GM is initiated by alterations in the local breast microenvironment. Factors such as nipple retraction, HPRL, local trauma, surgery, or infection may act independently or in concert to cause ductal obstruction and subsequent milk stasis (23, 30). When milk remains stagnant in the ducts for an extended period, it can lead to ductal obstruction and increased intraluminal pressure. This pressure progressively damages the ductal wall, ultimately resulting in ductal rupture. Consequently, lipid components and other degraded milk constituents may extravasate into the adjacent breast tissue (31).

When these components extravasate from the damaged ducts into the breast tissue, they are displaced from their normal anatomical compartment. The breast parenchyma then recognizes these degraded milk substances as “damage-associated molecular patterns”(DAMPs) (32). The release of these endogenous DAMPs from dead or damaged cells activates innate immune cells and pro-inflammatory signaling, thus launching the local immune response (33, 34).

Notably, HPRL plays a dual role in this phase: it not only creates conditions for mechanical obstruction by promoting milk stasis but also, as an immunomodulatory hormone, may pre-condition the immune cell landscape within the breast tissue, thereby priming it for subsequent exaggerated inflammatory responses (23, 35).

As shown in Figure 1, following their release, DAMPs rapidly activate pro-inflammatory signaling cascades (33). Neutrophils, as the earliest and most abundantly recruited innate immune cells, are subsequently chemotactically drawn to the site of injury (36). They capture and eliminate pathogens through degranulation, phagocytosis, and the release of neutrophil extracellular traps (NETs) (37). Although NETs serve as a defensive mechanism against pathogens, their excessive or dysregulated release within the chronic inflammatory milieu of GM can instead exacerbate tissue damage. Furthermore, through mechanisms such as the exposure of autoantigens, NETs may initiate and amplify subsequent autoimmune responses. Aberrant NETs formation has now been implicated in a variety of autoimmune diseases (38, 39).

Subsequently, macrophages emerge as the central players on the inflammatory stage of GM. These cells represent the most widely distributed immune cell population within human tissues (40). Within GM lesions, they are recruited by local pro-inflammatory signals and undergo phenotypic and morphological differentiation, a process known as macrophage polarization (41). In the specific microenvironment of GM, IFN-γ produced by activated Th1 cells synergizes with DAMPs to collectively drive macrophage activation predominantly towards the M1 phenotype. M1 macrophages adopt a pro-inflammatory functional state characterized by potent phagocytic activity and cytotoxicity (42). They secrete large quantities of key pro-inflammatory cytokines such as IL-6 and IL-1β, amplifying both systemic and local inflammatory responses. This further recruits additional immune cells, thereby establishing a vicious cycle (43). Concurrently, M1 macrophages directly attack and induce damage and necrosis in breast tissue cells through the release of toxic mediators, such as reactive oxygen species and substantial amounts of nitric oxide. This represents the central and direct mechanism underlying the ongoing tissue destruction in GM (44, 45).

NK cells constitute another essential component of the innate immune system. They participate in immunomodulation through cytotoxicity and cytokine secretion. In GM, their activity is likely modulated by the distinct local microenvironment. It is established that NK cells express prolactin (PRL) receptors, and a subset of GM patients presents with elevated serum PRL levels (35). Relevant basic research indicates that PRL can directly enhance NK cell activation and cytotoxicity by upregulating the autocrine IL-2/IL-2Rα and IL-15/IL-15Rα pathways (46, 47). Therefore, given the inflammatory context of GM, locally elevated PRL levels likely exert a similar activating effect on NK cells. Activated NK cells secrete copious amounts of IFN-γ, which is a key factor driving macrophage polarization toward the pro-inflammatory M1 phenotype (48). Based on this, a theoretical model can be constructed: a positive feedback loop potentially exists among PRL, activated NK cells, and M1 macrophages—where PRL activates NK cells, which induce M1 macrophages via IFN-γ, and the inflammatory milieu generated by M1 macrophages may in turn further stimulate NK cells. This hypothetical model may provide novel insights into explaining the rapid escalation of the initial inflammatory response in GM.

