Testicular microlithiasis (TM) is an entity of unknown etiology that results in formation of intratubular calcifications. It is often detected incidentally when scrotal ultrasonogram is done for various indications. Testicular microlithiasis are often multiple, uniform, small, echogenic polytopic intratubular calcifications without acoustic shadows. Despite the reports of association of TM and testicular tumor, there is no uniform consensus regarding the need for evaluation and method of follow-up of these patients. This review is focused on issues regarding the etiopathogenesis, clinical conditions associated with TM, methods of follow-up and about who should be followed. Relevant literature was also obtained from various published updates and case reports.


This review addresses the issues on etiopathogenesis of testicular microlithiasis (TM), associated clinical entities, evaluation and follow-up of patients with TM. TM is an uncommon entity among adult males, resulting from intratubular calcifications. The reported incidence of TM is highly variable. With the increasing frequency of ultrasound examination in scrotal and testicular conditions and with the advent of high frequency transducers, TM is increasingly being reported. TM is associated with many benign and malignant conditions of testes but the possible association of TM with testicular cancer has been a matter of concern. Though a few sporadic cases of testicular malignancies have been reported, it is believed that a conservative approach is warranted in the absence of high risk factors, in view of the low risks for invasive cancers. There is no uniform protocol for the evaluation and follow-up of the patients with TM. Those with high risk factors like contralateral testicular tumour, chromosomal anomalies, gonadal dysgenesis, cryptorchidism and definite ultrasound pattern of TM should be advised to have further evaluation. Incidentally detected asymptomatic TM during ultrasound examination does not warrant aggressive measures and it can be followed with self examination.


The origin of testicular microlithiasis is unknown. Numerous theories have been proposed including liquefaction of protoplasmic dendritus of a spermatocyte or coalescence of colloid droplets, ectopic oocytes in dysgenetic testes, displaced spermatogonia, undifferentiated or desquamated calcified cells, deposition of glycoprotein around the nidus of cell material sloughed into the tubular lumen and abnormal  Sertoli cells More Details activity. Staged development of microliths resembling crystal-matrix formation of urinary calculi was also suggested.  Vacuolized degenerating cells not phagocytized by sertoli cells were suggested to form the nidus of microlith within the tubular lumen. Vegni-Talluri et al. have described two zones within the microliths. The central calcified zone is surrounded by a zone of concentrically layered collagen fibers. Further, the diminished capability of sertoli cells to phagocytize the degenerating cells was accounted to the proximity of carcinoma in situ (CIS) in testis.  

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