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Journal of Orthopedics & Bone Disorders Research Article 30 min read

Osteonecrosis of Femoral Head with a Special Note on COVID 19

Itha R* and Ravali RS*
* Corresponding author
ISSN: 2577-297X  10.23880/jobd-16000230  Received: February 09, 2023  Published: February 24, 2023
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Keywords
Osteonecrosis Avascular COVID Arthroplasty Core Decompression Stem Cell
Abstract

Background: A prevalent condition in hip joint surgery is osteonecrosis of the femoral head (ONFH). The blood supply to the femoral head is damaged or disrupted for a variety of reasons, which is followed by a succession of pathological alterations and ultimately irreversible destruction of the hip joint. The disease SARS COVID 19 itself and the treatment of the condition with corticosteroids may cause ONFH. Various treatment methods have been described in literature depending on the stage of disease process. Purpose and Methods: The purpose of this review paper is to provide up to date details of the clinical evaluation, current diagnostic tools, and treatment modalities. We shall also mention a special note on the COVID 19. We reviewed several articles in the literature (Pubmed, Scopus, and Google Scholar) on this topic especially the mechanism of injury, diagnosis, and treatment methods to produce a review article. Conclusion: Osteonecrosis of the femoral head is caused by many conditions which ultimately cause the disruption of blood supply to the femoral head. The treatment methods vary with stage of the disease. The early stages can be managed with conservative methods and hip preserving surgeries whereas late stage condition with advanced osteoarthritis requires arthroplasty. The early recognition by clinical and radiological features the progression is reversed or slowed down. The high usage of corticosteroids during COVID 19 and its association with ONFH is a warning sign for the judicious usage of the same in future.

Introduction

Osteonecrosis of femoral head is characterized by bone cell death in a particular segment of the subchondral bone due to disturbance in blood supply to the femoral head. The prominent French anatomist Jean Cruveilhier documented extensive distortion of the femoral head as a consequence of trauma, possibly as a result of vascular injury [1]. On the other hand, Freund is widely regarded as the first author to provide a full description of the avascular necrosis of the both hips [2]. The aetiology of AVN in the hip is unknown, although it is the ultimate common mechanism of traumatic or nontraumatic events that harm the femoral head’s already vulnerable circulation. Gradually, the femoral head collapses and the hip joint is rapidly destroyed which ultimately leads to osteoarthritis.

Epidemiology

A prevalent condition in hip joint surgery is osteonecrosis of the femoral head (ONFH). The blood supply to the femoral head is damaged or disrupted for a variety of reasons, which is followed by a succession of pathological alterations and ultimately irreversible destruction of the hip joint. Statistics show that there are more than 20 million ONFH patients worldwide, with roughly 5-7.5 million instances in China, and that there are between 150 and 200 thousand new cases per year [3, 4]. The United States sees 10,000–20,000 new cases of ONFH each year [5, 6]. Males in their 40s and in females in their 30s are more likely to develop it in Japan [7]. According to reports, Korea’s peak age range is 40-59 years [8]. In the UK, patients’ ages were on average 57.6 years old [9].

Etiology

Among the factors that predispose a subject to ONFH are hip trauma, including femoral neck and acetabular fractures, hip dislocation, sprain or contusion (no fracture but sometimes intra‐articular hematoma) [10] long‐term high‐ dose glucocorticoids [11, 12, 13, 14] long‐term heavy consumption of alcohol [15] thrombophilia and hypofibrinolysis and autoimmune diseases treated with glucocorticoids [16, 17, 18] and a history of having used decompression chambers [19]. It is idiopathic in around 30% of individuals (Table 1) [20]. Males are more often affected than females, and bilateral presentation is usually noted [21]. Within two years, roughly 55% of patients could develop a contralateral hip problem [22]. Ongoing ONFH will be present in about 75% of patients with other sites of involvement [23].

Deranged lipid metabolism,Systemic steroid administration, Habitual alcohol use, Hyperlipidemia, Pancreatitis
Disturbed arterial supplyTrauma: Fractures and dislocations of the hip
Disturbed arterial supplyIatrogenic: Following surgical intervention around hip
EmbolicGauchers disease, Sickle cell disease Dysbarism (caissons disease)
Coagulation disorders (thrombotic)Thalassemia, Polycythemia, Myeloproliferative disorders, Ionizing radiations
Miscellaneous and multifactorialSlipped capital femoral epiphyses, Legg-Calve-Perthes disease, Congenital hip dislocation, Gout, Systemic lupus erythematosus, Rheumatoid arthritis, Organ transplantation, Pregnancy, Cytotoxic agents, HIV (Human immunodeficiency virus)

Table 1: Prevalent causes of femoral head avascular necrosis.