Furthermore, certain DAMPs can directly activate the complement alternative pathway. Clinical studies have confirmed significantly elevated levels of the intrinsic complement components C3 and C4 in both the serum and lesion tissues of GM patients, which markedly decrease following treatment, suggesting a close association with disease activity (35, 49). C3 and C5 are components of the complement system and can be cleaved by proteases via the classical, alternative, or lectin pathways, generating the potent inflammatory mediators known as anaphylatoxins C3a and C5a. These anaphylatoxins bind to their specific receptors, C3aR and C5aR1, respectively, thereby inducing histamine release from mast cells and basophils and potently recruiting polymorphonuclear leukocytes—such as neutrophils and eosinophils—to the site of inflammation (50). Further research revealed that exosomes derived from GM lesions are highly enriched with C3a and C5a. Concurrently, the expression of the C3/C3a-C3aR and C5/C5a-C5aR1 signaling axes is synchronously upregulated. These findings suggest that the complement system further amplifies and sustains inflammatory signaling in a spatial manner through this “vesicle-mediated delivery” mechanism (51).

Treg cells are essential for maintaining immune tolerance. However, during the active stage of GM, both their numbers and function are impaired. Studies have confirmed that GM patients exhibit a reduced population of Treg cells in peripheral blood, accompanied by significantly decreased expression of FOXP3, the key transcription factor essential for their identity and suppressive function (73, 83). This deficit directly results in a relative predominance of effector T cells, leading to an imbalance in the Teff/Treg ratio. Consequently, the immune system fails to adequately restrain the overactive inflammatory response (35). Notably, HPRL may further compromise Treg function. PRL binds to receptors on the Treg cell surface, interfering with their suppressive activity. This indirectly fuels the proliferation of effector cells and the secretion of the pro-inflammatory cytokine IFN-γ, thereby creating a vicious cycle (73). Based on current evidence regarding Th17 cells and GM, it is reasonable to hypothesize that an imbalance between Th17 and Treg cells exists in GM patients, which hinders the effective resolution of inflammation.

Breg cells represent another crucial class of immunoregulatory cells (84). Their functional impairment in GM, coupled with the aforementioned Treg cell deficiency, constitutes a dual failure of immunoregulation. Breg cells, particularly the subset that exerts its function via IL-10 secretion, are essential for maintaining immune tolerance and homeostasis. They directly suppress the activity of various pro-inflammatory immune cells, including Th1, Th17, and CD8 + T cells, as well as NK cells and dendritic cells. Furthermore, they can induce the differentiation of naive CD4 + T cells into Treg cells, thereby establishing a critical peripheral immunosuppressive barrier (85). However, this regulatory barrier is markedly compromised in GM patients. Studies reveal that patients in the active stage exhibit a significantly reduced proportion of Breg cells in peripheral blood (73). Correspondingly, serum levels of the key anti-inflammatory cytokine IL-10 are also found to be low in these patients (86). The reduction in Breg cells and the low levels of IL-10 indicate an impaired capacity of this pathway to suppress excessive immune responses. This impairment may allow effector cell reactions, such as those driven by Th17 cells, to proceed unchecked, hindering the self-containment of the inflammatory process. Currently, research on the precise regulatory mechanisms governing Breg cells in GM remains relatively limited. Therefore, exploring how to correct Breg cell deficiency and restore IL-10-mediated immunoregulatory function represents a promising direction for future research into GM treatment mechanisms.

This immune imbalance in GM is not confined to the active stage alone. A longitudinal study revealed that, even during the asymptomatic remission phase when lesions had subsided, the expression level of Foxp3, the master transcription factor for Treg cell function, remained significantly lower in patients’ peripheral blood compared to healthy controls (73). Another study similarly reported that the serum levels of soluble triggering receptor expressed on myeloid cells-1, a biomarker reflecting the activation state of myeloid cells such as macrophages and neutrophils, remained persistently higher in patients during remission compared to healthy controls (87). These findings collectively suggest that the “clinical remission” of GM may signify only a temporary quiescence of local inflammation, while the underlying systemic immune dysregulation does not resolve. This persistent systemic immune abnormality likely explains the high risk of recurrence even after clinical remission is achieved.

Common laboratory tests include a complete blood count, erythrocyte sedimentation rate, purified protein derivative testing, and inflammatory markers such as C-reactive protein and serum PRL. Immunologic tests may include an antinuclear antibody profile and rheumatoid factor.

First, complete blood count is typically not significantly abnormal in the early stages of GM. However, as the disease progresses, especially during the abscess formation stage, the white blood cell count may increase, indicating an acute inflammatory response (100). erythrocyte sedimentation rate is a nonspecific indicator of inflammatory activity in the body. During the acute or abscess phase of GM, some patients may show an increased erythrocyte sedimentation rate, which suggests ongoing inflammation (101). Although the purified protein derivative test has little value in diagnosing GM itself, it is still helpful when TM needs to be ruled out (2).

