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 Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 27  |  Issue : 3  |  Page : 461-463

Chameleon of head and neck diseases: Intraoral actinomycosis


Department of Oral Medicine and Radiology, Farooqia Dental College and Hospital, Mysore, Karnataka, India

Date of Submission14-Apr-2015
Date of Acceptance11-Nov-2015
Date of Web Publication25-Nov-2015

Correspondence Address:
Bharathi Ullagaddi
#2617, Vontikoppal, Valmiki Road, Mysore - 570 002, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-1363.170487

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   Abstract 

Actinomycosis is a chronic infectious granulomatous disease caused by saprophytic Actinomyces species. The case discussed in this report is of an adult female patient with a large actinomycotic lesion in the region of the mandibular left second premolar, first and second molars. Provisional diagnosis was made as extragingival pyogenic granuloma. Definitive diagnosis was based on histopathological examination. Since actinomycotic infection has opportunistic characteristics, early diagnosis and proper management of the disease is mandatory to prevent further complications.

Keywords: Actinomycosis, cervicofacial, eosinophilic, extra gingival, hematoxyphilic pyogenic granuloma, pyogenic granuloma, suppurative


How to cite this article:
Basappa S, Ullagaddi B, Shivalingu MM, Lingaraju LN. Chameleon of head and neck diseases: Intraoral actinomycosis. J Indian Acad Oral Med Radiol 2015;27:461-3

How to cite this URL:
Basappa S, Ullagaddi B, Shivalingu MM, Lingaraju LN. Chameleon of head and neck diseases: Intraoral actinomycosis. J Indian Acad Oral Med Radiol [serial online] 2015 [cited 2020 Jul 11];27:461-3. Available from: http://www.jiaomr.in/text.asp?2015/27/3/461/170487


   Introduction Top


Actinomycosis is a suppurative bacterial infection most commonly caused by Actinomyces israelii. It is a slow progressive infection which usually manifests as a soft tissue swelling, abscess, or mass lesion that is often misdiagnosed as a neoplasm. [1] Clinical manifestation occurs in one of the three forms: Cervicofacial, abdominal-pelvic, or pulmonary actinomycosis. [2] Approximately 60% of the actinomycotic infections in humans are cervicofacial. Intraoral infections are relatively rare and usually are accompanied by the cervicofacial type. Lesions in the oral cavity frequently involve the mandible, tongue, lips, and oral mucosa. [3] Gingival involvement is rare.


   Case Report Top


A 39-year-old female patient presented to our department with a chief complaint of missing teeth in lower left back teeth region and desired to get them replaced. Past dental history revealed that she underwent extraction of her mandibular teeth 1 year back which was uneventful. Her medical history and personal history were not significant. On general physical examination, the patient's gait was unaltered, and she was moderately built and nourished. General intraoral examination revealed missing 31, 32, 36, 37, 41, and 42. There was presence of a proliferative growth extending from the distal aspect of 35 posteriorly up to the region of 38 and mesiodistally covering the entire alveolar mucosa in relation to 36, 37, and 38. The tooth structures of 36, 37, and 38 appeared to be missing. The surface of the lesion appeared edematous and erythematous. Suppurative discharge from the sulcular region of 35 was seen [Figure 1]. On palpation, the proliferative growth was soft to firm in consistency, with mild tenderness, immobile, minimally bleeding, and associated with suppurative discharge from the sulcular region of 35. Provisional diagnosis was made as extragingival pyogenic granuloma in relation to the alveolar mucosa of 36, 37, and 38. Differential diagnoses considered were peripheral ossifying fibroma, peripheral giant cell granuloma, and actinomycosis finally. Complete hemogram was within normal limits. Panoramic radiograph (OPG) showed a well-defined, scooped out or saucer-shaped radiolucency around the roots and periapical regions of 33, 34, and 35 [Figure 2]. Generalized loss of interdental bone was seen. Excisional biopsy of the lesion was carried out under local anesthesia and the specimen was sent for histopathological examination. Histopathological section showed stratified squamous epithelium and underlying connective tissue [Figure 3]. Connective tissue was moderately vascular with diffuse intense mixed inflammatory cell infiltrate predominantly consisting of neutrophils, and numerous colonies of microorganisms with central hematoxyphilic and peripheral eosinophilic rimming were present [Figure 4]. The histopathologic findings were similar to the characteristic features of actinomycosis. The patient was treated with amoxicillin 500 mg four times a day for a period of 21 days and followed up for 6 months which showed complete healing and no evidence of recurrence of the lesion.
Figure 1: Lesion seen in the mandibular left posterior edentulous area

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Figure 2: OPG showing generalized bone loss and scooped out radiolucency seen with respect to the mandibular left premolar region

