Idiopathic Orofacial Granulomatosis – A Diagnostic and Treatment Challenge

Rv, Rangdhol; N, Madhulika; Dany, A; Jeelani, Shazia; Gs, Asokan

doi:10.7860/jcdr/2014/10047.4961

Cited by 8 publications

(12 citation statements)

References 13 publications

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“…Gingival enlargement covers broad etiological entities classified into five general groups: Enlargement associated with non-genetic diseases GF can be directly or indirectly linked to poor nutrition (vitamin C deficiency) [ 42 ], systemic hormonal stimulation (pregnancy or puberty) [ 43 ], blood dyscrasias (leukemia) [ 44 – 47 ], Wegener’s granulomatosis [ 48 ], orofacial granulomatosis [ 49 ], pyogenic granuloma [ 50 ] and sarcoidosis [ 51 ]. It may also be associated with pseudotumors [ 52 , 53 ], benign neoplasms, e.g .…”

Section: Reviewmentioning

confidence: 99%

“…Regarding DIGO, it may occur not only for calcium channel blockers, CsA and phenytoin but also with other immunosuppressants or anticonvulsants, antibiotics, and oral contraceptives [ 149 ]. Differential diagnosis of GF with granulomatous lesions includes systemic diseases such as sarcoidosis, Crohn’s disease, and tuberculosis, as well as lesions localized to the orofacial region like orofacial granulomatosis [ 48 , 49 , 51 , 150 ]. Although leukemia is a malignant disease of the blood, where the uncontrolled proliferation of immature blood cells takes place, leukemic infiltration of oral tissues may occur, resulting in a pale mucosa, poor wound healing, and bleeding, which in some cases can resemble GF [ 45 , 46 ].…”

Section: Reviewmentioning

confidence: 99%

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Gingival fibromatosis: clinical, molecular and therapeutic issues

Gawron

Łazarz‐Bartyzel

Potempa

et al. 2016

Orphanet J Rare Dis

103

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Gingival fibromatosis is a rare and heterogeneous group of disorders that develop as slowly progressive, local or diffuse enlargements within marginal and attached gingiva or interdental papilla. In severe cases, the excess tissue may cover the crowns of the teeth, thus causing functional, esthetic, and periodontal problems, such as bone loss and bleeding, due to the presence of pseudopockets and plaque accumulation. It affects both genders equally. Hereditary, drug-induced, and idiopathic gingival overgrowth have been reported. Hereditary gingival fibromatosis can occur as an isolated condition or as part of a genetic syndrome. The pathologic manifestation of gingival fibromatosis comprises excessive accumulation of extracellular matrix proteins, of which collagen type I is the most prominent example. Mutation in the Son-of-Sevenless-1 gene has been suggested as one possible etiological cause of isolated (non-syndromic) hereditary gingival fibromatosis, but mutations in other genes are also likely to be involved, given the heterogeneity of this condition. The most attractive concept of mechanism for drug-induced gingival overgrowth is epithelial-to-mesenchymal transition, a process in which interactions between gingival cells and the extracellular matrix are weakened as epithelial cells transdifferentiate into fibrogenic fibroblast-like cells. The diagnosis is mainly made on the basis of the patient’s history and clinical features, and on histopathological evaluation of affected gingiva. Early diagnosis is important, mostly to exclude oral malignancy. Differential diagnosis comprises all pathologies in the mouth with excessive gingival overgrowth. Hereditary gingival fibromatosis may present as an autosomal-dominant or less commonly autosomal-recessive mode of inheritance. If a systemic disease or syndrome is suspected, the patient is directed to a geneticist for additional clinical examination and specialized diagnostic tests. Treatments vary according to the type of overgrowth and the extent of disease progression, thus, scaling of teeth is sufficient in mild cases, while in severe cases surgical intervention is required. Prognosis is precarious and the risk of recurrence exists.

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Section: Reviewmentioning

confidence: 99%

Section: Reviewmentioning

confidence: 99%

Gingival fibromatosis: clinical, molecular and therapeutic issues

Gawron

Łazarz‐Bartyzel

Potempa

et al. 2016

Orphanet J Rare Dis

103

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“…The diagnosis of OFG involves the exclusion of other granulomatous diseases such as sarcoidosis. The patient undergoes a detailed oral examination, ultrasonography, haematoserological assays as well as histological examination of a biopsy taken from an appropriate site (Rangdhol, Madhulika, Dany, Jeelani, & Asokan, 2014). New biomarkers would supplement the diagnostic procedures and provide indicators to assist early diagnosis and facilitate monitoring of disease activity.…”

Section: Introductionmentioning

confidence: 99%

Salivary changes in oxidative stress related to inflammation in oral and gastrointestinal diseases

et al. 2020

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Objectives The early diagnosis and monitoring of Crohn's disease (CD) and orofacial granulomatosis (OFG) might be facilitated by assaying potential disease biomarkers in saliva. Markers of oxidative stress and inflammation were assayed in salivas from patients with CD, OFG and concurrent OFG and CD (OFG + CD). Subjects Unstimulated whole mouth saliva was collected from 93 subjects, and immunoglobulin A (IgA), lactoferrin (LF) and myeloperoxidase (MPO) were determined by ELISA. Markers of oxidative stress and antioxidant status were assayed spectrophotometrically. Results Immunoglobulin A was significantly (p < .03) higher in experimental groups vs the control group. LF was significantly (p < .01) higher in OFG + CD compared to CTRL and CD. Ferric reducing antioxidant power was lower (p ≤ .009) in all experimental groups, and advanced glycation end products were higher (p ≤ .01) in CD and OFG + CD patients. Conclusion Oxidative stress is increased in saliva in CD and OFG. Although MPO, a product of inflammatory cells, was not significantly increased, the other innate immune markers, IgA and LF, which are also secreted by salivary glands, were increased. This study suggests that saliva might be utilized in monitoring CD and OFG but further longitudinal studies focused on analysing a panel of salivary markers are needed.

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“…Etyopatogenezi tam olarak bilinmemekle beraber, genetik yatkınlık, immün yetmezlik, enfeksiyöz etkenler, besin intoleransı, stres gibi birçok faktör suçlanmıştır. Nadir görülen bir dermatoz olup genellikle 10-30 yaşlar arasında ve kadınlarda sık görülmektedir 1,2,3 . Burada 27 ve 35 yaşlarında keilitis granülomatosalı iki kadın olgu sunulmaktadır.…”

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“…Rekürren fasiyal sinir paralizisi, skrotal dil ve orofasiyal ödem triadı ile bilinen MelkerssonRosenthal sendromunun bulgularından birisidir. Bu sendromda klasik triadın görülmesi nadirdir ve genellikle monosemptomatik veya oligosemptomatik tutulum izlenir 1 Etyolojisi tam olarak bilinmemekle birlikte otozomal dominant olduğu 9p 11 kromozomunun sorumlu gen olduğu öne sürülmüştür 4 . Genetik yatkınlık, immün yetmezlik, enfeksiyöz etkenler, besin intoleransı, stres gibi birçok faktör suçlanmıştır 3 .…”

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