Introduction
Given that tibial plateau fractures (TPF) are rare, they may pose a challenge to the treating surgeon due to their variety of complex fracture patterns [
1]. There are numerous approach concepts to improve surgical outcome of TPF, including the updated three-column, the revised three-column, which is a mechanism-driven approach, and the ten-segment concept [
1‐
5]. Nonetheless, persistent pain, impaired range of motion (ROM), and/or instability are repeatedly described. While short- and mid-term outcomes have been associated with a low return-to-sports rate and a low patient-related outcome compared to healthy individuals (Knee Injury and Osteoarthritis Outcome Score), a good-to-excellent knee function in the long term has been reported (Rasmussen and Hospital for Special Surgery Knee Scoring System) [
6‐
10]. Several studies have identified potential fracture-specific and surgery-related risk factors for impaired patient outcomes [
6‐
11]. As a result, there is general consensus that anatomical reconstruction within a 2–3-mm articular step-off, a straight leg axis, and stable bony and ligamentous fixation should be considered [
9,
11‐
14].
While some studies have also analyzed the influence of patient-specific risk factors, medication, or comorbidities, their association with bone metabolism and its impact on patient outcomes has not been in the focus [
6,
7,
10,
15‐
17]. Instead, impaired bone metabolism (IBM) and its association with patient-specific risk factors such as vitamin D deficiency, thyroid dysfunction, chronic kidney disease (CKD) or liver failure, systemic immunodeficiency after organ transplantation or with HIV, or osteoporosis itself have most commonly been studied in relation to fracture risk of vertebral and hip fractures. The influence of vitamin D deficiency on bone health is undisputed and seems to have a negative impact on fracture healing [
18]. Other endocrine diseases like hyperthyroidism, renal, or liver failure are also common in descending order of prevalence and relate to increased fracture risk (hyperthyroidism: from 17 to 97%) depending on location of the fracture site [
19,
20].
While the exact prevalence of IBM is unclear, many of its associated risk factors such as a vitamin D deficiency (up to 40.4%), which may be called pandemic in western Europe, CKD (up to 10.6%), and hyperthyroidism (up to 1.3%) are common [
21‐
23]. Osteoporosis, the most obvious reason for IBM, is prevalent in 35% of all postmenopausal white women, further increasing with age [
24]. Therefore, the impact of a potential IBM on fracture risk, subsequent fracture healing, and postoperative patient outcome in TPF is conceivable and still underrated.
The aim of this study was to analyze patient outcome after surgical treatment of TPF and to evaluate the potential influence of patient comorbidities affecting bone metabolism on surgical outcome. We hypothesized that patients with accompanying bone metabolism-affecting comorbidities or medication showed a worse outcome than patients without known potentially impaired bone metabolism (IBM). We also aimed to present an individual failure analysis of patients with a poor-to-fair functional outcome (Rasmussen) after open reduction and internal fixation (ORIF) of TPF.
Discussion
The present study demonstrated a good-to-excellent clinical outcome in more than 95% of the cases [
1,
27‐
30]. Specifically, 41-type B fractures showed a better outcome than that of 41-type C fractures. We found that the presence of potential IBM due to influencing comorbidities or medication was an independent risk factor for a poor or fair clinical outcome, especially in 41-type B fractures. In accordance with the previous studies, a great number of patients with severe bony destruction reported a good-to-excellent clinical outcome despite postoperative radiological peculiarities [
8,
14,
16,
36,
37] as well as an even better outcome with unilateral plateau fracture [
10,
15,
38].
Common comorbidities, such as type II diabetes or arterial hypertension, have not been associated with clinical outcomes [
6,
7,
10]. However, reports analyzing the risk factors of bone metabolism in a cohort of TPF are rare. In the current study, all but one patient with a fair-to-poor clinical outcome demonstrated at least one risk factor for IBM and consequent fracture healing (Table
5). One patient showed secondary loss of reduction in the posterolateral and posteromedial segments, and that patient presented with HIV and ART with abacavir, lamivudine, and nevirapine. HIV itself is a risk factor for impaired fracture healing [
39]. Treated patients with HIV have a 1.98-to-3.69 times higher fracture rate compared to healthy controls [
40]. In addition, ART regimens induce increased bone loss [
41]. However, modern regimens with abacavir–lamivudine and nevirapine have demonstrated fewer decreases in bone mineral density and fewer increases in bone turnover [
42]. In addition, the patient was exposed to long-term PPI therapy; this causes iatrogenic hypochlorhydria, which itself is associated with decreased bone mass, decreased bone mineralization, and consequently increased fracture risk [
43‐
45]. PPI-induced hypochlorhydria was also detected in another patient with bilateral fractures and secondary loss of reduction. She presented with chronic type-c gastritis, a subsequent chronic hypocalcemia, and unknown collagenosis, which were responsible for a number of insufficiency fractures in the patient’s history. She also suffered from myasthenia gravis, which is associated with significant bone loss independent of corticosteroid use [
46]. Common risk factors for delayed fracture healing or fragility fractures, such as chronic alcohol abuse and severe smoking, were not statistically associated with impaired clinical outcomes in the present study, but they may have been one of the major triggers in one patient with secondary loss of reduction and a substantial subchondral bone loss (Fig.
2) [
47]. Additionally, vitamin D deficiency was commonly observed, and even though its role in fracture healing is still under debate, it constitutes one of the most important determinants of skeletal health [
47,
48].
Numerous studies that have analyzed the outcome of TPF have identified several risk factors for poor clinical and radiological outcome, such as fracture complexity, leg axis malreduction [
9], involvement of the posterior column [
7], residual articular depression of more than 2 mm [
9,
13], or postoperative malreduction due to an impaired intraoperative fragment visualization [
26,
49], while the impact of associated soft-tissue injuries is still under debate [
50,
51]. In the individual failure analysis of the present study, two of six cases may be explained solely by a potential IBM. The other four fractures showed secondary loss of reduction. While risk factors for a potential IBM were found in all cases, surgical considerations should also be included. Two cases involved the posterior column with specific involvement of the PLL, PLC, and both posteromedial segments (posteromedial shear fragments) without a supporting posteromedial buttress plate, a direct subchondral screw placement with the strongest bone stock in the tibial plateau, or malreduced posterolateral fragments due to an insufficient initial surgical approach. Addressing the posterior column has been identified as an important prognostic factor with respect to functional outcomes [
6,
7].
The most important objective clinical limitation, even in patients with good-to-excellent clinical outcome and especially in 41-type C fractures, was impaired ROM. All patients were encouraged to achieve full ROM within three months after surgery through strict rehabilitation protocols. ROM may still be improved up until the sixth month after surgery, but it may be impaired afterwards if it is not fully accomplished by the sixth month [
52]. The most important risk factor is time spent on the external fixator and bicondylar fracture involvement, which is supported by the present results [
53]. Hence, limited ROM in TPF is common and should be the focus of postoperative rehabilitation [
53,
54].
This study has some limitations. Due to its retrospective nature, data acquisition was based on patient records without a standardized assessment of systemic bone mineral disorders, including dual-energy X-ray absorptiometry or serum analyses of 25-OH vitamin D, phosphate, or creatinine levels. All medical records were carefully screened, with a special emphasis on calcium levels and secondary indicators for potential IBM. Additionally, given the complexity of different fracture patterns, the methods of ORIF differed among the fracture types, resulting in treatment bias [
5,
37]. However, this limitation reflects everyday clinical practice in orthopedic trauma surgery [
15]. In addition, postoperative CT scans were performed in only 28 patients. However, radiological evaluation to assess the Rasmussen score is established on plain radiographs [
33,
55].