Summary

Introduction: Bone edema is caused by an inflammation of the internal part of the bone caused by the accumulation of fluids and blood (red and white blood cells and platelets), thus producing edema. It can have different origins such as trauma (fractures), continuous overload or even a degenerative injury. The main symptom is localized pain in the affected area of the bone due to the increased pressure caused by the accumulation of fluids. Material and methods: Patients with the presence of post-traumatic bone edema without additional injuries to the knee and ankle were selected, treatment and functional evaluation were carried out according to conservative post-treatment knee and ankle scale.
Results: There were 4 patients, 3 with knee bone edema, 2 women aged 53 and 15 years, a 53-year-old man, and a 34-year-old ankle patient, all with traumatic causes, 3 of them received conservative treatment, and one with knee bone edema apart from conservative treatment received intraosseous ultrasound-guided PRP. According to the Lysholms scale, patients with knee bone edema with excellent Lysholms Scale score. Ankle bone edema patient with Maryland scale with good results.
Discussion: Bone edema, bone inflammation with fluid buildup, is often caused by trauma or overuse, leading to pain. It can resolve or worsen. Initial treatment is rest and medication, but if that fails, interventions like PRP injections can be used. MRI is key for diagnosis. Physical therapy focuses on reducing inflammation and restoring function. Early, appropriate treatment, starting conservatively, is important, with surgery considered for persistent cases or severe bone damage.
Conclusion: Favorable results in bone healing can be observed in the short-, medium- and long-term using MRI control in the ankle and knees. However, research is needed to demonstrate the efficacy of the various treatments in bone edema.

Keywords:Bone edema; Inflammation; Fluid accumulation; Trauma; Post-traumatic bone edema; Conservative treatment; Intraosseous PRP

Abbreviations:CT: Computed tomography; MRI: Magnetic resonance imaging; BMI: Bone marrow edema

Introduction

To understand what bone edema is and how it occurs, it is important to know how the bone is formed [1-3] Bone is made up of compact bone and cancellous or trabecular bone. Compact bone forms the cortex of cortical bones and is what provides bone strength [4-6]. The inner part of the bone is spongy, it is formed by trabeculae. Its function is to give extra strength to the bone and support the bone marrow. Bone edema occurs when the cancellous or trabecular bone becomes inflamed. 5 Bone marrow is made up of fat-rich tissue (at peripheral sites of bone). This tissue has a characteristic signal pattern on MRIs [7-11]. Bright images can be seen in T1-weighted images and a dark signal in T2 [12-16] Any change in these images is the consequence of the change of fat tissue for water-rich material. This injury is called “bone edema” and is characterized by an altered signal in the spinal cord area in which the T1 signal is decreased and the T2 signal is increased. This usually occurs in a specific part of the bone marrow where fat tissue is replaced by water [1,4,12,13]. The cause of bone edema, in some cases, is unknown, but most cases are due to different pathologies that may be responsible: trauma (fracture, direct injury, ligamentous damage), degenerative (osteoarthritis),neoplastic (primary or secondary bone cancer), infectious (septic arthritis), inflammatory (inflammatory arthritis), metabolic, iatrogenic (after radiotherapy), ischemic and neurological [1,12]. As for the clinical manifestations, edema is usually accompanied by edema of the soft tissues and joint effusion. Patients usually report joint pain spontaneously. It mainly affects the joints of the lower limbs. The symptoms are inflammation, pain that increases when loading the joint and impotence [2,12]. Diagnosis is very important to rule out different pathologies because early differentiation from other pathologies is essential to avoid unnecessary treatments [12]. This diagnosis will be made through different tests, depending on the time that has passed since the onset of symptoms and what you want to observe in the test [1,17- 19].

Courtesy: Rev Esp Traum Lab. 2022; 5(2): 86-94.

