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ISSN (Print) 1013-9052
EISSN 1658-3558
The Saudi Dental Journal,
P.O. Box 52500,
Riyadh 11563,
Kingdom of Saudi Arabia
Tel.
966-1-467-7328
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933-1-467-7308 /
966-1-467-7534
Email
saudidj@ksu.edu.sa

SDJ

Localized Inflammatory Hyperplasia Of The Oral Cavity:

Clinico-Pathological Study Of 164 Cases

Nii Otu Nartey, BDS, MSc, MRCD{C}, Hezekiah A. Mosadomr, DMD, MS,
Maan Al-Cailani, BDS, PhD, Aziza Al-Mobeerik, BDS
King Saud University College of  Dentistry, P.O. Box 60169, Riyadh 11545, Saudi Arabia

Abstract 

 
One hundred and sixty-four cases of localized inflammatory hyperplasia of the oral cavity namely, focal fibrous hyperplasia, pyogenic granuloma, peripheral giant cell granuloma and peripheral ossifying fibroma were studied. The inflammatory hyperplasia occurred more commonly in females except focal fibrous hyperplasia, which showed male predilection. In this series, the occurrence of peripheral giant cell granuloma and peripheral ossifying fibroma exclusively on the gingiva supports previous assertion that these lesions probably arise from the superficial periodontal fibers.

Introduction

 
The localized inflammatory hyperplastic lesions are the most frequently encountered oral mucosal lesions in humans.1 Localized inflammatory hyperplasia include focal fibrous hyperplasia (FFH) pyogenic granuloma (PC), peripheral giant cell granuloma (PGCG) and peripheral ossifying fibroma (POF). Although some of these lesions were described in a textbook of oral pathology as benign tumors,2 they are non-neoplastic inflammatory response of the connective tissue or superficial periodontal ligament to low grade chronic irritation.3,4 The term epulis is used clinically to describe any localized growth on the gingiva, but histological examination of such lesions indicate that the majority of them are FFH, PG, PGCG and POF.5 Their histopathological features are quite distinct but considerable overlap still exists among these lesions. For this reason, some authors2,4,5 have postulated that inflammatory hyperplasia may be the same lesion at different stages of maturation. Eversole and Rovin5 speculated that the different histological entities of inflammatory hyperplasia may be due to connective tissue response to varied intensities of mucosal irritation. This response may be influenced by the serum levels of certain endocrine hormones.
This study reviews the pathogenesis, clinical, and histopathological features of the four main types of localized inflammatory hyperplasia of the oral mucosa and compares the clinico-pathologic profiles of the diseases to those previously reported.
The localized inflammatory hyperplastic lesions are the most frequently encountered oral mucosal lesions in humans.1 Localized inflammatory hyperplasia include focal fibrous hyperplasia (FFH) pyogenic granuloma (PC), peripheral giant cell granuloma (PGCG) and peripheral ossifying fibroma (POF). Although some of these lesions were described in a textbook of oral pathology as benign tumors,2 they are non-neoplastic inflammatory response of the connective tissue or superficial periodontal ligament to low grade chronic irritation.3,4 The term epulis is used clinically to describe any localized growth on the gingiva, but histological examination of such lesions indicate that the majority of them are FFH, PG, PGCG and POF.5 Their histopathological features are quite distinct but considerable overlap still exists among these lesions. For this reason, some authors2,4,5 have postulated that inflammatory hyperplasia may be the same lesion at different stages of maturation. Eversole and Rovin5 speculated that the different histological entities of inflammatory hyperplasia may be due to connective tissue response to varied intensities of mucosal irritation. This response may be influenced by the serum levels of certain endocrine hormones.
This study reviews the pathogenesis, clinical, and histopathological features of the four main types of localized inflammatory hyperplasia of the oral mucosa and compares the clinico-pathologic profiles of the diseases to those previously reported.

Materials and Methods

 
A search through 1,594 consecutive biopsies submitted to the Oral Pathology Diagnostic services at the College of Dentistry, King Saud University in Riyadh, Saudi Arabia, over an eight-year period (1984-1991) yielded a total of 164 lesions which could be categorized as localized and inflammatory in origin. The microscopic sections were reviewed and histologic diagnoses were made according to the criteria of Daley et al.5 The available clinical data on the location of the lesions, sex and age of the affected patients at the time of excision were recorded and tabulated.

Results

 
During the eight-year interval, 164 localized inflammatory hyperplasia of the oral cavity were recorded from a total biopsy of 1,594 cases. This constituted 10.3% of the total biopsy accessioned during this period. Focal fibrous hyperplasia [Figs. 1 a and 2] was the most common (93; 57%). Fifty-two cases (32%) were pyogenic granuloma [Figs. 1b and 3]. Ten cases (6%) were peripheral giant cell granuloma [Figs. 1c and 5].
Table 1 shows that the distribution of the lesions according to sex, age range and mean age of the patients. Figure 6 illustrates the distribution of the individual lesion with respect to age of the patients at the time of excision. Figure 7 represents the site distribution of each lesion in the oral cavity.

