Adenomiosis adalah salah satu masalah ginekologi yang sering dikeluhkan oleh perempuan usia reproduksi yang sangat mengganggu kualitas hidup pada sebagian besar perempuan. Kondisi adenomiosis dicirikan dengan adanya sel epithel endometrium dan fibroblast stroma yang ditemukan di myometrium secara abnormal, dimana sel tersebut menimbulkan hiperplasia dan hipertrofi dari sel otot polos disekelilingnya. Beberapa teori terkait patogenesis adenomiosis telah banyak diteliti karena etiologi penyakit ini masih belum jelas.Banyak penelitian menunjukkan bahwa faktor inflamasi, angiogenik, pertumbuhan, dan hormonal mungkin memainkan peran utama dalam perkembangan adenomiosis. Sebagai salah satu upaya untuk memahami berbagai proses tersebut dikembangkan berbagai model hewan adenomiosis untuk mengenali patofisiologi dari adenomiosis.Penelitian ini merupakan penelitian uji pra-klinis in vivo menggunakan model adenomiosis tikus yang dilakukan selama bulan Agustus - Desember 2024 di ARF IMERI FK-UI disertai penelitian in vitro untuk mengetahui ekspresi reseptor estrogen pada jaringan uterus model hewan adenomiosis. Model tikus adenomyosis dilakukan pada 10 tikus SD model endometriosis yang dibagi menjadi 2 kelompok yang berbeda: kontrol negatif dan perlakuan. Model adenomiosis dibuat sesuai teknik mekanik yang dimodifikasi dari penelitian oleh Amaral dkk., lesi adenomiosis akan dilihat dengan laparatomi pertama pada hari ke 14 kemudian diberi perlakuan berbeda sesuai kelompok penelitian. Selanjutnya dilakukan laparotomi ke-2 pada hari ke 65 untuk menilai perkembangan lesi adenomiosis serta dilakukan pewarnaan HE dan IHK untuk menilai reseptor estrogen A dan NGF jaringan adenomiosis.Laparotomi pada tikus untuk induksi adenomyosis dilakukan setelah tikus memasuki fase estrus yang dibuktikan dengan swab vagina harian hingga 18 hari. Setelah tikus masuk ke fase estrus maka dilakukan perlakuan berupa induksi mekanik pada kornu uteri dengan ditusuk secara mekanis dengan frekuensi 100x/1cm. Tampak lesi adenomyosis pada 60% tikus di hari ke-14 dan 80% tikus di hari ke-65. Lesi berupa berupa massa kistik yang dikelilingi epithelium kuboid selapis dan stroma endometrium yang tertanam di dalam myometrium. Luas lesi di hari ke-65 lebih besar dibandingkan di hari ke-14, ( 42.83 +28.54 vs 22.87 +9.08) namun perbedaan rerata luas tersebut tidak signifikan secara statisik (P >0.05). Intensitas IHK Reseptor Estrogen Alfa menunjukkan adanya positivitas sedang (+2) pada lesi adenomyosis tikus.Kesimpulan: Teknik mekanik dapat menginduksi adenomyosis pada model hewan coba tikus SD secara efektif serta tampak ekspresi reseptor estrogen A pada hewan coba yang diinduksi adenomyosis.

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Adenomyosis is one of the gynecological problems that is often complained of by women of reproductive age which greatly disrupts the quality of life in most women. Adenomyosis conditions are mixed with the presence of endometrial epithelial cells and stromal fibroblasts found in the myometrium abnormally, where these cells cause hyperplasia and hypertrophy of the smooth muscle cells around them. Several theories related to the pathogenesis of adenomyosis have been widely studied because the etiology of this disease is still unclear. Many studies have shown that inflammatory, angiogenic, growth, and hormonal factors may play an important role in the development of adenomyosis. As an effort to understand these various processes, various animal models of adenomyosis have been developed to recognize the pathophysiology of adenomyosis.

This study is a pre-clinical in vivo trial study using a rat adenomyosis model conducted during August - December 2024 at ARF IMERI FK-UI accompanied by an in vitro study to determine the expression of estrogen receptors in the uterine tissue of the adenomyosis animal model. The adenomyosis rat model was carried out on 10 SD rats with an endometriosis model which were divided into 2 different groups: negative control and treatment. The adenomyosis model was made according to a mechanical technique modified from research by Amaral et al., adenomyosis lesions will be seen with the first laparotomy on the 14th day then given different treatments according to the research group. Furthermore, a 2nd laparotomy was performed on the 65th day to assess the development of adenomyosis lesions and to perform HE and IHC staining to assess estrogen A and NGF receptors in adenomyosis tissue.

Laparotomy in rats for adenomyosis induction was performed after the rats entered the estrus phase as evidenced by daily vaginal swabs for up to 18 days. After the rats entered the estrus phase, treatment was carried out in the form of mechanical induction on the uterine horn by mechanically piercing it with a frequency of 100x/1cm. Adenomyosis lesions were seen in 60% of rats on day 14 and 80% of rats on day 65. The lesions were cystic masses surrounded by simple cuboidal epithelium and endometrial stroma embedded in the myometrium. The area of ​​the lesion on day 65 was larger than on day 14, (42.83 +28.54 vs 22.87 +9.08) but the difference in the average area was not statistically significant (P>0.05). The intensity of the Alpha Estrogen Receptor IHC showed moderate positivity (+2) in the rat adenomyosis lesions.

Conclusion: Mechanical techniques can effectively induce adenomyosis in the SD rat animal model and the expression of estrogen receptor A is seen in the animal model that induces adenomyosis.