One of the diagnostic tests that can be done is the X-ray (X-ray). With it, you can see the bone demineralization that usually accompanies edema. Initially, no change can be seen on the x-ray. The first changes in the bone are visible from 3-8 weeks after the onset of symptoms. Complete bone mineralization can take anywhere from a few weeks to 2 years after the patient becomes asymptomatic [1,12]. Another possible test is computed tomography (CT). It cannot detect bone edema, but if MRI is contraindicated in patients, it is useful to observe the initial bone demineralization, before it is seen on the X-ray [1,12]. The most effective test is magnetic resonance imaging (MRI). This test can detect bone edema that cannot be seen in the other tests described above. It is observable after 48 hours of the onset of symptoms. The edema can spread through the spinal cord to other areas further away. Also, joint synovial effusion or proliferation and periarticular soft tissue edema can be observed. Before the advent of MRI, edema was very difficult to assess because the cortex is often intact [1,2,20]. Bone marrow edema (BME) is a medical disorder characterized by specific concerns and an unclear etiology, a nonspecific finding that is identified on magnetic resonance imaging (MRI) as an area of low signal intensity at T1 and high intensity at T2 [2,4,9,11, 21,22]. However, although MRI detects true local edema, histological studies have revealed that there is also lymphocyte infiltration, fibrous tissue, increased vascularization, and decreased bone mineralization [6,23,24,25]. For this reason, BME has been included in a broader concept of osteochondral unit lesions. MRI is considered the gold standard for detecting changes in the bone marrow and guiding the decision-making process. Clinically, MRI can detect BME in both symptomatic and asymptomatic people, including highlevel athletes and military recruits, but also in non-professional athletes [1,7,12,26]. Even changes in training protocol, equipment used, or the start of a new sport are common causes of stress injuries. The most used treatment is preservative. A partial joint discharge is performed through which the pain is reduced. It should be considered that if a prolonged total discharge of the joints is performed, it can promote bone demineralization. Therefore, it is important that patients walk using crutches that allow this partial discharge and to keep the joints in use. Mild pain relievers (pain relievers, NSAIDs) may also be given [7,12]. In addition, it is recommended to take calcium and have sessions with physiotherapy, in which massage therapy, relaxation therapy and magnetotherapy sessions will be carried out [2,24].

Nonsurgical treatments include

Partial or complete rest, medications such as NSAIDs, bisphosphonates, and monoclonal antibodies.

Some medications used:

Studies have shown that zoledronic acid can relieve pain and speed up recovery in high-performance athletes, and combined with partial weight bearing for a month improves mobility and reduces BME. The efficacy of ibandronate and denosumab in the treatment of pain associated with knee BME has been demonstrated. Küchler et al. reported that a single intravenous dose of ibandronate reduced pain in patients with knee BM, regardless of the severity detected on MRI. Rolvien and colleagues found that a single dose of denosumab led to the near-complete disappearance of BME in 93% of patients with idiopathic lower extremity BM, in addition to a significant reduction in pain perception and markers of bone metabolism. Teriparatide is used in the treatment of fractures with repair complications and in conditions such as complex regional pain syndrome I (CRPS I) with the presence of BME on magnetic resonance imaging. Galluccio et al. suggest, based on their clinical experience, that teriparatide is effective in the treatment of BME secondary to CRPS I, with long-lasting effects in pain reduction and functional improvement of the joint due to its anabolic capacity in the cellular pathways of bone metabolism. Therefore, they recommend short-term administration [4,7,11,19,16,27,28].

Vitamin D: Identified as an effective strategy for treating BME due to its role in bone environment homeostasis. This is precisely because BME is produced due to an alteration in bone turnover. Consequently, the authors considered that an inadequate level of vitamin D may be a cofactor in the occurrence of BME [2, 5,15,29,30].

Result

We present 4 patients, 3 with Bone Edema of the knee of which 2 were women of 53 years of age right knee and 15 years of age left knee, a man of 53 years of age right knee, and a patient with edema of the left ankle of 34 years, all with traumatic cause, 3 of them received conservative treatment, and one with bone edema of the knee apart from conservative treatment with:

i. Relative rest for 2 weeks,

ii. Physical therapy, especially with magnetotherapy, 20 sessions each session for 20 minutes and functional exercises from diagnosis. Ibandronate belongs to a class of drugs called bisphosphonates. It was indicated that the 150 mg tablet should be taken on an empty stomach on the same date each month.

iii. Cholecalciferol 1 amp orally weekly for 3 months.

iv. Analgesia in case of pain.

The variables analyzed were:

In 1 patient with bone edema of the knee, although he received conservative treatment, he received intraosseous PRP guided echo, which improved his symptoms. According to the Lysholms scale, patients with knee bone edema resulted in excellent Lysholms Scale scores. Patient of bone edema of the Ankle with Maryland scale with results of good, we did not improve we found that the cause was his work activity and his overweight.

Courtesy: Rev Esp Traum Lab. 2022; 5(2): 86-94.

