Abstract
Background
Orofacial tumours and tumour-like lesions encompass a diverse spectrum of benign and malignant conditions. Understanding their demographic distribution is essential for early diagnosis and optimal treatment planning. This study aimed to evaluate the prevalence and histopathological spectrum of OT/TLL in a Nigerian tertiary hospital and to compare findings with reports from other regions of the country.
Methods
Histopathology records of all orofacial lesions diagnosed between January 2015 and December 2024 were reviewed. Data on demographics, anatomical sites, and histological diagnoses were analyzed. Lesions were categorized as benign or malignant and Chi-square tests, logistic regression, and odds ratios were calculated using SPSS version 26.
Results
A total of 588 patients were studied. Benign lesions predominated (84.0%) and reactive follicular hyperplasia was the most common diagnosis (47.0%) peaking in childhood. Ameloblastoma (8.6%) was the leading benign odontogenic neoplasm, especially in the 10–19 age group. Malignancy rates increased progressively by odds of 9.6% with each additional year of age (OR = 1.096, 95% CI: 1.067–1.126, p < 0.001). Squamous cell carcinoma (59.6%) as the most frequent with 73.2% of cases occurring in patients aged ≥ 50 years (χ²=112.4, p < 0.0001). Benign tumours showed a slight female predominance, whereas males had significantly higher malignancy rates than females (χ²=7.82, p = 0.005) and independently conferred 86% higher odds (OR = 1.86, 95% CI: 1.16–2.98, p = 0.010). The mandible was the main site for ameloblastoma, while SCC often involved the larynx and nasopharynx.
Conclusion
Benign orofacial lesions are highly prevalent, with reactive follicular hyperplasia being most common. Ameloblastoma and SCC represent the most significant benign and malignant neoplasms, respectively with age and male gender independent predictors of malignancy. These findings highlight the need for improved diagnostic services, oral health interventions, and strengthened cancer screening programs for early detection at high-risk sites.
Keywords: Orofacial tumours, Maxillofacial lesions, Ameloblastoma, Squamous cell carcinoma, Reactive follicular hyperplasia, Pleomorphic adenoma
Introduction
Orofacial tumours and tumour-like lesions (OT/TLL) represent a diverse group of conditions affecting the oral cavity, jaws, salivary glands, and adjacent facial structures [1]. These lesions vary widely in biological behaviour, ranging from benign growths to aggressive malignant neoplasms, and pose diagnostic and therapeutic challenges due to overlapping clinical and radiographic features [1–3] .Early and accurate diagnosis is essential for appropriate management and improved patient care and outcome; with tissue biopsy remaining the gold standard for definitive diagnosis, treatment planning, and prognostication [3, 4].
The prevalence and pattern of OT/TLL show considerable geographic variation, influenced by cultural, social, occupational, and climatic factors [5, 6]. In Nigeria and other parts of sub-Saharan Africa, increasing attention has been directed toward their epidemiological and histopathological characteristics, providing insights into population-specific trends and risk factors [7–10] However, disparities in healthcare access and limited regional data continue to hinder comprehensive understanding [10].
This study aimed to evaluate the prevalence and histopathological spectrum of OT/TLL in a Nigerian tertiary hospital and to compare findings with reports from other regions of the country.
Materials and methods
This retrospective, descriptive study was conducted in the Departments of Pathology and Dentistry, University of Ilorin Teaching Hospital (UITH), Ilorin, Nigeria. Ethical approval was obtained from the University of Ilorin Teaching Hospital Ethics Committee prior to study commencement.
Histopathology records of all orofacial tumours and tumour-like lesions diagnosed between January 2015 and December 2024 were retrieved from the hospital records. All the incomplete data were excluded from the study. Extracted data included patient age, sex, anatomical site, and histopathological diagnoses. Lesions were classified as benign or malignant based on histopathology and according to the World Health Organization Classification of Head and Neck Tumours, 5th edition (2024), into reactive/non-neoplastic lesions, odontogenic tumours, malignant epithelial tumours, haematolymphoid tumours, and salivary gland tumours. Age at diagnosis was categorized into 7 groups (0–9, 10–19, 20–29, 30–39, 40–49, 50–59 and ≥ 60 years).
Data were analyzed using SPSS version 22 (IBM Corp., Armonk, NY, USA). Frequencies and percentages for categorical variables; means and standard deviations for continuous variables. Chi-square tests (or Fisher’s exact test when expected cell counts < 5) for associations between categorical variables. Binary logistic regression to identify independent predictors of malignancy and Odds ratios (OR) reported with 95% confidence intervals (CI). Statistical significance at p < 0.05 (two-tailed) and the study adhered to STROBE reporting guidelines.