.Inflammatory markers are helpful for assessing how active GM is. For instance, C-reactive protein, a common acute-phase protein, often rises during flares or if infection is present. Shifts in C-reactive protein levels can help gauge how severe the inflammation is. Some GM patients also show higher serum PRL, especially when breast tissue is damaged or inflamed. Therefore, if PRL is high, doctors usually recommend checking it again later to monitor any changes over time (100).

Immunological tests are used to rule out other immune disorders in the diagnostic process for GM. Therefore, if signs like erythema nodosum appear, it suggests possible immune-related mechanisms, as some GM patients do exhibit irregularities in their immune function (102, 103). In these situations, antinuclear antibody testing is useful to detect systemic lupus erythematosus or other connective tissue diseases. For GM patients with joint symptoms, rheumatoid factor testing helps exclude rheumatoid arthritis (91). Measuring immunoglobulins and complement proteins is also important for evaluating immune function and detecting possible immune issues, particularly in GM patients with systemic conditions or immune dysregulation (49, 103).

Breast ultrasound (USG) serves as the primary imaging technique for patients suspected of having GM. It clearly visualizes the lesion and can determine the number, size, and position of any abscesses. Common ultrasound features include irregular hypoechoic masses (Figure 3A) and multiple fluid-filled abscesses (Figures 3B,C). These findings are often accompanied by skin thickening, subcutaneous edema, and axillary lymphadenopathy (Figure 3D). Tubular hypoechoic areas on ultrasound may suggest duct involvement or fistula formation. Concurrently, color Doppler imaging frequently demonstrates increased blood flow around abscesses, aiding in the assessment of inflammatory activity and severity (104).

Magnetic resonance imaging (MRI) plays a useful role in both diagnosing and monitoring GM. MRI provides excellent soft tissue resolution, making it a key tool for complex cases. This version uses “provides clear pictures” and “how well treatment is working” for simpler expression, and connects the two sentences with “Because of this capability” for natural flow. MRI provides clear pictures that help doctors evaluate a lesion’s size, level of inflammation, and how well treatment is working. Because of this capability, it is especially valuable when ultrasound findings are inconclusive or when more precise details about the lesion are needed (105).

On MRI, GM most commonly presents as non-mass enhancement. This pattern frequently occurs in a segmental, ductal, or regional distribution, suggesting inflammatory changes. When a mass is present, it typically exhibits irregular borders and marginal enhancement, potentially indicating abscess formation or necrotic tissue (106). On T1-weighted images, these lesions usually appear as low signal intensity. On T2-weighted fat-suppressed sequences, lesions appear hyperintense, reflecting their fluid-rich, inflammatory nature. Although most GM lesions exhibit a Type I time-signal curve, a minority demonstrate a Type III curve. This Type III pattern overlaps with the typical curve seen in breast cancer (107). Diffusion-weighted imaging frequently demonstrates diffusion restriction in GM lesions, manifested as low apparent diffusion coefficient values—a feature also observed in inflammatory breast cancer (IBC). Accurate diagnosis requires integrating these MRI findings with clinical presentation and other imaging results for comprehensive interpretation (108). In the management of GM, MRI serves several important purposes. Firstly, it helps determine the exact location and extent of lesions. It also monitors how the disease changes throughout treatment. Furthermore, MRI assesses long-term treatment effectiveness, offering essential imaging support across the entire care process (105).

In its symptoms and imaging features, GM can look very similar to a common breast abscess or to cancers like IBC. Because of this similarity, a definite diagnosis cannot be made on clinical and radiological findings alone and usually requires a core needle biopsy for tissue analysis (98). The key pathological feature of GM is non-caseating granulomatous inflammation centered on breast lobules. Lesions are often distributed in multiple foci, which can partially or completely destroy the normal lobular architecture. The inflammatory infiltrate consists of neutrophils, lymphocytes, plasma cells, eosinophils, and epithelioid histiocytes. These cells gather to form granulomas within the affected area, sometimes accompanied by sterile microabscesses, as shown in Figures 4, 5 (23, 95). Some cases also show dilation of ducts within and between lobules, along with fat necrosis and fibrosis. These features are important for diagnosing GM and distinguishing it from other conditions (23).