Discussion

Bone edema is a common clinical condition that can be painful and can be caused by multiple causes, in our work we present the Traumatics, for The evolution of this etiology that is very variable, can be resolved either by spontaneous and complete changes or by evolution towards the advance of chondral erosions and joint annihilation according to the publication of the work of U. Tarantino [2,3,7,9,24,27,31-35]. If mechanical joint overload due to physical activity is the primary cause of the occurrence of BME, the clinician should consider the intensity and mode of training, as well as rest periods from exercise. In the absence of acute trauma but with painful symptoms, the first approach is conservative treatment: immobilization for short periods, rest from training and pharmacology. Treatments (such as NAID, bisphosphonates, and monoclonal antibodies) [18]. However, disrupting the dynamics of the lesion with simple rest seems to be insufficient for optimal regression of the lesion. Bone edema injury in cases where conservative treatment fails, invasive strategies such as decompression and sub chondroplasty can be used [3,30]. An important aspect within the results of this research was the location of the lesion, in which a predominance of the internal femoral condyle was observed, representing 67% of the population, while the external femoral condyle and the tibial plate constitute 13% each. Finally, it is evident that the least frequent location is that of the internal tibial plate, which is represented by 7%. Another relevant aspect is to highlight the importance of the magnetic resonance study to confirm the diagnosis of bone edema, because all patients previously underwent a radiological study, which showed no signs of bone edema. As for physical therapy, this depended on each patient and the characteristics of the injury. But it is evident that the most used therapeutic agent was magnetotherapy, because it has great benefit for the reabsorption of inflammatory fluid. Another of the most used agents was ultrasound, but in this case focused on the associated injury. On the other hand, the laser, despite the studies on its efficacy described in the research, was the least used agent with a value of 20% of the patients [5,21,23]. Different types of therapeutic exercises were performed, their progression depends on each patient and the associated injury, but most of them performed active-assisted, free and resisted exercises from the beginning of rehabilitation. In addition, it was observed that the work of the Core to prevent decompensation at the level of the lower limbs was not largely addressed, but that it was preferred to approach the knee with proprioceptive work, in cases in which the bone edema was accompanied by a sprain. It is imperative to perform the appropriate treatment which we present in this work, identifying the condition as soon as possible. The first step is a conservative approach, reserving the surgery for a specific period. For those situations where there is no improvement. At least 3 months or in individuals that larger osteonecrotic obstructions are present, which are more prone to collapse [36,37].

Conclusion

BME presents a clinical pattern with an unclear etiology, which can manifest in people with and without symptoms. Although it is commonly detected by magnetic resonance imaging in the symptomatic population, its finding does not always coincide with clearly defined symptoms. However, its treatment will always depend on the situation in which it occurs: incidental or symptomatic. The need for an MRI to confirm the presence of the lesion is verified. Regarding treatment, the use of magnetotherapy in all patients, the performance of active exercises from the beginning of rehabilitation and the importance of specific training before returning to sport are highlighted. In our cases, followup is recommended through MRIs and clinical reevaluations with pharmacological interventions or PRP infiltrations, in case conservative therapies are not sufficient (1 case only). Histological evaluation may be of predictive use, especially in severe cases requiring surgery and the control MRI scans to determine if BME is the cause of the pain.

Funding

No funding or conflict of interest to declare.