Role of Covid-19 as a Disease Process and the Treatment with Steroids

The long-term effects of the COVID-19, which also affect the musculoskeletal system, have been extensively documented in investigations [24]. The physiology of bone and joint tissue in COVID-19 individuals may be influenced by systemic inflammation [25]. CXCL10, IL-17, and TNF- alpha are cytokines that COVID-19 induces [24]. They prevent osteoblasts from proliferating and differentiating as much. Furthermore, several genes encode proinflammatory proteins, such as IL-1b, IL-6, and IL-8, which are associated with hypercoagulability and bone necrosis in COVID-19 patients [26]. Vasculitis and hypercoagulability can interfere with the blood flow in bone vessels and contribute to bone necrosis if they are combined [26]. Viral invasion can cause ACE2 deficiency, which can result in bone matrix degradation [27]. Since Coronaviruses infect the upper respiratory tract by binding to ACE2 receptors in ATII cells, ACE2-dependent effects on bone tissue are also relevant. As a result of Infection with COVID19, ACE2 is a potential factor that regulates bone biology [28, 29].

The majority of COVID-19 hospital patients who get corticosteroids also experience negative effects on their bone tissue [30, 31]. After steroid therapy, there is a 6- to 1-year window during which AVN risk increases [32]. There is disagreement on the dose and length of corticosteroid therapy as a risk factor for developing AVN. According to one prospective study, a dose of more than 20 mg/day considerably increases the incidence of AVN [33].

Clinical Evaluation

A thorough history of the patient is obtained, followed by a physical examination is helpful, In order to suspect that ONFH is present. Symptoms of ONFH may not appear for some time after the onset. Most commonly, groin pain is the main clinical sign. In some cases, pain may occur in the buttocks or knees on the ipsilateral side. Rest cures the symptoms, while weight bearing worsens them. There is a restriction of range of motion, particularly on the inside and outside of the hips, and uncomfortable logrolling (passive rotation of the interior and exterior of the hips) is present [34].

The efficacy of ON treatment is correlated with the stage at which care is began, hence early identification is essential [35].

Over 16 different classifications have been published in the literature for ONFH, based primarily on MRI and radiography. It allows for the determination of prognosis and provides directions for treatment options. The classification systems Ficat and Arlet (63% of studies; Table 2; Figure 1), Steinberg (20%; Table 3), Association Research Circulation Osseous (ARCO) (12%), and the Japanese Orthopedic Association (5%), are the most frequently employed in the literature [36].

StageFindings
1Normal radiograph
2Normal femoral head sphericity. Some signs of bone remodelling such as cysts or osteosclerotic regions
3Subchondral collapse or flattening of the femoral head
4Degenerative changes are seen in the acetabulum with narrowing of the joint space

Table 2: Ficat and Arlet classification.

StageFindings
0No symptoms
Normal radiograph
MRI non-specific
1Mild pain in the affected hip, or pain with internal rotation
Normal radiograph
MRI diagnostic
2Worsening or persistent pain
Increased sclerosis or cysts in the femoral head
3Subchondral collapse (crescent sign)
4Flattening of the femoral head
Normal joint space
5Narrowing of the joint space with/without femoral head involvement
6Advanced degenerative changes

Table 3: Steinberg classification.

Ultimately, all of these classifications are meant to distinguish between pre-collapse lesions, which can be treated conservatively, and post-collapse lesions, which typically require total hip arthroplasty.

Role of Radiology in Treatment and Prevention

Common hip joint disorders like ONFH can be a turning point in the development of a disease. Patients enter the irreversible late stage once it happens [37]. For the purpose of choosing the best course of treatment and enhancing the prognosis, it is essential to be able to estimate the likelihood of femoral head collapse. According to studies, the size and location of the lesion play a significant role in femoral head collapse [38, 39, 40, 41]. The location and extent of the lesion have been depicted using a variety of methods, although they have always relied on MRI or radiography [38, 39, 40, 41, 42, 43].

The following auxiliary investigations are advised in addition to collecting the history and clinical symptoms and signs, which is the first step in making a diagnosis.

Plain Radiography

Ankylosing spondylitis, hip dysplasia, osteoarthritis, and rheumatoid arthritis can all be ruled out using X-ray films. ONFH can be diagnosed by identifying the crescent sign, which represents segmental collapse and necrosis surrounded by sclerotic bone. In advanced cases global arthritis of hip joint is seen. (Figure 1).

Figure 1: Various stages of osteonecrosis of femoral head.
Click to enlarge
Figure 1: Various stages of osteonecrosis of femoral head.