Therapeutically, GM presents a distinct clinical challenge. As an idiopathic granulomatous inflammation of unknown etiology, its management remains controversial in clinical practice. Commonly employed treatment modalities include observation, oral antibiotics, glucocorticoids (GCs), surgical excision, and oral traditional Chinese medicine therapy (6). GM is considered to have a self-limiting nature. According to the literature, approximately 50% of GM patients may experience a natural remission period ranging from 2 to 24 months (2). Studies have shown that for localized lesions that are small, unilateral, and have not formed abscesses or chronic sinus tracts, some patients can undergo spontaneous resolution without pharmacological or surgical intervention (109). Therefore, for patients with mild, localized clinical symptoms that show no signs of rapid progression, a conservative strategy of regular clinical surveillance is justifiable after thorough patient-clinician communication. However, a meta-analysis incorporating 4,735 patients indicated that the recurrence rate under a simple watchful waiting approach was significantly higher compared to other active interventions (110).

In the therapeutic management of GM, antibiotic use should be reserved for cases with clear indications and requires prudent consideration. This recommendation primarily stems from the possible concomitant bacterial infection observed in some cases, with Corynebacterium being a notable example (111). A retrospective study utilizing clarithromycin as first-line therapy reported an average time to clinical remission of approximately 8 months, suggesting its potential efficacy in specific scenarios. However, the therapeutic benefit is significantly limited, as antibiotic monotherapy often proves insufficient to adequately control the disease course. The same study found that nearly one-third of patients experienced recurrence during follow-up, and almost half required combination therapy with GCs to effectively manage inflammation (112). Consequently, current consensus emphasizes that once GM is diagnosed, empirical long-term antibiotic therapy without clear indications should be avoided (104).

GCs currently represent an effective therapeutic approach for GM (113). Clinical studies have confirmed that approximately 80% of GM cases respond effectively to GC treatment, making GCs a first-line option for moderate to severe or progressive GM (114). However, there is no standardized protocol for the clinical use of GCs. The typical initial dose ranges from 0.5 to 1 mg/kg/day in prednisone equivalent, maintained for several weeks, and is then tapered gradually based on the treatment response (114, 115). This systemic administration can achieve complete remission in most patients, although the treatment duration is prolonged, with a median time to remission reaching 159 days in one study (116). GC therapy is confronted with two major challenges: a high recurrence rate and significant side effects. Approximately 50% of responders experience relapse within 1–2 months after discontinuation, with some patients even requiring a second treatment course (114). Furthermore, long-term or high-dose use can lead to adverse effects such as Cushing’s syndrome, weight gain, and hyperglycemia (2, 117).

While traditional oral systemic administration remains the mainstay of treatment, topical application of GCs is emerging as an alternative approach that reduces systemic side effects and is gaining recognition (114, 118). Studies indicate that topical therapy can induce a clinical response in over 80% of patients within 12 weeks, with associated lower rates of recurrence and side effects (118).

Prior to the use of GCs for GM management, surgical excision was the primary therapeutic approach (5). Surgical options included procedures such as wide local excision, partial mastectomy, and total mastectomy, with the goal of completely removing the involved inflammatory tissue (8). For cases complicated by abscess formation, ultrasound-guided needle aspiration or surgical incision and drainage are essential interventions (119). However, surgical intervention carries significant limitations. The foremost concern is the high recurrence rate. According to the literature, the overall recurrence rate of GM ranges from 5 to 50%, whereas recurrence following surgical excision can be as high as 50% (13). Furthermore, surgery may lead to a range of complications, including delayed wound healing, poor cosmetic outcome, mammary fistula formation, nipple retraction, skin flap necrosis, hematoma, and chronic pain (120). Given these limitations, surgery is not considered an essential or first-line treatment for GM. It is primarily indicated for the following scenarios: 1 failure of pharmacological therapy; 2 contraindications to drug treatment, such as pregnancy; and 3 localized abscesses that have failed needle aspiration drainage (109, 117, 121). For the rare, refractory cases in which all other medical approaches have been exhausted, mastectomy may be considered as a last resort (114).

For GM patients who have not responded to antibiotics, GCs, or surgery, immunosuppressants serve as an important subsequent treatment option. Among these, methotrexate is the most widely used agent, typically employed as second-line therapy or in combination with GCs (114). Studies have demonstrated that for cases refractory to antibiotics, GCs, and surgery, treatment with methotrexate achieved improvement in 94% of patients and clinical remission in 75% after a 15-month course (15). When an methotrexate and GC combination regimen is employed, case series reports indicate that complete symptom resolution can be achieved in 72 to 100% of patients, typically within 2 to 4 months of treatment (114). However, potential side effects, such as elevated liver enzymes and alopecia, necessitate its use under the collaborative management of rheumatology and breast specialists (122).

