Arthroscopic treatment for anterolateral impingement of the ankle: Systematic review and exploration of evidence about role of ankle instability.

Background: Arthroscopic debridement is a common surgical treatment for patients with anterolateral impingement (ALI) of the ankle. Although they often have a history of ankle sprain, information regarding the role of ankle instability in ALI is limited. The aims of this review were to: 1) assess the clinical outcomes of arthroscopic surgical treatment for ALI of the ankle; and 2) review the data regarding anterior talofibular ligament (ATFL) injury and lateral ankle instability in patients who underwent arthroscopic surgery for ALI.

All-inside endoscopic anatomic reconstruction leads to satisfactory functional outcomes in patients with chronic ankle instability.

Purpose: Ankle sprain is a common injury that can be treated conservatively, though many injured patients do not seek treatment or are not adequately managed, both of which can lead to subsequent chronic ankle instability (CAI). The purpose of this study was to evaluate the functional scores and complication rates of an all-inside anatomic reconstruction technique to treat CAI at a minimum follow-up of 24 months.

Methods: The authors retrospectively collected the records of 41 patients that underwent all-inside endoscopic anatomic reconstruction of the ATFL and CFL including demographics, complications, satisfaction, American Orthopaedic Foot and Ankle Society (AOFAS) score, Karlsson score, and ankle activity score (AAS), at a minimum follow-up of 24 months.

All-Inside Endoscopic Broström-Gould Technique.

Ankle sprain is the most frequent sports trauma. Surgical treatment is needed in case of chronical instability, after failure of conservative treatment. The technique established today worldwide consists in repairing the ligament (Broström technique) and strengthening the repair by adding extensor retinaculum (Gould technique).

Arthroscopic classification of chronic anterior talo-fibular ligament lesions in chronic ankle instability.

Background: The surgical treatment of chronic ankle instability (CAI) relies chiefly on anterior talo-fibular ligament (ATFL) repair (with or without augmentation) or anatomical reconstruction with a tendon graft. Arthroscopy enables not only a complete assessment and the same-stage treatment of concomitant articular lesions, but also an accurate assessment of ligament lesions. Pre-operative imaging studies (MRI, CT, US) may fail to provide sufficient detail about chronic ATFL lesions to guide the decision between repair and reconstruction.

Mice Deficient in Angiopoietin-like Protein 2 (Angptl2) Gene Show Increased Susceptibility to Bacterial Infection Due to Attenuated Macrophage Activity.

Macrophages play crucial roles in combatting infectious disease by promoting inflammation and phagocytosis. Angiopoietin-like protein 2 (ANGPTL2) is a secreted factor that induces tissue inflammation by attracting and activating macrophages to produce inflammatory cytokines in chronic inflammation-associated diseases such as obesity-associated metabolic syndrome, atherosclerosis, and rheumatoid arthritis. Here, we asked whether and how ANGPTL2 activates macrophages in the innate immune response.

ANGPTL2 increases bone metastasis of breast cancer cells through enhancing CXCR4 signaling.

Bone metastasis of breast cancer cells is a major concern, as it causes increased morbidity and mortality in patients. Bone tissue-derived CXCL12 preferentially recruits breast cancer cells expressing CXCR4 to bone metastatic sites. Thus, understanding how CXCR4 expression is regulated in breast cancer cells could suggest approaches to decrease bone metastasis of breast tumor cells.

Angiopoietin-like protein 2 renders colorectal cancer cells resistant to chemotherapy by activating spleen tyrosine kinase-phosphoinositide 3-kinase-dependent anti-apoptotic signaling.

Angiopoietin-like protein 2 (ANGPTL2) plays an important role in inflammatory carcinogenesis and tumor metastasis by activating tumor angiogenesis and tumor cell chemotaxis and invasiveness. However, it is unclear whether ANGPTL2 expression has an effect on tumor cell survival. Here, we explored that possibility by determining whether ANGPTL2 expression altered survival of human colorectal cancer cell lines treated with antineoplastic drugs.

