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The calcification of knee ligaments is a finding noted only in a handful of case reports. The finding of an anterior cruciate ligament calcification has been reported once in the literature. Comparable studies involving the posterior cruciate ligament, medial collateral ligament and an ossicle within the anterior cruciate ligament are likewise discussed in reports of symptomatic patients. We report a case of incidentally discovered anterior cruciate ligament calcification. We discuss the likely etiology and clinical implications of this finding.
An 82-year-old male with a history of hypertension, diabetes and unconfirmed asbestosis was a restrained driver in a motor vehicle accident. The patient presented with lacerations to his face, right upper and lower extremities. The patient was found to have sustained a tibial plateau fracture and a non-operable right transverse process fracture at L2 and L3. In addition to the comminuted Schatzker II fracture of the lateral right tibial plateau with depression, chondrocalcinosis and severe joint disease, calcification of the anterior cruciate ligament was found. The patient did not report knee trauma prior to his motor vehicle accident and presentation to the emergency room, he stated only that he was a retired brick layer with to-be-expected joint pain.
On admission, antero-posterior and lateral radiographs of the right knee demonstrated the tibial plateau fracture (figure 2). A CT of his lower extremity revealed a comminuted fracture of the lateral right tibial plateau with depression, chondrocalcinosis of the medial meniscus, severe degenerative disease and calcification of the anterior cruciate ligament (figure 1).
Shortly thereafter, the patient underwent open reduction internal fixation of his tibial plateau fracture. Submeniscal arthrotomy revealed a medially displaced lateral meniscus with displaced and depressed fracture fragments some of which were intraarticular. Fragments were pinned, a lateral tibial plateau periarticular nonlocking plate was implanted and lateral meniscus was repositioned and sutured in place. Provided the various traumatic injuries the anterior cruciate ligament calcification could not be appreciated. Unfortunately, pathological tissue could not be acquired for histological examination.
Blood tests performed during his 7 day hospital stay revealed normal range calcium at 9.2 mg/dL. The patient had normocytic anemia with hemoglobin of approximately 10 gm/dL. Glucose ranged from 136 to 201 in the setting of acute trauma. The patient developed a mild leukocytosis following his operation which normalized. Hematologic and biochemical tests were otherwise within normal limits.
Antero-posterior and lateral radiographs of the right knee following the procedure demonstrated the tibial plateau fracture in near anatomic alignment with hardware in place (figure 2).
Following the surgery, the patient was able to perform range of movement exercises without difficulty and basic transfer of weight exercises with minimal assistance. The patient refused acute inpatient rehabilitation and so was discharged. He failed to return 2 weeks after discharge to orthopedic clinic for wound check and staple removal. As such, delayed post-procedure imaging could not be attained.
Few cases involving largely isolated symptomatic calcifications of a ligament within the knee have been reported. Of note, trauma is not clearly identified in all cases as the clear etiology [1, 2]. In each case with exception of the medial collateral ligament wherein calcification is restricted in location to the femoral attachment without involvement of the whole ligament and discrete from the synovium, pain is assumed to be derived from increased pressure on the synovium which is exerted from deposition of calcium within the ligament .
As calcification of the anterior cruciate ligament is a rare occurrence in the literature discussed only in select case reports, determination of incidence, sex and age predilection is limited and unknown.
Trauma is the most likely predisposing factor for calcification within the ligaments in our patient population with mechanical stress to joints up-regulating mRNA for bone morphogenic proteins which play an important role in bone formation during development and fracture repair but can also induce ectopic osteogenesis [4, 5]. Other possible etiologies discussed in the literature include various endocrine disorders including thyroid disorders with associated osteopenia and traumatic sequelae, hypoparathyroidism which is associated with calcium deposition in various organ systems not excluding ligaments and diabetes. Vitamin D resistance which is thought to be associated with low calciuric response is implicated in the progression of ligament calcification, specifically of the spinal ligaments. Medication induced hypercalcemia and hypomagnesemia may contribute to ligament calcification in concert with trauma. Hypervitaminosis A administered to animal models in excess results in osteophytes and heterotopic ossification in tendons and joint capsules. Hormone supplementation, normal cyclic fluctuations of sex hormones and total estrogen levels are positively correlated with the extent of ossification of the posterior longitudinal ligament [4, 6].