While conventional treatments for GM often face challenges such as high recurrence rates and drug-related side effects, recent years have witnessed the emergence of novel therapeutic approaches targeting its immunopathological mechanisms, providing clinicians with expanded options.

For patients with refractory or severe GM who respond poorly to conventional therapies, biologic agents targeting TNF-α have shown promise. In one study, a patient who failed intensive GC and methotrexate therapy demonstrated marked improvement after treatment with the TNF-α inhibitor adalimumab (123). More compelling evidence comes from a well-documented case involving a GM patient with concurrent psoriasis. The patient’s symptoms resolved with adalimumab, recurred upon discontinuation, and rapidly improved again within 1 week of re-initiating the treatment, providing robust evidence for the drug’s direct therapeutic effect (124). These case reports suggest that TNF-α inhibitors may serve as a potential effective alternative to surgery and non-systemic GC therapy.

By blocking the JAK–STAT signaling pathway, JAK inhibitors broadly suppress the inflammatory response at its upstream source, offering a novel oral targeted therapeutic strategy for GM (23, 71). Although direct clinical data on JAK inhibitors for GM are still accumulating, their mechanism of action is highly relevant to the immunological features of GM. This relevance is supported by the established efficacy of JAK inhibitors in other conditions such as rheumatoid arthritis. Therefore, they offer a novel conceptual direction for GM treatment (23, 125, 126).

Intraductal lavage therapy represents an innovative local treatment, which involves pumping medicated irrigating fluid into the affected ducts for lavage. A prospective study demonstrated that this approach achieved a clinical complete remission rate exceeding 90% at 1 year, with no significant adverse events reported (127). This suggests that local intraductal lavage therapy may represent one of the future directions for therapeutic optimization.

Intralesional steroid injection involves the direct administration of GCs into granulomatous lesions, thereby achieving a potent localized anti-inflammatory effect while minimizing systemic exposure and associated side effects (124, 128). A prospective controlled study confirmed that patients receiving intralesional injection combined with topical steroid application demonstrated a significantly higher response rate at 3 months and a notably lower recurrence rate compared to those on oral steroids alone. Moreover, systemic side effects were predominantly observed in the oral steroid group (128).

While GCs and immunosuppressants form the cornerstone of conventional Western medical therapy for GM, their long-term administration is limited by associated side effects in clinical practice (2). Against this backdrop, Traditional Chinese Medicine (TCM), which emphasizes holistic regulation, has gained increasing attention as a complementary therapeutic approach. TCM treatment is not merely a list of herbal formulas but constitutes a systematic therapeutic strategy guided by its own theoretical framework. Based on clinical practice, different TCM practitioners hold varying interpretations regarding the pathogenesis of GM. For instance, Professor Lin Yi classifies GM within the TCM disease category of “sores and ulcers”, considering it predominantly a “Yin syndrome.” He emphasizes that internal treatment in the later stages should primarily focus on fortifying the spleen, replenishing qi, and harmonizing the nutrient aspect, aiming to promote wound healing and shorten the disease course (129). Professor Lou Lihua posits that the disease fundamentally involves Yang Qi deficiency with cold congelation and phlegm stagnation. The treatment should therefore follow the principles of warming Yang and dissipating cold, resolving phlegm and dispersing stagnation, as well as nourishing blood and freeing stagnation. The formula Yanghe Decoction, modified according to presentation, is applied. This approach is suitable for patients presenting with breast masses of a deficiency-cold nature (130).