References

1. Ahuja S, Bullough PG (1978) Osteonecrosis of the knee. A clinicopathological study in twenty-eight patients. J Bone Joint Surg Am 60(2): 191-197.
2. Cañellas Trobat A (2006) The Human Patella: Morphological, Anthropological and Anthropological Analysis pathological. Granada: University of Granada Press, Spain
3. Zufferey P, Boubaker A, Bischof Delaloye A, So AK, et al. (1999) Prognostic aspects of scintigraphy and MRI during the first 6 months of reflex sympathetic dystrophy of the distal lower limb: A preliminary prospective study of 4 cases. J Radiol 80(4): 373-377.
4. Carrión M, Ortiz C, Cabrera S, Contreras O (2005) Edema syndrome transient bone marrow of the foot. Chilean Journal of Orthopedics and Traumatology 59-65.
5. Góngora García L, Rosales García C, Rosales García I, Pujals V (2003) Knee joint and its joint mechanics.
6. Ripoll P, De Prado M, Yelo J (2009) Osteonecrosis of the knee. Perfusion iliac crested mesenchymal cells. Trauma Fund 20(4): 211-220.
7. Guillermo Fernandez-Canton (2009) From bone marrow edema to osteonecrosis. New concepts. Clinical Rheumatology 5(5): 223-227.
8. Garcia Gongora, L, Garci Rosales C, Fuentes González I, Pujals V (2003) Knee joint and its joint mechanics. Medisan 100-109.
9. Jordàn Sales M, Celaya Ibañez F, Gonzàlez Rodrìguez J, Sarasquete Reiri J (2009) Spontaneous osteonecrosis of the knee. Arthos, p. 4-13
10. Prentice W (2001) Healing Process and Pathophysiology of Muscle Injuries skeletal. In Rehabilitation Techniques in Sports Medicine pp: 17-41.
11. Lazzarini KM, Troiano RN, Smith RC (1997) Can running cause the appearance of marrow edema on MR images of the foot and ankle?. Doctors 202(2): 540-542.
12. Bahr R, Maehlum (2007) Sports injuries. Pan american.
13. Belmonte, Castellano, Rosas (2013) Rheumatic Society Update Valencian. Rheumatic Diseases.
14. Gòmez, Garcìa F (2013) Review of non-surgical treatment of necrosis aseptic of the femoral head. Acta ortopedica mexicana 27(4): 265-272.
15. Ratto GD, Moreno Cascales M, Fernandez M, Capel Aleman A, Domenèch Asensi P (n.d.) Anatomy and biomechanics of the knee. Murcia: Faculty of Medicine.
16. Darbois H, Boyer B, Dubayle P, Lechevalier D, David H, et al. (1999) MRI symptomology in reflex sympathetic dystrophy of the foot. J Radiol 80(6): 849-854.
17. Schweitzer ME, White LM (1996) Does altered biomechanics cause marrow edema?. Doctors 198(3): 851-853.
18. Doury P (1993) Bone-marrow oedema, transient osteoporosis, and algodystrophy. J Bone Joint Surg Br 75: 210-216.
19. Brunner F, Lienhardt SB, Kissling RO, Bachmann LM, Weber U (2008) Diagnostic criteria and follow-up parameters in complex regional pain syndrome type I-a Delphi survey. Eur J Pain 12(1): 48-52.
20. Guiraldes H, Paulós J, Hurete I (n.d.). Clinical anatomy of the knee. Anatomy clinic.
21. Kaltenborn FM (2004) Manual physiotherapy for extremities. Madrid: McGraw Hill Inter-American. Mont, M., Baumgarten, K., Rifai, A., Bluemke D, Jones L, Hungerford D (2000) Atraumatic osteonecrosis of the knee 1279-1290.
22. Zanetti M, Steiner CL, Seifert B, Hodler J (2002) Clinical outcome of edema-like bone Marrow abnormalities of the foot. Doctors 222(1): 184-188.
23. Gaeta M, Mazziotti S, Minutoli F (2002) Migrating transient bone marrow edema syndrome of the knee. MRI findings in a new case Eur Radiol 3: S40-S42.
24. Panesso C (2009) Clinical Knee Chemistry. Bogotá: Universidad de Rosario. Bibliography 65.
25. Pellicer V, Gutierrez P, Vidal J (2013) Applicability of analogues of the prostaglandin I2 in the treatment of bone marrow edema syndrome of the femoral head. Clinical case. Trauma Fundación MAPFRE 212-216.
26. Crozier F, Champsaurb P, Phamb T, Bartolia JM, Kasbariana M, et al. (2003) Magnetic resonance imaging in reflex sympathetic dystrophy syndrome of the foot. Joint Bone Spine 70(6): 503-508.
27. Fournier RS, Holder LE (1998) Reflex sympathetic dystrophy: Diagnostic controversies. Semin Nucl Med 28(1): 116-123.
28. Segarra V, Heredia J, Peña G, Sampietro M, Moyano M, et al. (2014) Core and neuro-motor control system: basic mechanisms for Stability of the lumbar spine. Brazilian Journal of Physical Education and Sport 28(3).
29. Ochoa JL (1999) Truths, errors, and lies around ‘reflex sympathetic dystrophy'' and ''Complex regional pain syndrome''. J Neurol 246(10): 875-879.
30. Veldman PH, Reynen HM, Arntz IE, Goris RJ (1993) Signs and symptoms of reflex sympathetic dystrophy: Prospective study of 829 patients. Lancet 342(8878): 1012-1016.
31. Gòmez M (2017) Traumatological Clinic.
32. Barcelona: Paidotribo.
33. Ross M, Pawlina W (2007) Histology text and color atlas with cell biology and molecular. Pan american.
34. Harden RN, Bruehl S, Stanton-Hicks M, Wilson PR (2007) Proposed new diagnostic Criteria for complex regional pain syndrome. Pain Med 8(4): 326-331.
35. Sanjeev P (2014) Primary bone marrow syndromes. Rheumatology 53(5): 785-792.
36. Sarfati G (2015) Prevention of injuries in sports. AATD.
37. Sepúlveda J (2012) Histology: cell and tissue biology laboratory instruction.