Results
A total of 588 cases of orofacial tumours and tumour-like lesions were analyzed comprising 293 males (49.8%) and 295 females (50.2%). The mean age was 35.6 years (SD = 19.2, range: 0–89 years).
Benign lesions accounted for 494 (84.0%) while malignant lesions were 94 (16.0%) (Tables 1, 2 and 3). There was a slight female predominance in benign tumours with the highest frequency at 0–9 years, however, malignant lesions were significantly male (63.8%) dominated with modal age group of ≥ 60 years (χ² = 112.4, df = 6, p < 0.0001) (Tables 1 and 4).
Table 1.
Age group and gender distribution of benign and malignant lesions
| BENIGN | MALIGNANT | ||||||
|---|---|---|---|---|---|---|---|
| M | F | Total | M | F | Total | % Malignant lesions per age group | |
| 0–9 |
115 58.4% |
82 41.6% |
197 100.0% |
2 100.0% |
0 0.0% |
2 100.0% |
1.0 |
| 10–19 |
28 34.1% |
54 65.9% |
82 100.0% |
4 57.1% |
3 42.9% |
7 100.0% |
7.9 |
| 20–29 |
27 34.6% |
51 65.4% |
78 100.0% |
2 50.0% |
2 50.0% |
4 100.0% |
4.9 |
| 30–39 |
14 34.1% |
27 65.9% |
41 100.0% |
8 80.0% |
2 20.0% |
10 100.0% |
19.6 |
| 40–49 |
17 45.9% |
20 54.1% |
37 100.0% |
12 75.0% |
4 25.0% |
16 100.0% |
30.2 |
| 50–59 |
18 50.0% |
18 50.0% |
36 100.0% |
16 59.3% |
11 40.7% |
27 100.0% |
42.9 |
| ≥ 60 |
14 60.9% |
9 39.1% 100.0% |
23 100.0% |
16 57.1% |
12 42.9% |
28 100.0% |
54.9 |
| Total |
233 47.2% |
261 52.8% |
494 100.0% |
60 63.8% |
34 36.2% |
94 100.0% |
16.0 |
M Male, F Female, % Percentage
Chi-square test (age group vs. malignancy): χ² = 112.4, df = 6, p < 0.0001
Table 2.
Age group and gender distribution of benign lesions
| Ameloblastoma | Polyps | Reactive follicular hyperplasia | Others | Total | ||||||
|---|---|---|---|---|---|---|---|---|---|---|
| M | F | M | F | M | F | M | F | M | F | |
| 0–9 |
1 0.9% |
1 1.2% |
2 1.7% |
1 1.2% |
100 87.0% |
69 84.1% |
12 10.4% |
11 13.4% |
115 100.0% |
82 100.0% |
| 10–19 |
2 7.1% |
7 13.0% |
1 3.6% |
5 9.3% |
12 42.9% |
24 44.4% |
13 46.4% |
18 33.3% |
28 100.0% |
54 100.0% |
| 20–29 |
2 7.4% |
3 5.9% |
5 18.5% |
10 19.6% |
2 7.4% |
15 29.4% |
18 66.7% |
23 45.1% |
27 100.0% |
51 100.0% |
| 30–39 |
4 28.6% |
2 7.4% |
1 7.1% |
3 11.1% |
2 14.3% |
2 7.4% |
7 50.0% |
20 74.1% |
14 100.0% |
27 100.0% |
| 40–49 |
1 5.9% |
6 30.0% |
2 11.8% |
0 0.0% |
4 23.5% |
0 0.0% |
10 58.8% |
14 70.0% |
17 100.0% |
20 100.0% |
| 50–59 |
6 33.3% |
0 0.0% |
3 16.7% |
2 11.1% |
0 0.0% |
0 0.0% |
9 50.0% |
16 88.9% |
18 100.0% |
18 100.0% |
| ≥ 60 |
4 28.6% |
0 0.0% |
2 14.3% |
0 0.0% |
1 7.1% |
1 11.1% |
7 50.0% |
8 88.9% |
14 100.0% |
9 100.0% |
| Total |
20 8.6% |
19 7.3% |
16 6.9% |
21 8.0% |
121 51.9% |
111 42.5% |
76 32.6% |
110 42.1% |
233 100.0% |
261 100.0% |
Table 3.