Discussion

 
This study is the largest report on the incidence of the four main histological types of localized inflammatory hyperplasia of the oral mucosa in the Kingdom of Saudi Arabia. Focal fibrous hyperplasia (fibroma) was the most common lesion occurring over a wide age range, with a peak incidence in the third decade. These observations were in agreement with previous studies.3,4,5 However, a male predilection was noted in this study which differs from the other previous reports.3,4,5
Pyogenic granuloma occurred more frequently in the third and fourth decades and showed a female predilection in this study. Similar observations were reported by Kfir et al4 and Angelopoulous6 who suggested that the age incidence and female predilection of PG may reflect the influence of pregnancy on the pathogenesis of the disease. Recently, Daley et al7 reported a positive relationship between the incidence of PG and the serum progesterone and estrogen concentrations in pregnant women. It was speculated in this report that the two hormones render the gingival tissue more susceptible to chronic irritation caused by plaque and calculus.
Peripheral ossifying fibroma and peripheral giant cell granuloma occurred more frequently in females than males. There were bimodal peak incidences at the third and sixth decades for PGCG, which agreed with reports from other studies.3,5,8 The peak incidence for the peripheral ossifying fibroma was in the third decade followed by a definite decline. Peripheral ossifying fibroma has a marked predilection for the younger age-group.3,4,5 Eversole and Rovin3 suggested that the loss of periodontium that accompany tooth loss in old age may explain the greater occurrence of POF in the younger age-group.
This study supports previous assertions3,5,6,7 that FFH and PG may occur on any oral mucosal site with special preference for the gingivae while PGCG and POF occur exclusively on the gingivae. Eversole and Rovin3 suggested that limitation of PGCG and POF to the gingivae supports a possible histogenic derivation from the superficial periodontal ligament, which contains cells capable of producing bone and cementum. Daley et al5 felt that the high incidence of PGCG anterior to the molars in children may be related to the presence of odontoclast during physiological resorption of the deciduous teeth.
Considerable overlap exists among the different histological entities3,4,5 of the localized inflammatory hyperplasia but whether or not they represent the same lesion at different developmental stages as suggested by some workers2,5 is debatable. The predominantly vascular component of PG may be subsequently replaced partially or completely by fibrous tissue and, hence, diagnosed as organizing pyogenic granuloma or a fibroma.2,5 The frequent location of the inflammatory hyperplasia on the gingiva appears to support the notion that they are the same lesion at different stages of histological maturation. However, if this is true, then a definite age grouping for the different histological entities should be obvious. The mean ages for various lesions should reflect the progressive development of the lesion through the different histological stages, but this was not the case in our studies or any of the previous reports. We are of the opinion that FFH, PG, PGCG and POF are mucosal responses to chronic, low grade irritation caused by plaque and calculus, or any other irritant. However, the histological appearance of each entity may be influenced by the intensity of the irritation, duration of the lesion and possibly the metabolic effects of serum concentrations of hormones, such as estrogen and progesterone.

References

 

  1. Bouquot JE. Common oral lesions found during a mass screening examination, J Am Dent Assoc 1986;112:50-7.
  2. Shafer WG, Hine MK, Levy BM. A textbook of oral pathology. 5th ed. Philadelphia: WB Saunders Co, 1983;782.
  3. Eversole LR, Rovin S. Reactive lesions of the gingiva. J Oral Pathol 1972;1:30-8.
  4. Kfir Y, Buchner A, Hansen LS. Reactive lesions of the gingiva. A clinicopatho- logical study of 741 cases. J Periodontal 1980;51:655-61.
  5. Daley TD, Wysocki GP, Wysocki PD, Wysocki DM. The major epulides: Clinico-pathological correlations. J Can Dent Assoc 1990;56:627-30.
  6. Angelopolous AP. Pyogenic granuloma of the oral cavity: Statistical analysis of its clinical features. J Oral Surg 1971;29:840-47.
  7. Daley TD, Nartey NO, Wysocki CP. Pregnancy tumor: an analysis. Oral Surg Oral Med Oral Pathol 1991;72:196-99.
  8. Hassan MA, Hamed S. Peripheral giant cell granuloma -clinical, histological and histochemical study. Egypt Dent J 1985;31:25-44.
  9. Bhaskar SN, Cutright DE, Beasly JD, Perez B. Giant cell reparative granuloma (peripheral) report of 50 cases. J Oral Surg 1971;29:110-15.
  10. Miller CS, Henry RG, Damm DD. Proliferative mass found in the gingiva. J Am Dent Assoc 1990;121:559-60.

 

Tables

 


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