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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 13  |  Issue : 1  |  Page : 53-59

Pyogenic granuloma: A case report and a comprehensive review


1 Department of Periodontics, Kalka Dental College, Meerut, Uttar Pradesh, India
2 Department of Oral and Maxillofacial Pathology, Kalka Dental College, Meerut, Uttar Pradesh, India
3 Department of Orthodontics and Dento-Facial Orthopaedics, Kalka Dental College, Meerut, Uttar Pradesh, India

Date of Submission29-May-2020
Date of Acceptance22-Jan-2021
Date of Web Publication15-Feb-2021

Correspondence Address:
Shivani Sharma
Department of Periodontics, Kalka Dental College, NH-58, Partapur Bye-Pass, Meerut - 250 006, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jorr.jorr_47_20

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  Abstract 


Pyogenic granuloma (PG) is an inflammatory hyperplasia describing large range of nodular growths of the oral mucosa. PG commonly occurs on the skin or oral cavity but seldom in the gastrointestinal tract. It most commonly involves the gingiva. Extragingivally, it can occur on the lips, tongue, buccal mucosa, and palate. It is caused due to low-grade irritation, traumatic injury, or hormonal factors. Various authors have suggested other names for PG such as Crocker and Hartzell's disease, granuloma pyogenicum, benign vascular tumor and during pregnancy as granuloma gravidarum. Because it is possible to misdiagnose PG as peripheral ossifying fibroma, peripheral giant cell granuloma, hemangioma, and fibroma, its histopathological examination is essential for accurate diagnosis. Differential diagnosis is important because of its tendency to recur. This article presents a case of PG in a 17-year-old female along with a comprehensive review of the lesion.

Keywords: Granuloma, hormonal, irritation, oral, pyogenic, vascular


How to cite this article:
Sharma S, Singh S, Yadav L, Tyagi S. Pyogenic granuloma: A case report and a comprehensive review. J Oral Res Rev 2021;13:53-9

How to cite this URL:
Sharma S, Singh S, Yadav L, Tyagi S. Pyogenic granuloma: A case report and a comprehensive review. J Oral Res Rev [serial online] 2021 [cited 2021 Jun 21];13:53-9. Available from: https://www.jorr.org/text.asp?2021/13/1/53/309442




  Introduction Top


Pyogenic granuloma (PG) is a common tumor-like growth of the oral cavity?.[1] PG was first described by Hullihen in 1844[2] as a common nonneoplastic growth of the oral cavity; Hartzell in 1904[3] gave it the current term of “PG” or “granuloma pyogenicum.” The name PG is a misnomer as it is not associated with pus and does not represent a granuloma histologically.[1] PG has been described as “granuloma telangiectacticum” due to the presence of numerous blood vessels seen in histological sections.[4] Cawson et al.[4] described two forms of PGs, the lobular capillary hemangioma (LCH) and the non-LCH. PG commonly involves the gingiva in 75%–85% of cases; extragingivally, it can occur on the lips, tongue, and buccal mucosa.[1]

PG can be found at any age but is more commonly seen in children and young adults, especially females because of vascular effects of hormones.[1] Various stimuli such as trauma,[1] local irritation,[1] hormonal factors,[1] and certain drugs[5] have been suggested in its development. Clinically, these lesions usually present as a single nodule or sessile papule with smooth or lobulated surface.[1],[6] These vary in size from few millimeters to several centimeters.[1] Older PG resembles fibromas due to fibrous appearance.[7] A detailed history, clinical examination, and proper treatment plan are necessary to pinpoint PG as there are many lesions in the oral cavity that have appearance similar to PG. Surgical excision of the lesion with removal of irritants is the treatment of choice.[1]

This article presents a case of PG of the gingiva in a 17-year-old female patient with a localized gingival growth in the upper right quadrant of the jaw with review of literature.