Age group and gender distribution of malignant lesions
| Lymphoma | Mucoepidermoid carcinoma | Squamous cell carcinoma | Others | Total | Inferential statistics | ||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| M | F | M | F | M | F | M | F | M | F | Odds ratio | 95% CI | p-value | |
| 0–9 |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
1 50.0% |
0 0.0% |
1 50.0% |
0 0.0% |
2 100.0% |
0 0.0% |
1.00 (ref) | - | - |
| 10–19 |
1 25.0% |
0 0.0% |
0 0.0% |
1 33.3% |
0 0.0% |
0 0.0% |
3 75.0% |
2 66.7% |
4 100.0% |
3 100.0% |
8.41 | 1.59–44.5 | 0.012 |
| 20–29 |
0 0.0% |
0 0.0% |
1 50.0% |
0 0.0% |
0 0.0% |
1 50.0% |
1 50.0% |
1 50.0% |
2 100.0% |
2 100.0% |
5.05 | 0.90–28.4 | 0.065 |
| 30–39 |
1 12.5% |
0 0.0% |
2 25.0% |
0 0.0% |
4 50.0% |
2 100.0% |
1 12.5% |
0 0.0% |
8 100.0% |
2 100.0% |
24.09 | 5.06–114.7 | < 0.001 |
| 40–49 |
1 8.3% |
0 0.0% |
3 25.0% |
1 25.0% |
5 41.7% |
2 50.0% |
3 25.0% |
1 25.0% |
12 100.0% |
4 100.0% |
42.59 | 9.22–196.7 | < 0.001 |
| 50–59 |
0 0.0% |
2 18.2% |
0 0.0% |
0 0.0% |
14 87.5% |
7 63.6% |
2 12.5% |
2 18.2% |
16 100.0% |
11 100.0% |
73.92 | 16.30-335.2 | < 0.001 |
| ≥ 60 |
3 18.8% |
3 25.0% |
0 0.0% |
1 8.3% |
12 75.0% |
8 66.7% |
1 6.3% |
0 0.0% |
16 100.0% |
12 100.0% |
120.0 | 25.90-556.1 | < 0.001 |
| Total |
6 10.0% |
5 14.7% |
6 10.0% |
3 8.8% |
36 60.0% |
20 58.8% |
12 20.0% |
6 17.6% |
60 100.0% |
34 100.0% |
|||
Table 4.
Multivariate logistic regression for malignancy prediction
| Variable | β (SE) | Adjusted OR | 95% CI | p-value |
|---|---|---|---|---|
| Age (per year increase) | 0.092 (0.014) | 1.096 | 1.067–1.126 | < 0.001 |
| Male gender (vs. female) | 0.62 (0.24) | 1.86 | 1.16–2.98 | 0.010 |
| Constant | 4.38 (0.48) | 0.012 | - | < 0.001 |
Model fit: Nagelkerke R² = 0.31, Hosmer-Lemeshow p = 0.41, AUC = 0.857
Male gender was an independent risk factor for malignancy, conferring 86% higher odds after adjusting for age (OR = 1.86, 95% CI: 1.16–2.98, p = 0.010) (The area under the ROC curve was 0.857 (95% CI: 0.815–0.899) (Tables 1 and 4). Malignancy rates increase exponentially with age (OR = 1.096, 95% CI: 1.067–1.126, p < 0.001), from 1.0% in children to 54.9% in elderly patients, with patients aged ≥ 60 years having 120-fold higher odds of malignancy compared to children (OR = 120.0, 95% CI: 25.9-556.1, p < 0.001) (Tables 1 and 4).
Anatomical site distribution
The tonsils (27.9%, n = 126) was the most common sites for benign lesions with the mandible was the predominant site for ameloblastoma (7.1%, n = 32). For malignancies, the larynx (3.8%, n = 17) was frequently involved with the larynx (3.8%, n = 17) the most common affected in OSCC.
Histopathological spectrum of benign lesions
Reactive follicular hyperplasia was the most common benign lesion (47.0%) (M: F = 1.09:1) mostly in 0–9 years and ameloblastoma (7.9%) the most frequent benign odontogenic neoplasm (M: F = 1.09:1) with modal age group at 10–19 years) (Table 2).
Histopathological spectrum of malignant lesions
Oral squamous cell carcinoma (OSCC) accounted for 59.6% of all malignant cases. Notably, 73.2% of OSCC cases occurred in patients aged ≥ 50 years (χ² = 24.8, p < 0.0001) (Fig. 1). (Tables 1 and 4).
Fig. 1.
