Recently, the identification of fusion genes has enabled the accurate diagnosis of nodular fasciitis using small biopsy specimens. Consequently, as observed in our cohort, there has been an increase in cases managed through observation until tumor regression occurs following biopsy. A decrease in signal intensity on T2-weighted images over time has been previously reported [18, 19]. This change is believed to reflect a reduction in mucus and blood vessels, along with progressive accumulation of fibrous tissue [15, 22]. Shrinkage of the enhancing area over time has also been described by Sukpanichyingyong et al. [19]. These shrinkage features are clinically relevant because they support a benign process such as nodular fasciitis. However, such features can only be assessed through longitudinal observation. Therefore, progressive reduction in size and T2 signal intensity has limited clinical utility in differentiating benign from malignant tumors. Additionally, findings on T2-weighted imaging are highly variable and nonspecific [23], complicating reliable distinction between benign and malignant lesions.

Wang et al. reported contrast enhancement of the tumor periphery with a non-enhancing central region in nodular fasciitis, termed the “inverted target sign” [7]. This was attributed to peripheral hypervascularity and central cystic change. A histologic tendency for cyst formation in the central region of nodular fasciitis has also been described [3, 7, 8]. In our series, lesions were classified as either type 2 (central non-enhancement) or type 4 (predominantly non-enhancing), with type 2 occurring more frequently. Additionally, some lesions exhibited dynamic transitions between types during follow-up. Wang et al. [7] also reported that the enhancing portion of the “inverted target sign,” which corresponds to type 2 in our classification, gradually diminished over time, evolving into a pattern with peripheral-only enhancement. Although precise classification based solely on their data is difficult, the post-transition patterns appear to correspond to type 4a or type 4b. These imaging changes are consistent with our findings.

In summary, the reported MRI features of nodular fasciitis likely represent temporal phases in a dynamic biological process. This evolution may explain the spectrum of imaging findings described in previous reports.

The known histologic changes in nodular fasciitis over time, namely “progressive fibrosis and central cyst formation” [3, 6, 8], are considered primary contributors to the development of types 2 and 4. In our cases, we demonstrated that lesions can transform not only into types 2 and 4 but also into other types. For example, two lesions decreased in size while transitioning from type 4b to type 1 or type 3, suggesting that, in addition to fibrosis and cystic change, other histopathological processes may occur over time. Wang et al. further clarified that enhancing areas correspond to regions containing myxoid components, whereas non-enhancing areas reflect cystic cavities. The observed MRI findings are attributed to this heterogeneous tissue distribution [7]. These longitudinal changes in contrast-enhanced MRI features may reflect evolving distributions of mucinous and cystic content. Wang et al. also reported that central non-enhancing tissue often contains “more extracellular matrix, some fluid-filled spaces,” which differs from the histologic findings in our type 4b case. Taken together, these observations suggest that multiple factors likely contribute to the development of non-enhancing regions.

Among the 11 cases classified as type 4b, one exhibited size increase, nine showed regression, and one was resected, precluding clinical follow-up. These findings suggest that type 4b is strongly associated with a tendency toward tumor shrinkage. Histological evaluation of the resected type 4b specimen showed no necrosis. Although the tumor center exhibited low vascularity, a high density of vessels was observed outside the capsule. This vascular pattern likely contributes to the characteristic imaging features. Observed transitions from type 4 to type 2 or type 1 indicate that previously non-enhancing areas became re-enhancing over time. This supports the hypothesis that non-enhancing areas, defined by low cellularity and vascularity, may subsequently regain both. These findings suggest that nodular fasciitis may enter a phase in which apoptotic tumor cells [15, 24] coexist with proliferating cells, and vascular supply undergoes dynamic changes. This biologic interplay may account for the inconsistent patterns of contrast enhancement on MRI. If enhancement characteristics fluctuate over time, imaging findings will vary depending on scan timing, contributing to the wide spectrum of reported MRI features. Previous reports have highlighted the variability in T2-weighted and contrast-enhanced MRI findings of nodular fasciitis [8, 23, 25]. Our results offer a plausible explanation for this variability.

Wu et al. reported the presence of inverted target signs in 11% of cases [17]. Their study suggests that nodular fasciitis exhibits inverted target signs somewhat more frequently than other soft-tissue lesions. They also described one case (3.7%) with a finding resembling type 4b, termed the “solar halo sign,” considered a notable feature not typically observed in malignant tumors. In our study, type 4b was identified in 17% of cases. If this corresponds to the “solar halo sign” described by Wu et al., the frequency in our cohort is substantially higher. Because our study incorporated an analysis of temporal evolution, the increased detection of type 4b may be partly attributable to this longitudinal imaging approach. Currently, we cannot propose an alternative explanation. However, the higher frequency and dynamic nature of this finding, previously underemphasized, warrant further attention.

The chi-square test revealed that type 3 was significantly more frequent in malignant control group, whereas type 4 was significantly more frequent in nodular fasciitis. Type 1 also tended to be more prevalent in nodular fasciitis. These results imply that nodular fasciitis lesions tend to exhibit homogeneous enhancement or predominantly non-enhancing areas, suggesting relatively homogeneous tissue composition throughout their course. In contrast, malignant tumors were characterized by a higher frequency of type 3, reflecting their inherent internal heterogeneity, as previously recognized. Thus, the non-enhancing pattern classification likely reflects the distinct biological characteristics of nodular fasciitis and our malignant control group.

Type 4b was observed exclusively in nodular fasciitis and not in our malignant group. The temporal evolution of this pattern was inconsistent, with diverse imaging changes noted. In some cases, the type 4b pattern persisted as the lesion regressed, whereas in others, previously non-enhancing regions became enhanced. These findings are consistent with prior reports describing the heterogeneous MRI appearances of nodular fasciitis.

This study has several limitations. First, because it was retrospective and spanned a long period (2006–2021), the imaging protocols were heterogeneous. The contrast agent dose, injection rate, and administration method (manual versus power injector) were not standardized, and MRI examinations were performed on multiple scanners using different fat-suppression techniques. Although these factors introduced variability, the primary endpoint—a qualitative assessment of equilibrium-phase enhancement patterns—was considered minimally affected by such protocol differences.

Additionally, in current practice, the number of cases managed conservatively has increased, likely due to USP6 detection in needle biopsy specimens. Inter-reader reproducibility was not assessed because image interpretation was performed by consensus.

Type 4b patterns were not identified in our malignant control group and may be useful in differentiating nodular fasciitis from malignancy. However, the control group in this study was limited to pathologically confirmed tumors requiring histologic differentiation within a restricted size range for evaluating non-enhancing areas. Therefore, the control group may not represent the overall characteristics of malignant tumors.