Stage 1 : X-Ray Pelvis with both hips showing no radiological changes Stage 2: The femoral head contour is still normal with early signs of reactive change in the subchondral area.

Stage 3: Signs of osteonecrosis with evidence of structural damage and distortion of the bone outline. Collapse of the necrotic segment Figure 1: Various stages of osteonecrosis of femoral head.

Magnetic Resonance Imaging

MRI is the standard method for ONFH diagnosis [44]. The recommended sequence is T1WI, T2WI and fat suppression T2WI, coronal and axial scans, with specificity and sensitivity above 99%. The presence of bone marrow edema and joint effusion on T2WI with fat suppression indicates that the disease has advanced to the pre-collapse or subsidence stage.

CT Scanning

Although a coronal and axial two-dimensional reconstruction CT scan is advised, it cannot directly

Stage 4: Collapse of the articular surface and signs of secondary osteoarthritis determine the stage of ONFH but can clearly demonstrate subchondral bone plate fractures, necrosis, and the level of repair [45].

Scintigraphy

With a high sensitivity and low specificity, scintigraphy can offer hints for detecting stage I.

Treatment Methods

Depending on the cause of the condition, different treatments are used.

Nonoperative Treatment

Restricted weight bearing, pharmacological medications, and biophysical therapy methods are included in the nonoperative management of ONFH [46].

Non-Weight Bearing: During the early stages of osteonecrosis of the hip causing ON, restrictions of weight- bearing with a cane, crutches, or walker are beneficial (Ficat and Arlet Stage-I and II) [47].

Bisphosphonates: In osteonecrotic lesions, bisphosphonates are beneficial because they reduce osteoclast activity. When ON hip is treated in early stages, it delays the onset of subchondral fractures or collapses, and when collapse has already occurred, it delays the need for total hip replacement (THR) [48, 49, 50, 51, 52, 53, 54, 55].

Anticoagulants, Statins and Other Vasodilators: The pre-collapse stage of ONFH can be treated with anticoagulants (low molecular weight heparin), fibrinolysis promoters, and vasodilators. Thrombophilia and hypo fibrinolysis can be associated with ON, resulting in venous stasis, decreased arterial flow, increased intraosseous pressure, and hypoxic bone death [56, 57]. Systemic anticoagulation therapy initiated before irreversible segmental collapse of the femur head may be able to stop or, speculatively, reverse the progression of ischemia ON [58, 59]. In cases of idiopathic ON and/or corticosteroid-induced ON, anticoagulant medication has stopped the disease from progressing from the precollapsed stage to the advanced state [60]. Agents that reduce cholesterol are beneficial in ONFH, especially in cases where ON was brought on by steroids [61]. There is also an increase in fat content of the femoral head as a result of steroids causing hyperlipidemia [62]. Sinusoidal collapse and osteonecrosis occur due to increased intracortical pressure. Known as lipid-clearing drugs, statins reduce lipid levels in blood and tissues dramatically.

Physical Therapy: These techniques include extracorporeal shockwaves, high-frequency magnetic field therapy, hyperbaric oxygen therapy, and others.

  • Extracorporeal Shock Wave Therapy: It is still unclear exactly how ESWT helps in ONFH. However, researchers claim that it promotes neovascularization by encouraging the expression of angiogenic growth factors [63, 64, 65].
  • Pulsed Electromagnetic Therapy: Through promotion of osteogenesis and angiogenesis, similar to ESWT, pulsed electromagnetic therapy is expected to benefit early- stage ON [66, 67, 68, 69, 70]. There is currently little evidence in favour of electromagnetic stimulation, and more study is required to determine its potential impact on early- stage ON.
  • Hyperbaric Oxygen: An increase in microcirculation and a decrease in intraosseous pressure are the results of hyperbaric oxygen therapy’s improved oxygenation, vasoconstriction induced edema reduction, and angioneogenesis-induced edema reduction [71, 72, 73].

Surgical Treatment

Core Decompression: The most often used surgical technique for treating early ONFH is core decompression. It boosts neobone development by increasing blood flow to the necrotic area and reducing intraosseous pressure in the femoral head. The outcome of the treatment is heavily reliant on the etiology and radiographic factors such lesion size, location, or collapse [74, 75]. It has been thought to be the only surgical technique for ONFH that is cost effective [76, 77].

Implanting mesenchymal stem cells or using growth factor based therapies as treatments: An very promising strategy for treating ONFH in the precollapsing stage is the application of adult tissue derived mesenchymal stem cells (MSCs) [78]. Numerous studies have shown that people with ONFH have less colony forming units and endothelial progenitor cells than healthy individuals [79, 80]. Additional factors include increased cellular senescence and decreased angiogenesis in ONFH patients due to diminished endothelial progenitor cell migration capacity and cellular senescence [78].