Age distribution of squamous cell carcinoma
Age distribution of key lesions
Oral squamous Cell Carcinoma occurred predominantly among the 50–59 years age group (n = 21), with cases spanning the first to tenth decades of life (Fig. 1). Dentigerous cysts had a mean age of 22.6 ± 10.2 years, consistent with presentation in young individuals.
Ameloblastoma: Most prevalent in the second decade (10–19 years, n = 9), but observed across a wide age range (0–89 years) (Fig. 2; Table 2).
Fig. 2.
Age distribution of ameloblastoma
Distribution of other lesions
Salivary gland tumours
Pleomorphic adenoma constituted the majority (55%, n = 23) of salivary gland tumours especially at 30–39 years with strong female predilection (77.3% female, p = 0.0008), followed by mucoepidermoid carcinoma (21.4%), male predominance (M: F = 2:1) with the highest frequency at 40–49 years (Table 5).
Table 5.
Age groups and gender distribution salivary gland tumours
| Pleomorphic adenoma | Adenoid cystic carcinoma | Mucoepidermoid carcinoma | Mucocele | Lymphoepithelial sialoadenitis | Fibromyxoma tumour | |||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| M | F | M | F | M | F | M | F | M | F | M | F | |
| 0–9 |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
1 1.2% |
0 0.0% |
0 0.0% |
| 10–19 |
0 0.0% |
4 7.0% |
0 0.0% |
0 0.0% |
0 0.0% |
1 1.8% |
0 0.0% |
0 0.0% |
0 0.0% |
1 1.8% |
0 0.0% |
0 0.0% |
| 20–29 |
3 10.4% |
2 3.8% |
0 0.0% |
0 0.0% |
1 3.4% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
| 30–39 |
0 0.0% |
6 20.7% |
0 0.0% |
0 0.0% |
2 9.1% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
| 40–49 |
0 0.0% |
2 8.3% |
1 3.4% |
0 0.0% |
3 10.3% |
1 4.2% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
1 4.2% |
| 50–59 |
2 5.9% |
3 10.3% |
1 2.9% |
1 3.4% |
0 0.0% |
0 0.0% |
0 0.0% |
1 3.4% |
0 0.0% |
1 3.4% |
0 0.0% |
0 0.0% |
| ≥ 60 |
0 0.0% |
0 0.0% |
1 3.3% |
0 0.0% |
0 0.0% |
1 4.8% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
| Total |
5 1.7% |
17 5.8% |
3 1.0% |
1 0.3% |
6 2.0% |
3 1.0% |
0 0.0% |
1 0.3% |
0 0.0% |
3 1.0% |
0 0.0% |
1 0.3% |
Fibro-osseous lesions
Fibrous dysplasia was the most common (2.7%) with 81.6% female (p = 0.01), followed by ossifying fibroma (1.7%, M: F = 2:1) mostly at 10–19 years (Fig. 3; Table 6).
Fig. 3.
Distribution of fibro-osseous lesions
Table 6.
Age group and gender distribution of fibrous osseous lesions
| Age groups | Fibrous dysplasia | Ossifying fibroma | Non-ossifying fibroma | |||
|---|---|---|---|---|---|---|
| M | F | M | F | M | F | |
| 0–9 |
1 0.9% |
2 2.4% |
0 0.0% |
1 1.2% |
0 0.0% |
0 0.0% |
| 10–19 |
1 3.1% |
1 1.8% |
4 12.5% |
0 0.0% |
0 0.0% |
0 0.0% |
| 20–29 |
1 3.4% |
3 5.7% |
2 6.9% |
0 0.0% |
0 0.0% |
0 0.0% |
| 30–39 |
0 0.0% |
3 10.3% |
0 0.0% |
0 0.0% |
0 0.0% |
1 3.4% |
| 40–49 |
0 0.0% |
2 8.3% |
0 0.0% |
1 4.2% |
0 0.0% |
0 0.0% |
| 50–59 |
0 0.0% |
1 3.4% |
0 0.0% |
0 0.0% |
0 0.0% |
0 0.0% |
| ≥ 60 |
0 0.0% |
1 4.8% |
0 0.0% |
1 4.8% |
1 3.3% |
0 0.0% |
| Total |
3 1.0% |
13 4.5% |
6 2.0% |
3 1.0% |
1 0.3% |
1 0.3% |
Discussion
The predominance of benign lesions observed in this study constituting (76.9%) of all cases agrees with the established global and regional literature, where benign neoplasms and reactive conditions are consistently reported as more common than their malignant counterparts in the orofacial region [1, 5, 6]. The high prevalence of benign lesions underscores the critical role of histopathology in providing definitive diagnoses, thereby preventing overtreatment and guiding appropriate conservative or surgical management [3, 4]. The demographic distribution revealed interesting patterns. The slight female predominance in benign tumours has been reported in some studies [8, 11], though the reasons remain multifactorial and may involve hormonal influences or healthcare-seeking behaviour.
