• 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • In this study all tumors were Campanacci stage


    In this study, all tumors were Campanacci stage 3, which is a significantly higher proportion than in our database [9]. Such a high stage usually suggests that a tumor is highly aggressive and may be a high-risk factor for lung metastasis. Previous reports have also suggested that the stage of a GCTB may be related to lung metastasis. Chan et al. [13] reported that all patients with lung metastasis had stage 3 tumors, and Dominkus et al. [7] reported that most patients with lung metastasis had stage 3 tumors. Faisham et al. [18] reported that the metastasis rate of Campanacci stage 3 GCTB was as high as 30%. The recurrence rate in our database [9] was 12.4%, and that in the present study was 73.9%. This significant difference suggests that local recurrence is correlated with pulmonary metastasis. Niu et al. [9] reported that the metastasis rate was 8.6% in patients with recurrence and only 2.4% in those without recurrence. Rock [19] reported that the metastatic risk in patients with recurrence was six times higher than that in patients without recurrence. Many other reports [5,16,20–22] have also supported that the recurrence is a high-risk factor. A study at the Rizzoli Institute [4] revealed a 71% recurrence rate among patients with metastasis and only a 29% recurrence rate among those without metastasis. Therefore, monitoring of the pulmonary condition is very important for patients with postoperative recurrence. Some authors [23,24] have suggested that pulmonary metastases are related to the type of surgery performed for the primary tumor. The surgery itself, not the invasiveness of the tumor, might lead to vascular differentiation because surgical manipulation enables implantation of tumor protoporphyrin ix in the lung. Most pulmonary metastases occur postoperatively, but this does not occur for several years or even >10 years postoperatively in some patients. Therefore, there is not enough evidence to prove the relationship between surgery and metastasis. Kay et al. [25] suggested that the surgical method was a risk factor. All six patients with pulmonary metastasis had undergone curettage of the primary tumor, but not resection. The present study showed similar results in that the patients who underwent resection of the primary lesion had a lower metastasis rate. This should be related to the lower rate of local recurrence among patients who underwent resection. In our previous study [9], the local recurrence rate in the resection group (1.6%) was significantly lower than that in the curettage group (8.6%). A low local recurrence rate is related to a low lung metastasis rate. Curettage is currently the most common and effective method for the treatment of GCTB. We applied extended curettage for GCTB and achieved satisfactory local control. Therefore, even if an association between surgery and pulmonary metastasis exists, the benefits (good local control and retention of the articular surface) are obvious. With respect to the relationship between vascular invasion and lung metastasis, Sladden [26] reported five patients with tumor invasion of blood vessels, but no metastasis was found. Other studies [27,28] have shown that the presence of an intravascular tumor thrombus did not increase the risk of pulmonary metastasis.
    Conflict of interest statement
    Ethical review committee statement
    Conflict of interest statement
    Introduction Breast cancer is the most frequent cancer in women leading to a significant morbidity and mortality [1]. Early diagnosis and improved treatment regimens have significantly increased survival leading to a greater potential for experiencing long term side effects from cancer treatments including bone loss and fractures. Skeletal homeostasis is achieved through coupled and balanced bone resorption and bone formation. Several local and systemic factors regulate these processes, including estrogen, a key regulator of bone resorption. Physiologic decreases in estrogen levels after menopause lead to an increased risk for osteoporosis (low bone mineral density [BMD]) and fractures, and this risk can be exacerbated by breast cancer and its therapies [2]. Systemic therapies for breast cancer can additionally interfere with bone turnover, either through their effects on gonadal steroid hormone production or by inhibiting peripheral aromatization into estrogen [2–4]. In addition, some therapies for breast cancer might directly affect bone formation [5]. Regardless of the underlying mechanism, patients with breast cancer are at risk for cancer treatment-induced bone loss (CTIBL).