Here, we adopt the framework outlined in the Beijing Expert Consensus on the Integrated Traditional Chinese and Western Medicine Diagnosis and Treatment of Granulomatous Mastitis (2025 Edition), classifying GM into three fundamental patterns for pattern-based treatment: Liver Qi Stagnation with Phlegm Coagulation Pattern, Intense Heat Toxin Pattern, and Yang Deficiency with Toxin Accumulation Pattern (131). The Liver Qi Stagnation with Phlegm Coagulation Pattern predominantly manifests in the early stages of the disease. It is treated by soothing the liver and regulating qi, resolving phlegm and dissipating nodules, with a representative formula being the classical formula Chaihu Qinggan Tang from The Orthodox Lineage of External Medicine (131, 132). Studies have demonstrated that the combination of Chaihu Qinggan Decoction with prednisone can modulate immune function. This is specifically manifested as an increase in peripheral blood levels of CD3 + and CD4 + T cells and the CD4+/CD8 + ratio, alongside a reduction in immunoglobulin levels such as IgG, IgA, and IgM. These findings suggest that the therapeutic effect may be mediated by restoring the balance of T lymphocyte subsets and suppressing excessive humoral immunity (132). The Intense Heat Toxin Pattern corresponds to the stage of acute inflammation or abscess formation. The treatment principle focuses on clearing heat and draining fire, cooling blood and resolving toxin, typically using modified formulations based on the Heat-Clearing and Toxin-Resolving Formula (131). Research indicates that the Heat-Clearing and Toxin-Resolving Formula not only significantly reduces the area of breast redness and swelling as well as the size of masses, but also decreases serum levels of white blood cell count, neutrophil count, and C-reactive protein, demonstrating both anti-inflammatory and immune-modulating effects. Modern pharmacological studies confirm that core herbal components of the formula, such as Forsythia suspensa and Taraxacum mongolicum, may alleviate the inflammatory response by inhibiting signaling pathways including NF-κB, thereby downregulating the expression of pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α (133). The Yang Deficiency with Toxin Accumulation Pattern is commonly seen in a state of deficiency and lingering illness, characterized by protracted disease course and non-healing wounds. Yanghe Decoction, as a representative formula for warming Yang and freeing stagnation, can improve the local microenvironment of yin-cold congelation and stagnation, thereby promoting tissue repair and wound healing (131). Zhang et al. (134) found that Yanghe Decoction combined with surgical intervention demonstrated a higher cure rate and a lower recurrence rate compared to surgery alone, suggesting its therapeutic potential in the management of GM. Moreover, modern research has found that Modified Yanghe Decoction can downregulate the expression of pyroptosis-related proteins, such as NLRP3 and Caspase-1, in GM lesions. Given that the pyroptosis pathway has been shown to be activated in GM lesions, this finding suggests that the herbal formula may exert its therapeutic effect by modulating this inflammatory cell death pathway (135, 136).

For GM cases that have progressed to abscess formation or ulceration, external treatment methods such as Tounong San irrigation and drainage or external application of Jinhuang Gao can be employed to promote pus discharge, reduce swelling, and alleviate pain (86, 137). A clinical study demonstrated that the combined use of Chinese herbal decoctions with external application of Jinhuang Gao effectively increased the proportion of peripheral blood Treg cells and the levels of IL-10 and TGF-β1, thereby regulating the Treg/Th17 immune balance. This regimen also showed favorable safety and a lower recurrence rate (86). Additionally, therapies such as fire-needle cupping and pricking-cupping can clear meridians and drain heat-toxins through physical stimulation (35). A large-scale clinical observation demonstrated that the therapeutic approach of “Regulating Qi and Harmonizing the Nutrient System” combined with fire-needle cupping achieved a total effective rate of 86.38% in treating GM. This regimen significantly increased the levels of peripheral blood CD3+, CD4+, and CD8 + T cells, while reducing the levels of NK cells, IgM, and complement components C3/C4, thereby improving clinical symptoms and comprehensively modulating immune function (138).

TCM treatment alone offers advantages such as a favorable safety profile and preservation of breast aesthetics, but it typically requires a relatively long treatment duration (35, 139). Therefore, integrated traditional Chinese and Western medicine has become a key strategy in the current clinical management of GM. For instance, a study employing a combination of Chinese herbal medicine and surgical excision with suture reported that this regimen significantly improved the cure rate, shortened the treatment course, and reduced the rate of lesion suppuration (140). Furthermore, the combination of Western pharmaceuticals with targeted Chinese herbal penetration therapy has also demonstrated advantages in enhancing the overall response rate, reducing recurrence, alleviating symptoms, and preserving breast aesthetics (141).

In summary, through the principles of pattern differentiation and multi-pathway intervention, TCM demonstrates significant potential in the treatment of GM by enhancing therapeutic efficacy, reducing recurrence rates, and mitigating the side effects associated with conventional Western medications. Nevertheless, the current body of evidence predominantly originates from small-sample, retrospective studies, and the level of evidence requires further elevation. Future efforts should prioritize well-designed prospective randomized controlled trials to generate higher-level evidence, coupled with in-depth pharmacological research to elucidate the underlying mechanisms of action (142).