Our finding that malignancy rates increase progressively with age is consistent with global epidemiological data. Warnakulasuriya et al. (2021) reported similar age trends in a meta-analysis of 89 studies, with oral cancer incidence peaking in the 6th and 7th decades [12]. Our finding that 73.2% of SCC occurs in patients ≥ 50 years is consistent with global patterns where the mean age at diagnosis for oral SCC ranges from 60 to 65 years [13, 14]. Reason could be decline in immune surveillance with age permits the survival and proliferation of malignant cells [15, 16].
The study observed sharp increase after age 40 (OR = 42.6) probably suggest that this age window represents a critical period for diagnostic vigilance. This age threshold is in sharp contrast from reports from western countries with much older age which might be attributed to earlier exposure to risk factors such as tobacco, alcohol, and environmental carcinogens or the likelihood mutation of oncogene and tumor suppressor genes [13, 14, 17, 18].
The present study demonstrated male predominance in malignant lesions was in agreement with most studies worldwide in oral and maxillofacial oncology [17, 18]. The independent effect of male gender (OR = 1.86) after adjusting for age underlined in the current work is in tandem with a systematic review by Gupta et al. (2019) who reported a pooled OR of 2.1 for oral cancer in males compared to females [19]. The higher rates of tobacco use among males, heavy alcohol consumption among males and occupational exposures such as metal dust, chemicals more common in male-dominated industries have been suggested as plausible causes [15, 16]. These could be compounded by late presentation among males due to poor healthcare-seeking behaviours [20, 21]. Furthermore, estrogen may have protective effects against oral carcinogenesis, the differences in immune response and inflammatory pathways between genders, X-linked genes that influence cancer susceptibility [22–24]. However, this gender gap in some populations is reducing exponentially due to increasing tobacco use among females as reflected in some recent studies pointing to behavioural factors as probably playing more significant role in oral oncology [25, 26]. Therefore, we advocate the need to promote routine oral cancer screening at age 40 years with more focus and surveillance in males.
Ameloblastoma emerged as the most common benign odontogenic tumour, consistent with national and sub-Saharan data [1, 5]. Its predilection for adults and the mandible highlights its chronic course, emphasizing the need for ongoing surgical expertise and investigation into molecular pathways such as BRAF V600E mutations [9].
The high frequency of reactive follicular hyperplasia among tumour-like lesions may reflect the significant burden of chronic inflammation in the orofacial region, likely associated with poor oral hygiene and persistent infections. This finding contrasts sharply with earlier reports from Nigeria and other regions of the world, where benign lesions were predominantly odontogenic and non-odontogenic tumours [1, 27], This discrepancy may be attributed to the exclusion of reactive lesions in those previous studies.
The relatively low proportion of malignant lesions (16.0%) mirrors trends reported in recent Nigerian studies [8, 11]. Squamous cell carcinoma (SCC) was the predominant malignant tumour in the present research, accounting for nearly 60% of all malignant lesions with male at greater risk. This mirrors global trends, as SCC represents the most common oral malignancy worldwide [5, 8, 11]. The age distribution, peaking between the fifth and sixth decades, agrees with the established understanding that SCC is a disease of middle-aged and older adults. Environmental factors such as tobacco use, alcohol consumption, and viral infections (notably HPV) have been implicated in its pathogenesis. In recent years, there has been increasing recognition of the role of high-risk (HPV), particularly HPV-16, in the aetiology of oropharyngeal SCC. HPV is primarily transmitted through oro-genital sexual practices, and epidemiological studies indicate that individuals with a higher number of lifetime oral sex partners are at increased risk of developing HPV-positive oropharyngeal SCC [11], which commonly affects the tonsils and base of tongue and often presents in younger patients with fewer traditional risk exposures. This emerging pattern highlights the importance of HPV vaccination and sexual health education in reducing future disease burden. The male-to-female ratio observed in this work suggests a narrowing gender gap, possibly reflecting increasing exposure of women to known risk factors previously associated with men. The findings that the larynx and nasopharynx were frequent sites, alongside the more common oral cavity locations, underscores the need for a higher index of suspicion and thorough screening for SCC in these anatomical regions during clinical examination.