In our study, a calcified anterior cruciate ligament was discovered in the context of a post traumatic tibial plateau fracture. The patient though not clearly asymptomatic, had not pursued treatment for knee pain nor had he reported prior trauma. However, the severe degenerative disease of the knee joint seen on imaging may be consequence of his previous profession as a brick layer. With degenerative changes taken into account, traumatic etiology and prior hemorrhage cannot be excluded as a possible cause for the calcification within the ligament. Also of note, the incidental finding of chondrocalcinosis of the medial meniscus may be sporadic in 7–10% of patients over 60 years in age and bears association to osteoarthritis . Less likely is the supposition that the chondrocalcinosis is secondary to calcium pyrophosphate disease provided a lack of supporting history. The association of incidental chondrocalcinosis and separate calcification of a ligament is not well established although, if all causes for calcium deposition are to be entertained, affliction with both in this patient helps to direct suspicion of potential disease processes. Both chondrocalcinosis and calcification within ligaments and tendons is appreciated with hypoparathyroidism and hypothyroidism. However, these causes will be excluded based on the patient’s lack of supporting history and limited blood work including normal calcium levels.
Patients with diabetes mellitus have an increased risk of extraskeletal calcification. Studies have implicated diabetes in the development of hydroxypatite crystal deposition disease , diffuse idiopathic skeletal hyperostosis , calcific shoulder periarthritis , and ossification of the posterior longitudinal ligament . While the etiology by which diabetes mellitus incites these disease entities is not fully understood, studies have shown that diabetes induced angiopathy and associated decrease in blood flow may precipitate calcification of tendons . The decrease in cellular response to insulin or insulin deficiency in diabetics may contribute to the calcification of connective tissue and endochondral calcification as glycosamionoglycan production, collagen synthesis and hastening of the senescence of fibroblasts is retarded . Our patient does have a history of diabetes however; his initial glucose of 136 and high of 201 is not highly suspicious in the setting of his recent trauma and hospitalization. Unfortunately hemoglobin A1c was not attained and further conjecture can not be made on the role of diabetes on the development of his anterior cruciate ligament calcification. Ultimately, his history for repetitive overuse of his joints is most convincing as a cause for all of his incidental findings.
Calcification within a ligament can be seen on various modalities . As calcifications may be diffuse or speckled and evaluation of the joint space limited by technique, plain radiographs may not be as helpful in evaluation for calcification within a ligament. While ultrasound is infrequently the modality of choice for joint pain, calcification within the ligaments has been demonstrated as echogenic foci within the area of interest with variable presentation of acoustic shadowing. Computed tomography, a common modality for early evaluation of the extremity demonstrates calcium within the ligament; Hounsfield units are typically in excess of 200. Provided that the calcification of the ligament is a chronic and benign process, contrast administration should not result in enhancement within the region of calcification. While magnetic resonance imaging was not pursued in our case, a full evaluation of the tendons and ligaments would have been reasonable in our patient. MRI is often pursued in cases of ligamentous calcification as these patients will often present with chronic joint pain. Calcium within the ligament in a diffuse or speckled pattern appears dark on T1, T2 and PD imaging. While there are no reports within the literature of evaluation of anterior cruciate ligament calcification with positron emission tomography or other nuclear medicine modality, one would assume that based on likely chronicity and benignity of this finding that evaluation with PET would not be informative. Radiopharmaceuticals and fludeoxyglucose uptake should not be abnormal with exception of varied uptake secondary to trauma or arthritis.
In our study, antero-posterior and lateral radiographs of the right knee demonstrated the tibial plateau fracture but failed to show the anterior cruciate ligament calcification (figure 2). A subsequent CT of the lower extremity revealed a comminuted fracture of the lateral right tibial plateau with depression, chondrocalcinosis, severe degenerative disease and the calcification of the anterior cruciate ligament (figure 1).
The differential diagnosis for calcification of the anterior cruciate ligament is limited. Ossicles within the ligament, osteochondritis dissecans, chondrocalcinosis and joint space mass with associated calcification may be considered when confronted with what appears to be a calcification within the joint space.