Implantation Methods

Combination of Core Decompression and MSC Transplantation: The most common method for treating ONFH in its early stages is core decompression (CD), which lowers intraosseous pressure, eliminates necrotic tissue, and encourages the growth of new bone [81]. Positive results are only seen in patients with modest necrotic lesions, and core decompression’s effectiveness is inconsistent [82]. Consequently, a typical method for treating ONFH now involves combining core decompression with MSC transplantation. Together in brief, stem cells are separated from the pertinent tissue and then injected, after core decompression, into the necrotic area of the femoral head. Coupled core decompression and autologous bone marrow transplantation improved the Western Ontario and McMaster Universities Arthritis Index (WOMAC), visual analogue scale (VAS), Harris hip score (HHS), clinical score, and mean hip survival, promoted the repair of necrotic areas, reduced the size of lesions, improved the clinical symptoms, and slowed the disease progression of ONFH, according to a few studies [83, 84, 85] (Figure 2).

Figure 2: X-ray Pelvis with both hips showing bilateral core decompression with MSC insertion (along with artificial bone graft).
Click to enlarge
Figure 2: X-ray Pelvis with both hips showing bilateral core decompression with MSC insertion (along with artificial bone graft).

MSCs Arterial Perfusion: Another approach of treating ONFH is to increase the blood flow to the femoral head by perfusing MSCs through the arterial system. Multiple studies examining the beneficial effects of MSCs on angiogenesis found that arterial perfusion of MSCs encouraged angiogenesis and vascular repair of the femoral head by increasing the expression of VEGF, basic fibroblast growth factor (bFGF), and by increasing microvessel density (MVD), which helped improve the blood supply and renovation of the necrotic area [86, 87, 88].

Cytokine pretreated or gene-modified MSCs transplantation: Numerous cytokines, such as BMP, VEGF, bFGF, and tumor necrosis factor, have been shown in the recent research to contribute to MSCs’ osteogenesis and angiogenesis and to improve the repair of ONFH (TNF). Combination therapy could promote the growth of new bone in the necrotic region and stop the femoral head from collapsing; as a result, cytokines were thought to be used as a pretreatment for MSCs in ONFH [89, 90].

MSCs Transplantation and bone tissue engineering technology: The three main components of bone tissue engineering technology are seed cells, carriers, and scaffolds. Due to their great capacity for differentiation, high levels of proliferative activity, and low immunogenicity, MSCs are the best seed cells for bone tissue creation. In addition to integrating cells and receptors, the carriers or scaffolds can also be employed to support the necrotic area of the femoral head biomechanically, which can be used to regulate cellular function. As a result, a novel strategy for treating ONFH involves combining MSCs with carriers or scaffolds [91].

Role of Stem Cell Therapy

ONFH is a progressive disease that occurs when the blood supply to the femoral head is critically reduced, and intraosseous pressure is elevated. It is well acknowledged that a variety of traumatic and non-traumatic insults affect the femoral head’s already fragile circulation, resulting in bone marrow and osteocyte death—and ultimately the collapse of the necrotic segment. Molecular pathways implicated in the pathophysiology of ONFH have been the subject of recent research. In a study published in Baksh D, et al. [92] showed that multipotent mesenchymal stem cells (MSCs) can differentiate into a variety of cellular types, including osteoblasts, osteocytes, chondrocytes, and adipocytes while still maintaining mitotic proliferation [92]. When implanted in areas of necrotic bone, MSCs have been demonstrated to improve tissue regeneration [93]. According to Hernigou P, et al. [94]. S theory, multipotent MSCs in the bone marrow aspirate could repopulate the trabeculae of the necrotic zone within the femoral head, promoting regeneration and remodelling of the necrotic bone [94]. A study reviewed results implied that the implantation of autologous mesenchymal stem cells (MSCs) into the core decompression track, particularly when used at early (pre-collapse) phases of ONFH, might increase the survival of femoral heads and lessen the need for hip arthroplasty [95].

Nonvascularized Bone Graft

After removing the necrotic lesion from the femoral head, nonvascularized bone-grafts are employed to maintain the subchondral bone and articular cartilage. The osteonecrotic lesion is helped to heal by the osteoconductive and osteoinductive qualities of the bone graft. In precollapse and early postcollapse (2 mm collapse) ONFH cases when the articular cartilage is largely unharmed, this mode of treatment has been reported to be effective. When CD fails in Ficat stages I and II ONFH, the surgeons frequently use this method [58].

