Gian Luigi Canata and C. Niek van Dijk (eds.)Cartilage Lesions of the Ankle10.1007/978-3-662-46332-1_2

2. Conservative Treatment of Talar Osteochondritis Dissecans (OCD)

Ezequiel Palmanovich¹ and Meir Nyska¹

(1)

Foot and Ankle Unit – Orthopedic Department, Meir Medical Center – Israel, kfar Saba, Israel

Ezequiel Palmanovich

2.1 Introduction

Since 1922 when this syndrome was first described by Kappis [1], numerous terms have been used to describe chondral lesion of the dome of the talus including osteochondral fracture, osteochondritis dissecans, and talar dome fracture. This lack of well-defined terminology clearly demonstrates the unclear cause of the lesion [1]. In 1959, Berndt and Harty [2] proposed trauma as the principle etiological factor. In 1966, Campbell and Ranawat [3] proposed the name osteochondritis dissecans as a pathologic fracture resulting from necrotic changes due to ischemia. However, traumatic etiology plays an important role in the pathogenesis of osteochondral lesions of the talus. The lesion most likely represents the chronic phase of a compressed or avulsed talar dome fracture. Isolated incidents of macrotrauma or repeated cumulative microtrauma may contribute to initiation of the lesion in someone predisposed to talar dome ischemia. Osteonecrosis in a patient may cause the bone to collapse resulting in subchondral fracture and bony collapse. The subchondral cysts with overlying chondromalacia, osteochondral fragments, and loose bodies all represent stages in the progression of this disease [1].

2.2 Clinical Presentation

In acute injury, clinical presentation remains unrecognized. Pain and swelling interfere with the diagnosis. An x-ray performed in the emergency room may not reveal pathology or even a small area of radiolucency. An x-ray may reveal larger lesions. Lesions can heal spontaneously, or chronic symptoms may develop. Initially, the patient may experience pain during exercise or weight bearing; then deep joint pains may emerge. If symptoms continue for more than 4–6 weeks after “ligament injury” in the ankle, differential diagnosis of chondral defect must be ruled out. Morning or post-rest stiffness, chronic swelling, and catching [4, 5] are the most common symptoms.

As cartilage is aneural, the pain originates from the subchondral bone exposed beneath the cartilage defect [6]. In chronic cases, there is a delay in clinical manifestation.

2.3 Nonoperative Treatment

Prognosis depends on the patient’s age. Lesions which occur during childhood and adolescence tend to heal spontaneously, while the prognosis is poor for older patients and requires treatment [8].

Different treatment options depend on the lesion grade. Using computerized tomography (CT), lesions can be classified according to Ferkel et al. [9] from grade 1 to 4. Grade 1 includes cystic lesions with intact walls; grade 2 includes cystic lesions communicating with the talar dome, or full-thickness lesion with an overlaid fragment; grade 3 includes undisplaced lesions with lucency; and finally grade 4 includes free loose fragments [7].

Goals for treatment of talar OCDs are to decrease pain, improve function, and regenerate articular cartilage or prevent early joint degeneration [7].

For grades 1 and 2, nonoperative treatments are indicated [7].

Treatment in acute cases starts with rest and immobilization. Non-weight bearing physiotherapy is crucial to preserve range of motion.

2.3.1 Hyaluronic Acid (HA)

Treatment with hyaluronic acid, discovered in 1934 is well known as nonoperative treatment for knee and ankle osteoarthritis [9–12] and also for talar chondral lesions [4].

Hyaluronic acid (HA) is a glycosaminoglycan present in many tissues throughout the body and represents the major component of synovial fluid. At the cellular level, it is found in abundance in the extracellular matrices [4]. The rationale for the use of HA is based not only on the findings that the viscoelasticity of the synovial fluid is entirely due to its HA content and that HA forms an integral part of the proteoglycans of articular cartilage, but also on mounting evidence that HA may influence the disease by interacting with components of the synovial fluid and synovial cavity [13].

In 2008, Mei-Dan et al. [4] published results of the first prospective study on patients treated for OCD of the talus. In the study, 15 patients aged 18–60 with talar OCD were followed up 26 weeks after receiving three weekly injections. About 60 % of the patients had grade 3 lesions. On a scale for pain from 1 (no pain) to 10 (severe pain), mean VAS reported a decrease in pain from 5.6 to 3.2. There were also reports of an improvement in stiffness from 5.1 to 2.9 and function from 5.9 to 3.3, from baseline to week 26. Subjective global scores, on a scale from 0 to 100 (100 representing healthy normal function), reported an improvement, on average, from 57.3 at baseline to 74.3 by week 26. In this study, HA provided relief of pain, stiffness, and improved function. Efficacy of the treatment started at 3 weeks from the first intra-articular injection and peaked at 3–5 months with minimal safety concerns.

2.3.2 Platelet-Rich Plasma

Plasma rich in growth factor is a form of PRP [14] and is a biological delivery system of a complex mixture of bioactive proteins essential to natural repair, including anabolic and protective factors for cartilage, such as transforming growth factor-β1 (TGF-β1), platelet-derived growth factor (PDGF), and insulin-like growth factor (IGF-I) [7, 15]. The TGF-β1 is essential for cartilage integrity and is a powerful tool for prevention or repair of cartilage damage [16]. This growth factor is in its latent form while in the platelets and is activated by TSP-1 (thrombospondin), which is also released from platelet a-granules found in PRGF. As a result, intra-articular administration of PRGF could retard or prevent progressive degeneration of joint cartilage [7]

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