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Figure 3: H and E section showing connective tissue stroma with multiple actinomycotic colonies

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Figure 4: H and E section showing actinomycotic colony

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   Discussion Top


Actinomycosis was first explained in 1878 by Israel and Wolfe. It is caused by gram-positive anaerobic bacilli of the Actinomycetes family, predominantly A. israelii. [4] Currently, Actinomyces are grouped as bacteria. These bacteria can be classified into six subgroups: Israelii, odontolyticus, viscosus, meyeri, naeslundii, and pyogenes. Actinomycosis is rare; majority of reports cite an incidence of one case per year per institution. There is a slight male predilection with the ratio ranging from 1.5:1 to 3:1. Actinomycosis is commonly seen more in the 4 th to 6 th decades of life and is very rare in children. [2]

Actinomycosis in humans is caused primarily by A. israelii, bacteria of normal oral flora. Being an anaerobic gram-positive, filamentous bacterium, it is a commensal in periodontal pockets and gingival crevices, in carious teeth, dental plaques, and tonsillar crypts. Wounds like dental extraction and trauma facilitate its penetration. It is the most isolated pathogen, but not the sole causative agent of the disease. [5] The pathogenicity of the infection can be explained as ranging from an acute form of rapid onset with pus discharge from multiple sinus tracts to a slowly progressing chronic form which shows indurated fibrosis with little suppuration [6] and tender or non-tender woody hard multiple nodular lesions, usually situated at the angle of the jaw, multiple abscesses and sinuses that open onto the cheek, sulfur granules in the exudates, typical absence of lymphadenopathy, with or without trismus and fever. [7]

The infection most commonly occurs from a few weeks to months after the entry of organism through the oral portals of entry, such as facial bone fracture, periodontal pockets, site of extraction, pericoronitis, pulp and periapical inflammation, root canal treatment, or surgery involving the periodontium. Immunosuppression states were recently reported to be a predisposing risk factor, further enhancing the risk of an actinomycosis infection. [6] Invasion of the cranium or the bloodstream may occur if the disease is left untreated. [7] Actinomycosis is often challenging to diagnose and majority of the cases are misdiagnosed. Cervicofacial actinomycosis may resemble either a malignant neoplasm of the head and neck or chronic granulomatous lesions like tuberculosis. [2] Imaging modalities like computed tomography and magnetic resonance imaging give non-specific findings. [8] A. israelii is highly sensitive to commonly used antibiotics. Penicillin, being a narrow-spectrum antibiotic, is preferred as a good choice for treatment. In most cases of actinomycosis, antimicrobial therapy is sufficient. [2] Actinomycosis should be included in the differential diagnosis of commonly encountered lesions like pyogenic granuloma and of any homogenously enhancing soft tissue lesion associated with inflammatory reaction and infiltration of the cervicofacial area.

Acknowledgments

Dr. Nishath Khanum and Dr. Santosh Kanwar, Post Graduate students, Department of Oral Medicine and Radiology, Farooqia Dental College and Hospital, Mysore are acknowledged.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Naveen S, Seema S, Devendra Kumar R, Mohan Kumar, Manoj P. Actinomycosis of the mandible. World J Pathol 2012;1:44-6.  Back to cited text no. 1
    
2.
Rania R. Unusual presentation of actinomycosis misdiagnosed as severe periodontal destruction. JRMS 2012;19:53-6.  Back to cited text no. 2
    
3.
Sakallioðlu U, Açikgöz G, Kirtiloðlu T, Karagöz F. Rare lesions of the oral cavity: Case report of an actinomycotic lesion limited to the gingiva. J Oral Sci 2003;45:39-42.  Back to cited text no. 3
    
4.
De D, Dogra S, Kanwar AJ, Saikia UN. Actinomycosis presenting as a destructive ulcerated plaque on the palate and gingiva. J Am Acad Dermatol 2011;65:1235-6.  Back to cited text no. 4
[PUBMED]    
5.
Muharrem G. Cervicofacial actinomycosis: A case report. OHDMBSC 2005;4:58-61.  Back to cited text no. 5
    
6.
Nagler R, Peled M, Laufer D. Cervicofacial actinomycosis: A diagnostic challenge. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997;83:652-6.  Back to cited text no. 6
    
7.
Moniruddin AB, Begum H, Nahar K. Actinomycosis: An update. Medicine Today 2010;22:43-7.  Back to cited text no. 7
    
8.
Volante M, Contucci AM, Fantoni M, Ricci R, Galli J. Cervicofacial actinomycosis: Still a difficult differential diagnosis. Acta Otorhinolaryngol Ital 2005;25:116-9.  Back to cited text no. 8
    


    Figures

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



 

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