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Orthopedics
Musculoskeletal disorders, standing as the fifth leading cause of disability-adjusted life years globally, present significant challenges in orthopedics. Osteochondritis dissecans (OCD) and avascular necrosis (AVN) are distinct but closely related conditions within this spectrum, impacting patients’ quality of life with pain, limited mobility, and dysfunction. OCD, involving cartilage and bone detachment in joints, predominantly affects young athletes, but its exact etiology and optimal management remain subjects of ongoing research. Conversely, AVN, marked by bone tissue death due to compromised blood supply, is linked to systemic factors like corticosteroid use and traumatic injuries. Diagnosis for both conditions relies on radiography and magnetic resonance imaging. Conservative treatment for AVN includes the use of a cane or crutches, pharmacological therapy, or physical therapy. On the other hand, in OCD, the primary approach is activity/sports restriction. Surgical treatment options for AVN patients encompass core decompression, bone grafting, or, in the most advanced cases, total hip arthroplasty. OCD may be surgically treated through subchondral drilling or fixation of unstable lesions.
- osteochondritis dissecans
- avascular necrosis
- orthopedic
1. Introduction
Musculoskeletal disorders pose significant challenges in the field of orthopedics, affecting individuals of all ages and activity levels [1,2,3,4]. In 2017, musculoskeletal disorders ranked as the fifth leading cause of disability-adjusted life years (DALYs) worldwide and represented the primary contributor to global disability [5].
Among these disorders, osteochondritis dissecans (OCD) and avascular necrosis (AVN) stand out as two distinct but sometimes closely related conditions that can severely impact the quality of patients’ lives. Both conditions affect the integrity of bone and cartilage, often leading to pain, limited mobility, and long-term dysfunction [6,7,8,9,10]. De Smet [11] highlighted three key similarities between OCD and AVN. (1) The most frequent location for both types of lesions is the femoral condyles when the knee is affected. (2) In their advanced stages, both OCD and AVN can show similar radiographic features, such as the collapse of the subchondral bone plate, which can lead to the formation of intra-articular loose bodies. (3) Histologically, both conditions may present similarly with the presence of necrotic bone in the affected areas.
OCD, characterized by the detachment of cartilage and bone fragments within a joint, has long been a subject of clinical interest and debate. While it predominantly affects younger individuals, often athletes, and is believed to be linked to mechanical stress and repetitive trauma, its precise etiology and optimal management strategies remain topics of active research [8,9]. On the other hand, AVN, which most often occurs in the middle-aged and elderly, marked by the death of bone tissue due to compromised blood supply, is frequently associated with various factors, such as corticosteroid use, alcohol abuse, and traumatic injuries. Understanding the fundamental differences between these two conditions is vital for accurate diagnosis and timely intervention [6,7,11].
2. Nonsurgical Treatment
Nonsurgical treatment focuses on preventing bone collapse, delaying necrosis, and providing pain relief. It is primarily employed in patients with early-stage disease (Steinberg’s 0–1). The non-weight bearing, use of a cane, crutches, or a walker is one method to slow down disease progression [6,71,72,73]. The conservative treatment of humeral AVN involves lifestyle changes and avoiding intense shoulder movements like excessive abduction and flexion, while still maintaining flexibility through passive range of motion exercises [74].
Pharmacological treatment encompasses anticoagulants, statins, vasodilators, or bisphosphonates [73,75,76,77,78,79,80]. Enoxaparin is known to enhance arterial circulation and lessen hypoxia, potentially slowing down or reversing the effects of ischemic osteonecrosis [80]. In a similar vein, the bisphosphonate drug alendronate has demonstrated efficacy in reducing the occurrence of vertebral compression fractures, and it may also help prevent the deterioration of a femoral head affected by osteonecrosis [75]. Additionally, iloprost, a different medication, causes vasodilation, thereby improving microcirculation and boosting blood flow [79]. Regarding the treatment of AVN, statins work by inhibiting the formation of fat cells and encouraging the formation of bone cells. This is achieved through the downregulation of PPARγ2 and the upregulation of Cbfa1/Runx2 in bone marrow mesenchymal cells. The effect of statins is observed mainly in patients with corticosteroid-related AVN [77].
However, data on these drugs are limited, and specific guidelines for their use in AVN are lacking. Patients may also use pain relief drugs such as nonsteroidal anti-inflammatory drugs and acetaminophen [41].
