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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
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.
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.
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.
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.
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.
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