The recognition and treatment of osteochondral injuries of the talus have been the subjects of worldwide debate [7,8,9]. The exact history of the injury is hardly known in most cases, and medical records rarely document it because early asymptomatic injury can be easily overlooked . Studies have reported that 25–50% of patients with ankle sprains will experience chronic long-term ankle pain for several years after the initial injury (sprain) [11,12,13]. Therefore, the exact incidence of osteochondral injuries remains unknown, with only one study stating that 27 patients suffered from osteochondral injuries per 100 000 people between 1998 and 2008 . Draper et al. found that the incidence of chronic injuries to the talus due to ankle instability was up to 50% [15, 16].
Patients with chronic pain in the ankle joint are common in clinical practice . When the density of the talus is altered on the first radiograph, the attending physician often habitually diagnoses osteonecrosis of the talus. In the medical literature, the terms osteonecrosis and ischemic necrosis have been used interchangeably for bone death due to impaired circulation . This necrosis is often considered to be caused by a circulatory disorder. Thus, osteonecrosis of the talus seems to be a shorthand or synonym for ischemic necrosis of the talus. In contrast, the main clinical causes of ischemic necrosis of the talus are interruption of arterial blood supply and avulsion of the periosteal vascular network of the talar articular surface due to fracture of the talar neck and ankle dislocation. In our cases, there was no history of fracture or dislocation, and the local blood supply, bone metabolism, and pathology of the lesion showed different features from those of ischemic necrosis of the talus.
Three-phase bone imaging showed no ischemia in and around the cystic area of the talus. Compared with the healthy side, the cystic area showed significant concentrations of tracer and abundant blood flow. The blood flow and blood pool phases of the three-phase bone imaging represent the state of blood supply to the lower extremity (especially around the ankle joint) in the arterial and venous phases, respectively. The arterial phase of the affected side is congested, and the dorsalis pedis is patent without stenosis or occlusion, and slightly more congested than on the healthy side. The blood pool image is of the venous phase, with apparent concentrations of tracer at the talus, indicating stasis of blood flow in the venous phase. The static phase (the delayed phase) shows increased subarticular uptake, implying an active bone metabolism that extends over the entire medial or lateral aspect of the talus.
Different trauma mechanisms correspond to different injury sites. Some scholars believe that osteochondral injuries of the talus have a typical site of onset, namely the medial fornix or the lateral fornix of the talus, with the medial fornix being particularly common [19,20,21]. A study at Tong Ren Hospital in China found that medial injury accounted for 76% of injuries . Elias et al. found that injuries located in the medial third were larger and deeper than those located elsewhere . Cao et al. noted that deeper-position cystic changes in the medial subchondral talus were typical of patients over 60 years of age with talar cartilage injuries .
In this study, most of the patients had medial fornix injuries due to dorsal extension and internal rotation. In the more severe cases, the posterior part of the medial fornix was also involved, with almost no cases showing posterior involvement alone. In larger cases, the extent of injuries can extend from the anterior to the posterior part of the medial fornix of the talus. We conclude that cystic lesions typically begin from the anterior to the middle of the medial fornix, with the middle and anterior parts being the main areas of involvement. As the disease progresses, it continues to expand anteriorly and posteriorly. Distinguishing them from post-fracture talar necrosis, our cases, regardless of size, did not reveal nodal fracture or collapse of the talar fornix. The curvilinear morphology of the articular surface of the talar fornix remained, and the bony articular surface could be phenotypic but was never sunken. In contrast, ischemic necrosis of the talar articular surface often shows collapses of the necrotic bone tissue, loss of the normal morphology of the bony articular surface, and compression and flattening of the fornix.
The application of SPECT/CT, a new multimodality imaging method for patients with cystic lesions of the talus, allows assessment of the hemodynamic metabolic status of OLTs in real-time. The subchondral bone cystic lesion and surrounding area show the highest activity, whereas the rest of the talus presents a normal physiological bone metabolic zone [24,25,26]. The sclerotic zone is located at the junction of the lesion area and normal tissue, which is a zone rich in blood flow and new capillaries and shows active bone metabolism. An obvious concentration of tracer is located in the anterior part of the talar fornix and the stress point of the dorsal extension of the tibial talar joint, where the sclerotic zone is most concentrated, bone metabolism is most active, and blood flow is most abundant.
Simultaneous CT imaging showed alterations in the bone density of the talus, with the CT values varying greatly with the size of the cyst. This is because the smaller the cyst, the more it is affected by partial volume effects, with the measurement being subject to errors. Around subchondral bone cystic lesions, calcium salt deposits form unevenly-thickened sclerotic bands that provide strong mechanical support, especially in the weight-bearing zone of the tibial talar joint and at mechanical stress points. The sclerotic zone represents compensatory repair and an active response to injury. The joint is attempting to protect itself and restore the stability of its mechanical properties while restoring the original bone structure.
The functional imaging of blood metabolism on SPECT, the imaging of sclerotic zone morphology of CT, and the expression of multiple cellular components on pathology, comprehensively explain why collapse occurs in femoral head necrosis, but not in the articular surface of the talar vault. Although it is a weight-bearing joint like the hip and knee, the talus has a smaller weight-bearing area than the femur and carries almost the entire body’s mass. It is subject to more stress than the knee and hip and is more likely to be injured. Our SPECT/CT study confirmed that the blood supply to the affected limb was increased, and that the ankle joint showed rich blood circulation and active bone metabolism.
In the large cysts, the pathology showed the following features consistent with the SPECT/CT findings: (1) a tortuous fibrocystic wall; (2) numerous dense fibroblast proliferations and abundant collagen fibers; (3) granulation tissue and inflammatory cell aggregation around the cyst wall; and (4) chondrogenesis with ossification and active osteogenesis around the necrotic lesion. The pathologically-active chondrogenesis and ossification explain the abnormal concentration of tracers in the cystic cavity on SPECT/CT static fusion images. The presence of osteogenic repair activity within the cystic lesion is secondary to the injury. Focal necrosis of the talar injury occurs in conjunction with a marked congestive and inflammatory response, active fibrous and bone repair, and rapid formation of a sclerotic shell of protective new bone around the cystic lesion. It maintains the overall integrity and normal morphology of the articular surface of the talus under considerable stress. This is in contrast to the deformation of the femoral head caused by massive osteonecrosis in aseptic femoral head necrosis. However, many questions about the definite cause of cystic degeneration after talar injury and the process of its repair still remain for our further research. At present, it is still the best clinical treatment option, being minimally invasive and providing a means for bone grafting to revascularize and provide osteoinduction and osteoconduction [27, 28], thereby enhancing local support and improving ankle stability.
The causes of OLT formation are a popular issue of interest to many scholars, and these causes may be multifaceted. Cystic lesions are associated with trauma and are a part of osteochondral damage. Continuous small cystic lesion formation is typically distributed over the joint surface and occurs where the most force is exerted. When external forces are less than the shear forces that the cartilage can withstand but greater than those that the subchondral bone can withstand, a fracture or microfracture of the subchondral bone will occur in the presence of cartilage. Furthermore, the local microenvironment is altered, resulting in a focal necrotic capsular lesion. OLS differs from ischemic necrosis in that the talus is rich in blood flow and osteogenic activity, allowing for immediate repair and reconstruction. For treatment, minimally invasive surgery that takes full advantage of this and performs drilling combined with bone grafting is the recommended method. In conclusion, SPECT/CT three-phase bone imaging is advantageous for identifying the cause of talar injury, while SPECT/CT delayed imaging is advantageous for observing the location, extent of involvement, classification, and repair of cystic lesions in the talus.