Additional non-surgical therapies involve extracorporeal shockwave therapy or pulsed electromagnetic fields, which stimulate osteoblastic activity and alleviate pain [72,81,82,83]. Certain studies have reported positive outcomes with hyperbaric oxygen therapy in individuals with early-stage AVN. Hyperbaric oxygen enhances extracellular oxygen concentration, induces vasoconstriction, and reduces ischemia and edema [84,85].
Nonsurgical treatment for OCD is particularly intended for skeletally immature patients with stable lesions and minimal symptoms. The primary recommendation involves activity/sports restriction. Other procedures include immobilization through casting, bracing, splinting, weight-bearing restriction, and muscle-strengthening exercises. This form of treatment should be administered for a duration of 3–6 months [8,35,45]. Some authors have raised concerns about the consequences of prolonged immobilization, particularly regarding the development of stiffness [86,87]. Tepolt et al. suggested that short-term protected weight-bearing using crutches is likely advantageous. They also mentioned that the use of bracing could be based on the provider’s preference and a collaborative decision-making process involving the families [87].
Pharmacotherapy of OCD most often includes non-steroidal anti-inflammatory drugs [36].
3. Surgical Treatment
Surgical approaches for patients with AVN may differ based on whether it is in the early or late stages. In the early stages, core decompression is a common treatment method aimed at reducing intraosseous pressure and restoring normal blood flow. The method has evolved over time from single drilling to multiple drillings [88,89,90,91,92,93]. The number of drillings and trephine diameter should be chosen individually to minimize morbidity and the risk of bone weakening [94].
Bone grafts may be vascularized or nonvascularized and have various origins (allograft, autograft, or artificial). The procedure can be performed after core decompression or in combination using the core decompression tract. Vascularized grafting not only enhances subchondral architecture but also reinstates circulation in the affected area [95,96,97,98,99].
Total hip arthroplasty is considered for patients with significant femoral head collapse and a substantial decrease in quality of life. This method has shown good outcomes, and modern ceramic, low-wear, friction torques are a reasonable choice for young, active patients [100,101]. In patients with talus AVN, partial or total talar replacement has shown promising results [72]. Knee and humeral arthroplasty may also be successful treatments in advanced cases of AVN [102,103].
Surgical treatment for OCD is reserved for patients with unstable lesions after the failure of nonoperative treatment. In less advanced cases, subchondral drilling (transarticular or retroarticular) is commonly employed. This method stimulates the influx of mesenchymal cells and growth factors, leading to neovascularization and ossification of the cartilaginous lesion [35,36,37,104,105,106,107]. The results of OCD drilling are generally positive, showing high rates of healing and low complication rates in most cases [108,109].
Managing unstable OCD lesions involves articular surface restoration, fracture fixation, and vascular enhancement. Numerous techniques are available for fixing unstable OCD lesions, including screws, anchors, arrows, and pins, which can be implanted arthroscopically or during open surgery. Regardless, a critical step involves precise debridement for the removal of fibrotic tissue and drilling to create vascular channels, aiming to maximize revascularization and enhance the cure rate [8]. Fixation is recommended for detached osteochondral fragments, and a hybrid model, combining metallic or resorbable mechanical compression screws with osteochondral autograft transplantation, has been recently employed [8,36]. This procedure shows promising short-term outcomes with a low complication rate [37,110,111,112].
In large lesions with excessive fragmentation, fixation is not possible. In such cases, the affected fragment is removed, and cartilage salvage and resurfacing techniques are employed. These may include microfractures, autologous chondrocyte implantation, bone marrow stimulation, fresh osteochondral allografts, or autologous chondrocyte transplantation [8,45].
4. Biologic Treatment
Biological therapies for AVN primarily focus on treating the condition when it is present in the femur. The technique primarily involves the injection of mesenchymal stem cells or osteoinductive agents like bone morphogenic proteins. The goal of this approach is to initiate revascularization and regenerate bone [113,114]. It can be combined with core decompression, which has promising results [115]. The findings from two meta-analyses suggested that the combined use of core decompression and autologous bone marrow-derived mesenchymal stem cells is more effective in providing pain relief and improving clinical outcomes compared to core decompression alone in the treatment of osteonecrosis of the femoral head. Additionally, this combined approach can more effectively delay the collapse of the femoral head [116,117].
This entry is adapted from the peer-reviewed paper 10.3390/jcm13010287
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