  Case Report Top


A 17-year-old female patient was referred to the department of periodontics with the chief complaint of a swelling in gums in relation to the upper right back tooth region of the jaw since the last 20 days. The swelling was of pinpoint size when the patient first noticed it but had gradually enlarged to attain the present size. Intraoral examination of the patient revealed a poor oral hygiene with bleeding on probing. Soft-tissue examination showed a gingival growth in relation to 17 and 18 region which was reddish pink in color and had covered the entire crown of 17 up to the occlusal surface (2 cm × 2.5 cm) in size [Figure 1]. The swelling was firm in consistency and nontender on palpation. The patient's medical and family history was noncontributory, and general physical examination revealed no other abnormalities. Intra-oral periapical radiograph. [IOPAR] of the region showed no visible abnormalities, and the alveolar bone in the region of growth appeared normal [[Figure 1] inset]. The hematological and biochemical investigation of the patient was within normal limits. A provisional diagnosis of PG was made. The differential diagnosis included peripheral ossifying fibroma, peripheral giant cell granuloma, hemangioma, and fibroma.
Figure 1: Preoperative view showing gingival growth in 17 and 18 region. Inset shows an intraoral periapical radiograph with no underlying bone involvement in 17 and 18 region

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Oral prophylaxis was completed for the patient, and excisional biopsy was planned. Excision of the lesion up to and including the mucoperiosteum was carried out under local anesthesia using a Bard Parker handle and blade, followed by curettage in the involved teeth [Figure 2]. The excised tissue was sent for histologic examination [[Figure 2] inset].
Figure 2: Clinical image depicting excision of the lesion up to the mucoperiosteum. Inset shows excised growth

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Histopathological report showed parakeratinized epithelium. The underlying connective tissue stroma showed dilated and engorged small and large blood vessels, extravasated red blood cells, angiogenesis, few inflammatory cells, and bundles of collagen fibers. The diagnosis PG was confirmed [Figure 3].
Figure 3: Photomicrograph showing dilated and engorged blood vessels, angiogenesis, and bundles of collagen fibers (H and E, ×10)

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Patient was recalled periodically [Figure 4] to check for possible recurrence and showed no recurrence of the lesion at one year follow up [Figure 5].
Figure 4: One month follow up photograph showing uneventful healing'

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Figure 5: Clinical image of 17 AND 18 region at 1 year follow up

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  Discussion Top


Etiopathogenesis

PG has been regarded as an “infectious” entity. Shafer et al.[8] suggested that oral PG arises as a result of infection by either staphylococci or streptococci, partially because it was shown that these microorganisms could produce colonies with fungus-like characteristics. They also agreed that oral PG is the result of minor trauma to the tissues that allow nonspecific types of microorganisms to invade the tissues. Bhaskar and Jacoway[9] have demonstrated the presence of Gram-positive and Gram-negative bacilli in superficial areas of ulcerated forms of oral PG. This could justify the inclusion of the term “pyogenic” in PG. However, oral PG shows predominance of capillary growth within its granulomatous mass rather than the presence of real pyogenic organisms and pus, so the term PG is a misnomer and is not a granuloma in real sense.[1]

Other investigators consider PG as a “reactive” or “reparative” tumor process. Regezi et al.[6] have suggested that PG is an exuberant proliferation of connective tissue to a known stimulus or injury like calculus or foreign material within the gingival crevice. They also showed histopathological findings of prominent capillary growth in hyperplastic granulation tissue suggesting a strong activity of angiogenesis in oral PG. Two angiogenesis enhancers, i.e., vascular endothelial growth factor and basic fibroblast growth factor, and two angiogenesis inhibitors, i.e., thrombospondin-1 and angiostatin, have been implicated in mechanism for angiogenesis. Vascular morphogenesis factors Tie-2, angiopoietin-1, angiopoietin-2, ephrinB2, and ephrinB4 were also found to be upregulated in PG compared to healthy gingiva.[10]

Yih et al.[11] suggested hormonal influence in the development of PG on the basis of the observation that pregnancy tumor that occurs in the pregnant women also arises from the gingiva and has the same microscopic appearance. They concluded that morphogenetic factors were higher in PG as compared to normal gingiva and thus supported the mechanism of angiogenesis in oral PG in pregnant females. Due to its frequent occurrence in a pregnant female, PG is also called granuloma gravidarum or pregnancy tumor.[1] However, the role of hormones has been questioned by Bhaskar and Jacoway,[9] since these lesions are found in both males and females.

Cawson et al.[4] stated that PG represents vascular proliferations and does not represent a stage in the development of fibrous nodules or merely inflamed fibrous nodules. Thus, several “etiologic factors” such chronic low grade irritation, hormonal factors, traumatic injury, certain kinds of drugs, poor oral hygiene, injury to primary tooth, aberrant tooth development, have been suggested in patients presenting with pyogenic granuloma.[7]

In the present case, the patient was a 17-year-old healthy female, the probable etiology included the presence of large amount of calculus due to poor oral hygiene habits,[6] repeated trauma, and occlusal interference while eating due to the size and position of the lesion,[12] and as described by Ainamo,[13] recurrent trauma occurring during tooth brushing or function with the release of various endogenous and angiogenic factors could be contributing to the increased vascularity and development of the lesion.

