numerous vascular channels of varying caliber associated with intense inflammatory infiltrate (H and E, ×100)|
Click here to view
|Figure 2: View showing the greatest increase in blood capillaries and diffuse inflammation (H and E, 400)|
Click here to view
Excision and biopsy of the lesion is the recommended line of treatment unless it would produce a marked deformity and in such a case incisional biopsy is recommended. Conservative surgical excision of the lesion with the removal of irritants such as plaque, calculus, and foreign materials is recommended for small painless nonbleeding lesions. Excision of the gingival lesions up to the periosteum with through scaling and root planning of adjacent teeth to remove all visible sources of irritation is recommended. In the present study, forty lesions were surgically excised and scaling and root planning of the adjacent teeth was completed to remove all the local irritants, which could have been the primary etiologic factor in the present case.
In pregnant females, recurrence of oral PGs is common, so treatment should be preferably performed after parturition. However, if necessary treatment can be completed in the second trimester with follow-up of the case postparturition. In our study, out of four pregnant patients, only one female had been treated by surgical excision under general anesthesia. As the size of the lesion was large and causing difficulty in eating, other females were treated postdelivery.
Taira et al. have shown a recurrence rate of 16% in excised lesions and also described a case of multiple deep satellite lesions surrounding the original excised lesion in a case of Warner Wilson James syndrome. Incomplete excision, failure to remove etiologic factors, or repeated trauma contributes to recurrence of these lesions., Vilmann et al. emphasized the need of follow-up, especially in PG of the gingiva due to its much higher recurrence rate. In the present study, cases were followed up for a period of 1 year and no recurrence was observed for any case.
| Conclusion|| |
PGs are benign tumor-like lesions commonly encountered, but when presented late, especially when infected, they can pose diagnostic challenges by mimicking more sinister lesions, due to their remarkably large sizes. Knowledge of their clinical features and demographics is essential for all heath personnel who encounter this lesion. We presented a study carried out on patients with oral PG to evaluate its clinicopathological features and to determine the relative prevalence of the same in relation to age, sex, site, and various clinical variations.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Hullihen SP. Case of aneurism by anastomosis of superior maxillae. Am J Dent Sci 1884;4:160-2.
Hartzell MB. Granuloma pyogenicum (botryomycosis of French authors). J Cutan Dis 1904;22:520-3.
Verma PK, Srivastava R, Baranwal HC, Chaturvedi TP, Gautam A, Singh A. Pyogenic granuloma-hyperplastic lesion of the gingiva: Case reports. Open Dent J 2012;6:153-6.
Mathur LK, Bhalodi AP, Manohar B, Bhatia A, Rai N, Mathur A. Focal fibrous hyperplasia: A case report. Int J Dent Clin 2010;2:56-7.
Angelopoulos AP. Pyogenic granuloma of the oral cavity: Statistical analysis of its clinical features. J Oral Surg 1971;29:840-7.
Cawson RA, Binnie WH, Speight PM, Barrett AW, Wright JM. Lucas Pathology of Tumors of Oral Tissues. 5th
ed. Missouri: Mosby; 1998. p. 252-4.
Regezi JA, Sciubba JJ, Jordan RC. Oral Pathology: Clinical Pathologic Considerations. 4th
ed. Philadelphia: WB Saunders; 2003. p. 115-6.
Al-Khateeb T, Ababneh K. Oral pyogenic granuloma in Jordanians: A retrospective analysis of 108 cases. J Oral Maxillofac Surg 2003;61:1285-8.
Avelar RL, Antunes AA, Carvalho RW, Santos TS, Neto PJ, Andrade ES. Oral pyogenic granuloma: A epidemiologic study of 191 cases. RGO 2008;56:131-5.
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.
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.
Mubeen K, Vijaylakshmi KR, Abhishek RP. Oral pyogenic granuloma with mandible involvement: An unusual presentation. J Dent Oral Hyg 2011;3:6-9.
Saravana GH. Oral pyogenic granuloma: A review of 137 cases. Br J Oral Maxillofac Surg 2009;47:318-9.
Vilmann A, Vilmann P, Vilmann H. Pyogenic granuloma: Evaluation of oral conditions. Br J Oral Maxillofac Surg 1986;24:376-82.
Parisi E, Glick PH, Glick M. Recurrent intraoral pyogenic granuloma with satellitosis treated with corticosteroids. Oral Dis 2006;12:70-2.
Daley TD, Nartey NO, Wysocki GP. Pregnancy tumor: An analysis. Oral Surg Oral Med Oral Pathol 1991;72:196-9.
Whitaker SB, Bouquot JE, Alimario AE, Whitaker TJ. Identification and semi quantification of estrogen and progesterone receptors in pyogenic granuloma of pregnancy. Oral Surg Oral Med Oral Pathol 1994;78:755-60.
Kamal R, Dahiya P, Puri A. Oral pyogenic granuloma: Various concepts of etiopathogenesis. J Oral Maxillofac Pathol 2012;16:79-82. [Full text]
Mills SE, Cooper PH, Fechner RE. Lobular capillary hemangioma: The underlying lesion of pyogenic granuloma. A study of 73 cases from the oral and nasal mucous membranes. Am J Surg Pathol 1980;4:470-9.
Epivationas A, Antoniades D, Zaraboukas T, Zairi E, Poulopoulos A, Kiziridou E, et al
. Pyogenic granuloma of the oral cavity: Comparative study of its clinicopathological and immunohistochemical features. Pathol Int 2005;55:391-7.
Taira JW, Hill TL, Everet MA. Lobular capillary hemangioma (pyogenic granuloma) with satellitosis. J Am Acad Dermatol 1992;27:297-300.
Eversole LR. Clinical Outline of Oral Pathology: Diagnosis and Treatment. 3rd
ed. Hamilton: BC Decker; 2002. p. 113-4.
Steelman R, Holmes D. Pregnancy tumor in a 16-year-old: Case report and treatment considerations. J Clin Pediatr Dent 1992;16:217-8.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4]