Background: Dental implantation has emerged as a prominent alternative to traditional dental orthopedic approaches, however predicting and preventing implant failure remains a significant challenge.
Aim: To assess the gingival state at the pre-implantation stage to predict early implant failures in dental implantation
patients.
Material and methods: This retrospective case-control study involved 138 patients, of whom 124 were included in the
analysis set: ages 35-60, with a bounded edentulous space, satisfactory oral hygiene, and informed consent. Patients
with acute inflammation, generalized chronic periodontitis, severe systemic pathology, or smokers were excluded.
Gingival biopsies were collected pre-implantation, fixed in formalin, and analyzed using histological and
immunohistochemical (IHC) methods. The primary antibodies used included CD3, CD20, TBX21, GATA3, Foxp3,
CD68, CD80, and CD163. Statistical analysis was conducted using descriptive statistics, Chi-Square Test, and MannWhitney U Test.
Results:During the one-year follow-up, signs of early implant failure were observed in 21 out of 124 patients (16.9%).
Histopathological analysis revealed inflammatory changes in 18 out of 103 control group patients (17.5%) and 14 out
of 21 case group patients (66.7%) (P < 0.001). IHC analysis showed a predominance of CD3+ cells, particularly Th1
cells, and a significant portion of macrophages, mainly from the M2 subpopulation, in the case group. These findings
suggest a pro-inflammatory immune response in patients with implant failure.
Conclusion: The pre-implantation gingival state can be a valuable predictor of the early implant failure. A predominance
of T-cells, especially Th1 cells, along with a significant presence of macrophages, can indicate a higher risk for
developing implant failure due to inflammatory background and affected bone remodelling. Understanding and
addressing gingival inflammation before implantation can help minimize complications and improve implant success.
Further research is needed to explore these inflammatory mechanisms and develop targeted prevention strategies.
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