Both an ossicle within the ligament and osteochondritis dissecans with avulsed fragments may appear as radiopaque loose bodies within the region of a ligament on plain film . These benign calcifications may not look particularly dissimilar to calcified ligaments on ultrasound, computed tomography or magnetic resonance imaging. An ossicle however even within the ligament will appear as a well-defined calcification with possible bone marrow signal on MR in contrast to the speckled and diffuse appearance of the calcified ligament we have discussed in this case report. Osteochondritis dissecans can be differentiated typically by localization of the bone fragments which may be near impossible on plain films and ultrasound but should not be particularly difficult on CT or MRI. MRI may demonstrate a structure isointense to bone marrow with or without a hypointense rim within the region of interest. Like ligament calcifications, nuclear medicine studies will only be helpful in identifying inflammatory changes, trauma and arthritis in association with ossicles, loose bodies and bone fragments from osteochondritis dissecans.
In regards to calcification, chondrocalcinosis and renal osteodystrophy may present as radiopaque structures within the ligamentum flavum, joint capsule, menisci/hyaline cartilage, and within soft tissues and ligaments .
Based on the propensity for chondrocalcinosis and renal osteodystrophy to involve other ligamentous and cartilaginous structures, this etiology should only be entertained in the context of appropriate and contributory medical history and physical exam. If chondrocalcinosis and renal osteodystrophy is the suspected etiology of a calcification within a ligament, it will present very much like the benign calcification of the anterior cruciate ligament discussed in this case. Again, a calcification within a ligament secondary to chondrocalcinosis or renal dystrophy will not typically present as an isolated finding. Nuclear medicine imaging in this instance may be helpful in ascertaining the full extent of bone and soft tissue involvement. Erosive and inflammatory changes in addition to the potential for a superscan and pseudofractures may be evaluated on bone scan.
A number of rare soft tissue tumors may involve the joint space; necrosis and subsequent calcification may mimic the appearance of a solitary ligament calcification on plain film and occasionally on ultrasound . Synovial sarcoma may involve the joint typically secondary to local invasion from a juxtaarticular soft tissue primary which is readily identified on CT/MRI or nuclear medicine study. Malignant peripheral nerve sheath tumor is frequently associated with calcification but again an infiltrative mass should be seen on CT/MRI. Extraskeletal osteosarcoma has a soft tissue preference while extraskeletal mesenchymal chondrosarcoma typically occurs in the head and neck. Pleomorphic sarcoma (malignant fibrous histiocytoma) and solitary fibrous tumor may also exhibit calcifications but soft tissue components should not be missed on CT/MRI.
These soft tissue lesions are varied in appearance, etiology, incidence and require histologic examination for full evaluation. Scintigraphy and PET scan may be pursued and will demonstrate varied radiopharmaceutical and FDG uptake depending on aggressiveness and blood supply.
Unfortunately, the anterior cruciate ligament could not be examined intraoperatively, nor could a sample for histologic examination be attained from this patient.
In prior studies, histologic examination of removed material yielded calcium deposits and samples resembling that acquired from calcifying tendinitis [12, 13]. Previous case reports have reported that arthroscopic treatment and debridement of the calcium deposits have relieved pain in symptomatic patients . Destruction of calcium deposits may make it possible for calcium remnants to diffuse and reabsorb. Of note, extracorporeal shock wave lithotripsy has been pursued for complications of arthroplasty however, data supporting the use of lithotripsy for ligament calcifications is still lacking.
Regardless, this truly incidental finding of a calcified anterior cruciate ligament in the context of numerous findings suggestive of chronic degenerative change does not necessarily warrant intervention. Physical therapy may be a reasonable first step in a treatment plan and as pain from ligament calcification is thought to be secondary to increased pressure on the synovium, anti-inflammatory medication may serve some benefit. In terms of prognosis, it would seem that for both those patients wherein treatment through debridement is warranted and for those where it is not, prognosis is promising.
The significance of rarely discussed calcification within knee ligaments is uncertain with previous case reports drawing conclusions about the clinical implications of ligament calcifications based on symptomatic relief following surgical removal. Incidentally discovered and asymptomatic anterior cruciate ligament calcifications raise the possibility that such a finding when encountered in practice may represent a chronic benign condition of little to no clinical significance.