Prolyl-4-hydroxylase domain 3 (PHD3) is a critical terminator for cell survival of macrophages under stress conditions.

On a molecular level, cells sense changes in oxygen availability through the PHDs, which regulate the protein stability of the α-subunit of the transcription factor HIF. Especially, PHD3 has been additionally associated with apoptotic cell death. We hypothesized that PHD3 plays a role in cell-fate decisions in macrophages.

Serum ANGPTL2 levels reflect clinical features of breast cancer patients: implications for the pathogenesis of breast cancer metastasis.

Introduction: Breast cancer is a leading cause of cancer-related death in women worldwide, and its metastasis is a major cause of disease mortality. Therefore, identification of the mechanisms underlying breast cancer metastasis is crucial for the development of therapeutic and diagnostic strategies. Our recent study of immunodeficient female mice transplanted with MDA-MB231 breast cancer cells demonstrated that tumor cell-derived angiopoietin-like protein 2 (ANGPTL2) accelerates metastasis through both increasing tumor cell migration in an autocrine/paracrine manner, and enhancing tumor angiogenesis.

Angiopoietin-like protein 2 induced by mechanical stress accelerates degeneration and hypertrophy of the ligamentum flavum in lumbar spinal canal stenosis.

Chronic inflammation and subsequent fibrosis induced by mechanical stress play an important role in ligamentum flavum (LF) hypertrophy and degeneration in patients with lumbar spinal canal stenosis (LSCS). Angiopoietin-like protein 2 (Angptl2) is a chronic inflammatory mediator induced under various pathological conditions and increases the expression of TGF-β1, which is a well-characterized mediator in LF hypertrophy. We investigated whether Angptl2 is induced by mechanical stress, and whether it contributes to LF hypertrophy and degeneration by activating the TGF-β1 signaling cascade.

The secreted protein ANGPTL2 promotes metastasis of osteosarcoma cells through integrin α5β1, p38 MAPK, and matrix metalloproteinases.

The tumor microenvironment can enhance the invasive capacity of tumor cells. We showed that expression of angiopoietin-like protein 2 (ANGPTL2) in osteosarcoma (OS) cell lines increased and the methylation of its promoter decreased with time when grown as xenografts in mice compared with culture. Compared with cells grown in normal culture conditions, the expression of genes encoding DNA demethylation-related enzymes increased in tumor cells implanted into mice or grown in hypoxic, serum-starved culture conditions.

Angiopoietin-like protein 2 accelerates carcinogenesis by activating chronic inflammation and oxidative stress.

Unlabelled: Chronic inflammation has received much attention as a risk factor for carcinogenesis. We recently reported that Angiopoietin-like protein 2 (Angptl2) facilitates inflammatory carcinogenesis and metastasis in a chemically induced squamous cell carcinoma (SCC) of the skin mouse model. In particular, we demonstrated that Angptl2-induced inflammation enhanced susceptibility of skin tissues to "preneoplastic change" and "malignant conversion" in SCC development; however, mechanisms underlying this activity remain unclear.

Tumor cell-derived angiopoietin-like protein ANGPTL2 is a critical driver of metastasis.

Strategies to inhibit metastasis have been mainly unsuccessful in part due to insufficient mechanistic understanding. Here, we report evidence of critical role for the angiopoietin-like protein 2 (ANGPTL2) in metastatic progression. In mice, Angptl2 has been implicated in inflammatory carcinogenesis but it has not been studied in human tumors.

Angiopoietin-like protein 2 is an important facilitator of inflammatory carcinogenesis and metastasis.

Chronic inflammation plays important roles at different stages of cancer development, including carcinogenesis, tumor invasion, and metastasis, but molecular mechanisms linking inflammation to cancer development have not been fully clarified. Here, we report that expression of angiopoietin-like protein 2 (Angptl2), recently identified as a chronic inflammation mediator, is highly correlated with the frequency of carcinogenesis in a chemically induced skin squamous cell carcinoma (SCC) mouse model. Furthermore, Angptl2 expression in SCC is highly correlated with the frequency of tumor cell metastasis to distant secondary organs and lymph nodes.