Clinical features

Oral PG occurs over a wide age range of 4.5–93 years with the highest incidence in the second and fifth decades, with females slightly more affected than males.[9] It shows predilection for gingiva (75% of all the cases), with interdental papilla being the most common site. The maxillary gingiva is more commonly involved than mandibular gingiva, anterior areas are more frequently affected than posterior areas, and the facial aspect of the gingiva is more commonly involved than the lingual aspect, followed by lips, tongue, and buccal mucosa.[1] The incidence of PG has been described as between 26.8% and 32% of all reactive lesions.[14] Intraorally, it appears as an elevated sessile or pedunculated growth covered with red hemorrhagic and erythematous papules. It also shows ulcerations and is covered by a fibrinous membrane.[1],[6] Clinically, the lesion can be slow growing, asymptomatic, and painless, but it may also grow rapidly sometimes.[6] The color varies from pink to red to purple, depending on the age of the lesion, with young PGs being highly vascular, and older lesions tend to become collagenized and pink.[1] The case presented here shows a large growth localized to the buccal surface of the upper right posterior maxilla, involving the interdental and marginal gingiva; it was reddish pink in color and was present since 20 days. It had gradually increased in size to cover the occlusobuccal surface of the crown of 17, interfered with mastication, and resulted in intermittent bleeding which prompted the patient to seek treatment.

Histopathology

PG can be classified as the LCH type and non-LCH type. The non-LCH type consists of a vascular core which resembles a granulation tissue with foci of fibrous tissue. The central area has a greater number of vessels with perivascular mesenchymal cells which are nonreactive for alpha-smooth muscle actin as compared to LCH type. The LCH type on the other hand has proliferating blood vessels organized in lobular aggregates, and no specific changes such as edema, capillary dilation, or inflammatory granulation are seen. On comparison, the lobular area of LCH type has greater number of blood vessels with small luminal diameter than non-LCH type.[1],[7] PG is partly or completely covered by parakeratotic or nonkeratinized stratified squamous epithelium. The amount of collagen in the connective tissue of PG is usually sparse. The surface can be ulcerated, and in such ulcerated lesions, edema is a prominent feature and the lesion is infiltrated by plasma cells, lymphocytes, and neutrophils.[9]

The biopsy in this case showed a non-LCH type of PG with high vascular proliferation that resembles a granulation tissue along with numerous small and large endothelium-lined channels that are engorged with red blood cells. A mixed inflammatory cell infiltrate is also evident. The diagnosis of oral PG was confirmed from these findings.

Radiographic findings

Although radiographic involvement is usually absent, large and long-standing gingival PGs can cause localized alveolar bone resorption.[15] In this case, no obvious radiographic findings could be seen.

Differential diagnosis

Differential diagnosis of PG includes peripheral giant cell granuloma, peripheral ossifying fibroma, fibroma, peripheral odontogenic fibroma, hemangioma, conventional granulation tissue, hyperplastic gingival inflammation, Kaposi's sarcoma, bacillary angiomatosis, and non-Hodgkin's lymphoma[16],[17] [Table 1].
Table 1: Differential diagnosis of gingival growths resembling pyogenic granuloma[17],[18]

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Treatment

The treatment of PG consists of conservative surgical excision. For gingival lesions, excision should extend down to the periosteum and adjacent teeth should be thoroughly scaled to remove any source of continuing irritation.[1] Various other treatment modalities, such as use of neodymium-doped yttrium aluminum garnet laser, carbon dioxide laser, flash-lamp pulsed-dye laser, sodium tetradecyl sulfate sclerotherapy and use of intralesional steroids, and cryosurgery, have been used.[7] The treatment of lesion that develops during pregnancy is deferred unless significant functional or esthetic problems develop.[1] In the present case, the lesion was surgically excised and was sent for histopathologic examination. The scaling and curettage of the involved teeth was completed to remove all the local irritants, which could have been the primary etiologic factor in the present case.

