Open Access

Table I

Features and main outcomes of the included studies.

Author’s Geographic origin Method Type of lesions No. of samples Outcomes
Nakarin Kitkumthon et al. (2010) [6] Thailand PCR Group 1 :
AMB
SMA
UA
Group 2 :
Healthy controls
78
5325
94
The P53 Arg allele increases susceptibility to AMB, suggesting its importance in tumor etiology.
Noorieh Sharifisistani et al. (2011) [7] Iran IHC AMB follicular plexiform
UA
KOT
39
15
15
9
15
p53 was expressed in 77.8% of AMB and 100% of KOTs, while MDM2 was detected in 74.8% and 80% of cases, respectively. No statistically significant difference in p53 expression was observed among AMB subtypes or between AMB and KOTs (P > 0.05). A positive correlation between p53 and MDM2 expression was reported.
Amol Ramchandra Gadbail et al. (2011) [8] India IHC AMB
SMA
UA
KCOT
DC
NOM
FOM
23
14
9
32
30
12
10
No significant difference between UA and SMA (P = 0.388). p53 significantly higher in AMB compared with KCOT, DC, NOM, and FOM (P < 0.001).Positive correlation between Ki-67 and p53 (P < 0.001).
Olusegun Michael Adesina et al. (2022) [10] Nigeria IHC AMB
AOT
OKC
69
23
23
p53 immunoreactivity was significantly higher in AMB than in AOT and OKC (P < 0.05). The highest expression was observed in plexiform ameloblastoma, indicating increased proliferative activity
Zulfin Shaikh et al. (2015) [11] India IHC AMB
Follicular
Plexiform
Unicystic
AOT
25
12
4
9
25
p53 expression was observed in both AMB and AOT with no statistically significant difference between the two tumors (P = 0.554). The average percentage of p53-positive cells was 75.97% in AMB and 69.87% in AOT. In contrast, survivin expression was significantly higher in AMB than in AOT (P = 0.002), suggesting differences in apoptotic regulation and tumor behavior.
Adriano Mota Loyola et al. (2016) [12] Brasil IHC AMECA + atypical AMB 17 Strong p53 nuclear expression was observed in AMECA and was associated with a high Ki-67 proliferative index, supporting the role of p53 alterations in malignant transformation.
Zhu You et al. (2019) [13] China IHC AM-BC 6 p53 expression was positive in all AM-BC cases and significantly higher than in other ameloblastoma variants (P < 0.05), suggesting increased proliferative activity.
Jefferson-da Rocha Tenório et al. (2018) [14] Brasil IHC AMB
OKC
AOT
20
20
20
p53 expression was detected in all lesions, predominantly with low expression in AMB. No significant difference was observed between AMB, OKC, and AOT (P = 0.108). Non-significant positive correlation with Bcl-2 (r = 0.200) and negative correlation with Bax (r = −0.100).
Abhishek Singh et al. (2020) [15] India IHC SMA
OKC
UA
20
20
20
p53 expression was detected in all AMBs. No significant difference was observed between UA and SMA (P = 0.388), while expression was significantly higher in AMBs compared with other odontogenic lesions (P < 0.001). Positive correlation with PCNA was reported.
Jahanshah Salehinejad et al. (2011) [16] Iran IHC AMB
Plexiform
Follicular
Acanthom-tous
AOT
30
15
12
3
12
No statistically significant difference in p53 expression among ameloblastoma subtypes (P = 0.589). A significant difference in p53 expression was observed between ameloblastomas and AOTs (P < 0.001). The intensity of p53 staining was significantly higher in ameloblastomas. A positive correlation between PCNA and p53 expression was also reported.
Takeshi Beppu et al. (2015) [17] Japan IHC AMECA secondary type 1 An unusual case of AMB progressing to AMECA was documented, with increased Ki-67 and p53 staining, alongside changes in cytokeratin expression.
Hisashi Kato et al. (2012) [18] Japan IHC PA
AMB
1
4
Immunohistochemical analysis showed absence of p53 expression in both peripheral and intraosseous AMBs, while p63 was positively expressed in all samples. The Ki-67 labeling index was low (2.22% in PA and 1.37% in intraosseous AMBs), indicating low proliferative activity and supporting the benign biological behavior of these lesions.
Alma Florescu et al. (2012) [19] Romania IHC AMB 17 p53 expression was detected in 52.9% (9/17) of AMBs, with weak to moderate nuclear staining predominantly in peripheral columnar cells. The positivity index exceeded 50% in peripheral cells but remained below 10% in stellate reticulum cells. A significant difference in marker reactivity between epithelial compartments was observed (P < 0.001), while no association with histological subtype was found (P > 0.05).
Juan-Carlos de Vicente et al. (2010) [20] Spain IHC OKC
DCs 10 RCs
AMB
11
10
10
10
P53 immunoexpression was detected in 64% of OKCs, 40% of DCs and RCs, and 30% of AMBs. Immunolabelling for P53 was scattered and only occasionally clustered in AMB.
Daniela Adorno-Farias et al. (2018) [21] Brasil IHC AA 8 Weak to moderate nuclear p53 expression was detected in AA, associated with high Ki-67 proliferative activity, suggesting aggressive tumor behavior.
Thasvir Singh et al. (2016) [22] India IHC SMA
UA
33
6
UA showed significantly higher p53 expression than SMA (P = 0.03), with many cases demonstrating strong positivity (>50% tumor cells).
Adriano Mota Loyota et al. (2015) [23] Brasil IHC AA 5 Immunohistochemical analysis demonstrated weak to moderate nuclear p53 staining in all cases, with additional weak cytoplasmic expression in three cases. The tumors also showed a high proliferative activity with a mean Ki-67 index of 72.4 ± 24.9 positive cells per high-power field, supporting the aggressive biological behavior and high recurrence potential of AA.

AMB: ameloblastoma, SMA: solid ameloblastoma, UA: unicystic ameloblastoma, AM-BC: ameloblastomas with basal cell features, AA: adenoid ameloblastoma, PA: peripheral ameloblastoma, DC: dentigerous cyst, OKC: odontogenic keratocyst, AOT: adenomatoid odontogenic tumors, AMECA: ameloblastic carcinoma, RC: radicular cyst, NOM: normal oral mucosa, FOM: fetal oral mucosa.

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