Testicular microlithiasis (TM) is a syndrome of numerous calcified foci <3 mm in diameter diffusely distributed in the testicular varicocele, first reported by Priebe et al. in 1970. The etiology, pathogenesis, epidemiology and ultrasound manifestations of TM, especially its relevance to tumors and male infertility, have attracted the attention of scholars. I. Etiology and pathogenesis of TM TM is often found in conjunction with other diseases, but the causal relationship between TM and them is uncertain. TM has been found to be associated with the following internal and external testicular pathologies: male infertility, cryptorchidism, atrophic testis, testicular dysplasia, testicular tumor, testicular cyst, testicular epididymitis, testicular or testicular adnexal torsion, epididymitis, epididymal or spermatic cord cyst, testicular syringomyelia, varicocele, AIDS, neurofibromas, Klinefelter's syndrome, Down's syndrome, male pseudohermaphroditism, and post-mumps. It has also been reported that only TM was found without other internal or external lesions of the testis . It has been suggested that TM may be a systemic disease based on the finding of multiple extensive microliths in the lungs and nervous system. Peterson et al. investigated a group of military officers in training and concluded that the incidence of TM was 5.59%, which was significantly higher than those investigated by other authors; Frauscher et al [15] investigated a group of mountain bikers and found that they had a higher incidence of scrotal disease (including TM) than the general population. Mountain bikers and participating officers have a higher chance of injury to the perineum (especially the testes) than the general population due to their usual high volume of exercise and their specific exercise and training regimen. Thus, TM can be simply considered as a marker of different degrees of testicular damage, and the process of different diseases inside and outside the testis may accompany or trigger the occurrence of TM. Using light and electron microscopy, Vegni-Talluri et al. observed testicular biopsies from a group of patients with cryptorchidism with TM and described in detail the composition and occurrence of TM for the first time. Light microscopy revealed numerous lamellar arrangements of amorphous material surrounding the calcium nuclei, surrounded by degenerating cells and occasionally some vesicles. Electron microscopy reveals two main types of material - a central electron-dense nucleus surrounded by multiple layers of laminae composed of cellular debris (degenerating mitochondria) deposited in vesicles. Electron microprobe microanalysis suggests that the microlithic center contains only calcium and no other elements. Vegni-Talluri et al. suggested that microliths are formed in two stages: in the first stage, degenerated cells containing solid nuclei and vesicles are deposited in the varicose tubules to form calcium nuclei: in the second stage, layers of collagenous fibrillar-like tissue envelop the calcium nuclei. Talluri et al. found similar phenomena. In contrast, Nistal et al [13] proposed a process of microlith formation that begins with the aggregation of cellular debris in the varicoceles to form nucleoli, followed by the deposition of collagenous fibrous-like tissue around the nucleoli and finally by calcification. II. Epidemiology of TM A large number of investigations have been done by scholars regarding the incidence of TM. The incidence of testicular tumors in TM patients ranges from 31% to 46%, while the incidence of malignant tumors is 30%: the risk is 13.2 to 21.6 times higher than that of the normal population, but the risk of tumors in elderly patients is low[. Characteristic TM (classicTM, CTM) is more closely associated with testicular malignancy than limited TM (LTM), but the risk of TM developing into malignancy is low in short-term follow-up_2ll. The high incidence of germ cell tumors, mostly seminoma, among the tumors accompanying TM has attracted the attention of scholars at home and abroad. Berger et al. reviewed the literature and found that 24 (55%) of 44 testicular tumors associated with TM were seminomatous cell tumors. Thoracic germ cell tumors associated with TM have now been reported [9,23]. Thus, Cast et al. suggested that TM may be a marker of pre-germ cell tumorigenesis. Previously, TM was thought to occur simultaneously with testicular tumors, but long-term follow-up of TM revealed eight cases that occurred after the diagnosis of TM, with the longest time being 11 years and the shortest being 6 months. Derogee et al. suggested that TM is a precancerous lesion, but no definite evidence has been found because of this correlation between TM and testicular malignancy, and therefore TM cannot be simply considered as a benign lesion. The incidence of male infertility in M patients is 17% to 23%, and the incidence of TM in male infertility patients is 1.3% to 3.1%. Testicular biopsies of infertile patients with TM show atrophy of the varicocele and cellular debris in 30% to 40% of the varicocele. Degenerated varicocele affects sperm production, while atrophied varicocele, cellular debris and microliths impede sperm motility, which may be the cause of male infertility. Other diseases associated with TM are mostly reported in individual cases or rarely discussed. The ultrasound manifestation of TM was first described in detail by Doherty in 1987, and the ultrasound manifestation of TM is characteristic: most of them are dotted strong echogenicity <3 mm in diameter in the parenchyma of both testes, with no posterior shadow. The majority of cases of TM have been reported in the literature to develop slowly during follow-up, although cases of unilateral lesions developing bilaterally or bilaterally evolving to unilaterally have been reported. Kutlu et al [33] observed three TM patients with Doppler for more than 2 years of follow-up and found no characteristic blood flow changes. Xue Ensheng et al. performed color Doppler examination of the testes of seven TM patients, and punctate or striated blood flow signals were seen in the testes, with a maximum intra-testicular arterial flow velocity of 0.08-0.12 m/s and a resistance index of 0.45-0.54, which did not differ significantly from the normal testicular blood supply.Backus et al. made the first detailed observation of the number, morphology and distribution of microliths in TM ultrasound images and described that CTM should be : More than 5-6O punctate strong echogenic echoes <3 mm in diameter with no posterior acoustic shadow can be found in each section. These punctate strong echogenic echoes are independent of each other, mostly diffusely and symmetrically distributed throughout the testicular parenchyma, but also scattered only in the periphery of the testis. Many diseases inside and outside the testis can form calcified foci that appear as strongly echogenic lesions on ultrasound images, and their morphology, size, number and distribution differ from those of TM. Bushby et al. described in detail the ultrasound presentation of calcified foci inside and outside the testis. The intra-testicular foci of calcification are mostly venous stones, spermatogenic granulomas, vascular wall calcifications or tumors of testicular origin. Venoliths, spermatogenic granulomas or vascular wall calcifications are mostly isolated punctate strong echogenicity with posterior acoustic shadowing, a few may be arranged in clusters, but the number is TM less and confined to one part of the testis. These masses may be round, oval, or irregular in shape, vary in size, but are larger than TM, with more posterior acoustic shadows, isolated or few in number, and confined to the primary lesion or to a site in the testis. Epidermoid tumors have characteristic strong echogenic masses that can be distributed at the tumor margins or in an onion skin-like distribution. Simple cyst wall calcifications are mostly patchy and strongly echogenic, located at the periphery of the cyst, arranged in an arc, and may have a posterior acoustic shadow. Extra-testicular calcifications are more likely to occur than intra-testicular ones, mostly located in the epididymis, but also in the testicular sphincter, with pearly, punctate or linear strong echogenicity, with posterior acoustic shadowing, and in smaller numbers, mostly secondary to chronic epididymitis, but also to testicular syringomyelia, spermatogenic granuloma, trauma, etc.