Recurrence

Recurrence rate of 16% has been reported for gingival granuloma.[18] Incomplete excision, failure to remove etiologic factors, or repeated trauma contributes to recurrence of these lesions.[6] The recurrence rate is higher for PGs removed during pregnancy, and some resolve spontaneously after parturition.[1] Vilmann et al.[19] emphasized the need of follow-up, especially in PG of the gingiva due to its much higher recurrence rate. The present case was followed up for a period of 1 year, and no recurrence was observed.


  Conclusion Top


This article reports a case of PG in maxillary posterior gingiva of a female patient with an overview on etiology, clinical and histologic presentation, differential diagnosis, treatment modalities, and recurrence of PG. Even though PG is a common lesion of the oral cavity, especially the gingiva, a thorough knowledge of the lesion is necessary to differentiate it from similar presenting lesions and appropriate treatment modality should be adopted to yield excellent results.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Acknowledgments

We would like to acknowledge, Management, Kalka Group of Institutions, Meerut, for their constant support, in providing us the infrastructure and basic amenities to conduct this work.

Ethical clearance

Study was conducted after approval from the Institutional Ethics Committee.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Neville BW, Damm DD, Allen CM, Chi A. Soft tissue tumours. In: Neville BW, Damm DD, Allen CM, Chi AC, editors. Oral and Maxillofacial Pathology. 4th ed.. Amsterdam, Netherlands: Elseiver Inc.; 2016. p. 483-5.  Back to cited text no. 1
    
2.
Hullihen SP. Case of aneurism by anastomosis of the superior maxillae. Am J Dent Sci 1844;4:160-162.  Back to cited text no. 2
    
3.
Hartzell MB. Granuloma pyogenicum. J Cutan Dis Syph 1904;22:520-5.  Back to cited text no. 3
    
4.
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.  Back to cited text no. 4
    
5.
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;14:187-191.  Back to cited text no. 5
    
6.
Regezi JA, Sciubba JJ, Jordan RC. Oral Pathology: Clinical Pathologic Considerations. 4th ed.. Philadelphia, PA: WB Saunders; 2003. p. 115-6.  Back to cited text no. 6
    
7.
Jafarzadeh H, Sanatkhani M, Mohtasham N. Oral pyogenic granuloma: A review. J Oral Sci 2006;48:167-75.  Back to cited text no. 7
    
8.
Sivapathasundharam B, Gururaj N. Bacterial infections of the oral cavity. In: Shafer AW, Hine MK, Levy BM, editors. Shafer's Textbook of Oral Pathology. 7th ed.. Amsterdam: Elsevier Health Sciences; 2012. p. 1371-7.  Back to cited text no. 8
    
9.
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. 9
    
10.
Yuan K, Jin YT, Lin MT. Expression of Tie-2, angiopoietin-1, angiopoietin-2, ephrinB2 and ephrinB4 in pyogenic granuloma of human gingiva implicates their roles in inflammatory angiogenesis. J Periodontal Res 2000;35:165-71.  Back to cited text no. 10
    
11.
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. 11
    
12.
Witjaksono W, Al Ani BT. Epulis and pyogenic granuloma with occlusal interference. Dent J (Maj Ked Gigi) 2005;38:52-5.  Back to cited text no. 12
    
13.
Ainamo J. The effect of habitual tooth cleansing on the occurrence of periodontal disease and dental caries. Suom Hammaslaak Toim 1971;67:63-70.  Back to cited text no. 13
    
14.
Buchner A, Calderon S, Raman Y. Localized hyperplastic lesions of the gingiva: A clinic-pathologic study of 302 lesions. J Periodontol 1977;48:101-4.  Back to cited text no. 14
    
15.
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. 15
    
16.
Rajendran R. Benign and malignant tumors of the oral cavity. In: Shafer, Hine, Levy. Shafer's Textbook of Oral Pathology. 7th ed.. Amsterdam: Elsevier Health Sciences; 2012. p. 559-754.  Back to cited text no. 16
    
17.
Rees TD, Ambalavanan N. Pathology and management of periodontal problems in patients with human immunodeficiency virus infection. In: Newman MG, Takei HH, Klokkevold PR, editors. Carranza's Clinical Periodontolgy. 10th ed.. Philadelphia, PA: Saunders; 2006. p. 380-1, 521-4.  Back to cited text no. 17
    
18.
Kfir Y, Buchner A, Hansen LS. Reactive lesions of the gingiva: A clinico-histopathologic study of 741 cases. J Periodontol 1980;51:655-61.  Back to cited text no. 18
    
19.
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. 19
    


    Figures

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