Porous Tantalum Implant

Porous tantalum implants offer structural support similar to that of a bone graft while minimizing the risks of infection problems and donor site morbidity associated with using allografts and autografts, respectively. Due to the high level of porosity (>80% volume) in these rods, bone can grow quickly and securely [96, 97, 98, 99].

Vascularized Bone Graft

A suggested mode of treatment for early ONFH is vascularized bone grafting (Ficat stage I to III) [100, 101, 102, 103]. Joint collapse is avoided by the graft, which offers a strong structural support (for example, a vascularized fibula graft or iliac crest graft) [104]. In addition to enhancing bone repair at the site of the necrotic lesion, the graft possesses inherent osteogenic potential and preserves vascularity. The prognosis is less favorable in severe lesions, though, when the collapse is greater than 2 mm and more than 50% of the femoral head is involved. No patients should be considered for the surgery if they have a history of smoking, drinking, peripheral vascular disease, or any other risk factors. This technique’s primary drawbacks are the difficulty of the surgery and the longer surgery time [105, 106, 107, 108].

Vascularized Iliac Crest Graft

When necrosis does not yet encompass the entire femoral head, the procedure described is advised for therapy in Ficat stages II and early III. The use of vascularized iliac crest grafts in ONFH was found to have a 74% success rate (17 of 23 hips) in a research by Iwato H, et al. [104].

Proximal Femoral Osteotomy

The basic idea behind proximal femoral osteotomies in ONFH is to rotate the necrotic femur head away from the area that bears weight and replace it with the healthy, unaffected part of the head. Furthermore, it enhances vascularity and lowers intraosseus venous pressure. There are primarily two types of osteotomies discussed: transtrochanteric rotational osteotomies and intertrochanteric varus or valgus osteotomies (combined with flexion or extension). The reported success rates for these osteotomies range from 70% to 93% [109, 110, 111, 112]. The best candidates for osteotomies are those who are not receiving longterm steroid therapy, have little osteoarthritic alterations, no acetabular involvement or loss of joint space, and a small combined necrotic angle (Kerboul’s angle <200) [20].

Arthroplasty

When all other forms of therapy have failed or the joint is arthritic as a result of advanced collapse, patients with ONFH may require THR (more than 2 mm). Because ONFH victims are typically young individuals with significant functional demands and a high likelihood of needing revision arthroplasty, THR is regarded as a last resort of treatment. Sickle cell disease, Gaucher disease, end-stage kidney illness, and transplant patients all had greater revision rates when the patients were categorized according to their related risk factors. Patients with SLE, those without a known cause, and those who underwent heart surgery had a lower revision rate [20].

Conclusion

Osteonecrosis of the femoral head with subsequent arthrosis is one of the leading conditions for the total hip arthroplasty. It is caused by many conditions which ultimately causes the disruption of blood supply to the femoral head. COVID 19 disease itself and the treatment with steroids for the same, is implicated as a cause for the outbreak of ONFH following COVID 19. During initial stages it causes the collapse of femoral head but in advanced stages it is associated with secondary osteoarthritis results in more disability. The treatment methods vary with stage of the disease. The early stages can be managed with conservative methods and hip preserving surgeries whereas late stage condition with advanced osteoarthritis requires arthroplasty. The early recognition by clinical and radiological features the progression may be reversed or slowed down. The high usage of corticosteroids during COVID 19 and its association with ONFH is a warning sign for the judicious usage of the same in future.

Disclosures

  • Acknowledgement: None
  • Conflict of interest: None
  • Financial disclosures: None to disclose
  • Authors’ contribution: RI: Conceptualization, writing, revision, and final approval; RSR: Literature search, revision and final approval.
  • Ethical approval: Not required, being a narrative review and not involving any patients data or identity.

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@article{itha2023,
  title   = {Osteonecrosis of Femoral Head with a Special Note on COVID 19},
  author  = {Itha R* and Ravali RS},
  journal = {Journal of Orthopedics & Bone Disorders},
  year    = {2023},
  volume  = {7},
  number  = {1},
  doi     = {10.23880/jobd-16000230}
}
Itha R* and Ravali RS (2023). Osteonecrosis of Femoral Head with a Special Note on COVID 19. Journal of Orthopedics & Bone Disorders, 7(1). https://doi.org/10.23880/jobd-16000230
TY  - JOUR
TI  - Osteonecrosis of Femoral Head with a Special Note on COVID 19
AU  - Itha R* and Ravali RS
JO  - Journal of Orthopedics & Bone Disorders
PY  - 2023
VL  - 7
IS  - 1
DO  - 10.23880/jobd-16000230
ER  -