The relatively low frequency of salivary gland tumours (7.1%) in this study corresponds with reports from other Nigerian series [5, 8, 11]. Pleomorphic adenoma remained the most common benign salivary gland tumour, in agreement with global data. However, malignant salivary gland neoplasms such as mucoepidermoid carcinoma and adenoid cystic carcinoma were also encountered, emphasizing the importance of histopathological confirmation for accurate diagnosis.
A distinct geographic variation characterizes the epidemiology of fibro-osseous lesions (FOLs), with a clear divergence between patterns observed in developing nations and Western populations [7, 8] In Nigeria, collective data from Ibadan, Port Harcourt, Kano and Enugu has firmly established ossifying fibroma (OF) as the leading FOL subtype [8]. Contrary to these established national trends, our study identified fibrous dysplasia (FD) as the predominant lesion, with OF being the second most common. This finding, however, agrees with the epidemiological profile reported in Western communities [8], where FD is often the most frequent FOL. The reasons for this discrepancy are not yet defined but may include genetic predispositions, environmental influences, or variations in pathological classification.
In this study, the low frequencies of non-ossifying fibroma and cemento-ossifying fibroma likely reflect their true rarity, a pattern consistent with findings from previous reports where these subtypes were among the least commonly encountered fibro-osseous lesions [7–11]. However, this finding may also be influenced by the significant diagnostic challenges these lesions pose. Given their overlapping histopathological features, definitive diagnosis often requires careful correlation with clinical presentation and radiological findings to achieve accurate classification [9, 10].
The predominance of benign tumours and tumour-like lesions in the current study may reflect health-seeking behavior patterns in the region, where patients present earlier for less aggressive lesions than for malignant cases. The findings underscore the need for improved public awareness, early detection programs, and equitable access to diagnostic facilities across Nigeria.
When compared with previous Nigerian studies, our findings both confirm and contrast existing trends. The high prevalence of ameloblastoma and SCC is a consistent narrative across the country [1, 8, 9].
This study has several strengths, including its ten-year duration and comprehensive inclusion of histologically confirmed cases. However, limitations include its retrospective design, single-institution design, no risk factor data (tobacco, alcohol, HPV), cross-sectional nature, moderate sample size for rare diagnoses, potential underreporting due to incomplete records, and lack of detailed clinical follow-up data.
In conclusion, this study highlighted reactive follicular hyperplasia and ameloblastoma as the principal benign lesions. Squamous cell carcinoma as the most significant malignant neoplasm; age ≥ 40 years and male gender as independent risk factors for oral and maxillofacial malignancy in the local population.
Therefore, the study recommends improved diagnostic capacity/pathway and strengthened early-detection programs through allocation of adequate resources and implementation of fast-track biopsy for high-risk groups. We also advocate for promotion of improved oral hygiene practices, targeted public health awareness and prospective multi-centre studies. Future research should incorporate genomics, molecular and immunohistochemical profiling, prospective validation, inclusion of risk factor data will be valuable in understanding the biological behavior of these lesions and improving therapeutic approaches. Region-specific data such as these are critical for guiding effective health policy, enhancing oral pathology services, and ultimately improving patient outcomes in Nigeria.
Acknowledgements
We would like to thank the management of university of Ilorin Teaching Hospital (UITH) and all members of staff of department of Dentistry UITH for their generosity and cooperation in the realization of this study.
Authors’ contributions
Adeyemi Moshood Folorunsho conceptualized the study. Adegboye Oluwatosin wrote the manuscript. Agbonifo Desmond Osamede reviewed the manuscript. Muideen Sule put in the Tables and figures. Taiwo Olanrewaju Abdulrazaq analysed the data. The final manuscript was read and approved by all authors.
Funding
None.
Data availability
The datasets used and/or analysed during the current study cannot publicly be made available. However, the corresponding author on reasonable request can make deidentified data available.
Declarations
Ethics approval and consent to participate
Ethical approval was obtained from University of Ilorin Teaching Hospital, Ilorin of Ethical board committee of the institution with approval no: ERCPAN/2025/10/0659. The research was conducted based on the guidelines and protocol approved by these bodies in accordance with 1964 Helsinki declaration and its amendments.
The need for consent to participate in the study was waived by the University of Ilorin Teaching Hospital Ethics Committee (UITHEC) as regard retrospective studies.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The datasets used and/or analysed during the current study cannot publicly be made available. However, the corresponding author on reasonable request can make deidentified data available.