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M. Ozery et al.
been shown to be comparable to aseptic TKA in terms of range of motion, knee scores, patient satisfaction, and function scores (Lee etal. 2017).
Of note, recent evidence has shown that TKA per-
formed after an episode of septic arthritis is associated
In a recent investigation, in patients with history of previously treated native septic arthritis of the same joint, as high as 8% rate of periprosthetic joint infec­tions (5 out of 62 patients) was determined (Sultan etal.
2019).
with an increased risk of periprosthetic joint infection (Sultan etal. 2019). Factors such as smoking and poor glycemic control (uncontrolled diabetes mellitus) are associated with a higher risk of periprosthetic joint
7.6 Special Considerations forTKA
inPost-Septic Arthritis
infection after TKA for a native septic joint arthritis. This may be due to poor management of medical comorbidities such as diabetes, smoking, or immuno­suppression, which could have caused the initial septic arthritis. Nonetheless, with good management of comorbidities, aggressive physical therapy, and patient
7
education, good clinical outcomes can be achieved (Bauer et al. 2010). Additionally, better clinical out­comes may be achieved by waiting at least 1year, and preferably 2years after the initial infection has cleared, before attempting a TKA (Kim etal. 2003; Sultan etal.
2019; Tan etal. 2019).
While TKA is a relatively safe choice for treating degen­erative changes after septic arthritis, there are some con­traindications to be aware of. Patients with an ongoing infection of the knee or who have a condition that might preclude them from non-emergent surgery (such as a cardiovascular event or systemic immunosuppression) should not undergo a TKA (Schmitt etal. 2017). Other situations in which TKA is contraindicated are neuro­logical disease of the lower extremity (such as a non­functional extensor mechanism) and ischemic or thrombotic leg disease (Promish et al. 2018; Thornhill and Lee (n.d.), available at 7
https://jomi. com/arti-
cle/13/total- knee- arthroplasty).
7.5.2 Complication andRevision Rates
ofTKA
One should also take into account the medical pro­le and lifestyle of the patient. If the patient is unlikely to follow up with physical rehabilitation or cannot lose
Complications that arise from the use of TKA to treat septic arthritis are essentially the same as those that arise from any joint arthroplasty. The two categories of complications are broadly classied into:
weight, then TKA is not as likely to be successful. In these instances, alternative methods should be discussed. Finally, in cases where there is signicant destruction of the joint and there is severe bone loss or ligamentous incompetence, a constrained implant (Moussa et al.
5 Aseptic complications 5 Septic complications
2017) or on occasions a hinge prosthesis should be con-
sidered (Rodríguez-Merchán 2019).
When considering septic complications, the most com­mon pathogen remains Staphylococcus aureus¸ which may be treated empirically or through bacterial culture. Common causes of aseptic complications include peri­prosthetic fracture, aseptic loosening, and polyethylene wear, among others (Lee etal. 2017).
Revision rates after TKA in post-septic arthritis patients have been demonstrated to be much higher than that of TKA patient population, in general.
> In fact, the most common reason for revision in a
patient who has had septic arthritis is joint infection
(Yu etal. 2018).
It is noteworthy that revision rates for periprosthetic joint infection (PJI) for patients after TKA range from
0.8% to 1.9% in the general population (Ratto et al.
2017), whereas revision rates for PJI are much higher
(12%) in patients who received TKA for septic arthritis (Jenny and Diesinger 2011).
Conclusion
z
Post-septic arthritis can present either as an acute, qui­escent, or evolutive infection. In persistent progressive cases, it can result in degenerative joint disease. Based on the stage of the disease, patients should be treated with aspiration, irrigation, and debridement, or total knee arthroplasty, in combination with a tailored anti­biotic protocol depending on the infecting organism, if known. While arthroscopic irrigation and debride­ment seem to produce better clinical outcomes in the acute setting, total knee arthroplasty appears to be safe at least 1 year after septic arthritis and has been shown to ensure adequate infection control and func­tional joint outcomes. It is important to counsel patients about the elevated risk of periprosthetic joint infection in these cases. Strong evidence on the choice of surgical approach (one-stage vs. two-stage) in post-septic arthri­tis is still lacking. Overall, studies investigating total knee arthroplasty in setting of post-septic arthritis are scarce. Further research on this topic is warranted.
Post-Septic Arthritis
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7
Take-Home Messages
5 For an appropriate treatment, categorization of
post-septic arthritis into acute, quiescent, or evolutive is imperative.
5 Both one-stage and two-stage TKAs result in
favorable clinical outcomes, but seem to be associ­ated with high rates of postoperative PJI.
5 Old investigations suggest the choice of one-stage
TKA for quiescent, and two-stage TKA for evolu­tive septic arthritis.
5 Even today, strong evidence is still lacking on the
choice of one-stage versus two-stage TKA.
5 More studies focusing on the use of TKA for the
treatment of post-septic arthritis are warranted.
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Inuence ofLifestyle andRisk Factors ontheDevelopment ofKnee Arthritis andOutcomes Following Cemented Total Knee Arthroplasty: AUS Perspective
JonathanDattilo andWilliamHamilton
Contents
8.1 Introduction – 76
8.2 Patient andLifestyle Risk Factors Associated withtheDevelopment ofKnee Osteoarthritis – 76
8.2.1 Patient Factors – 76
8.2.2 Lifestyle Factors – 78
8
8.3 Patient Risk Factors forAdverse Outcome Following Cemented TKA – 80
8.3.1 Aseptic Loosening – 80
8.3.2 Function andPatient Satisfaction – 82
References – 83
© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2022 E. Hansen, K.-D. Kühn (eds.), Essentials of Cemented Knee Arthroplasty,
https://doi.org/10.1007/978-3-662-63113-3_8
76
J. Dattilo and W. Hamilton
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8.1 Introduction
Osteoarthritis (OA) is the most common form of arthritis, affecting over 27million people in the United States and over 250million people worldwide (O’Neill et al. 2018; Vos etal. 2012). Among patients aged 63 to 94years, 33% were found to have radiographic pres­ence of OA (Felson etal. 1987). Additionally, it has been estimated that 45% of adults will develop symptomatic knee OA between the ages of 45 and 85 (Murphy etal.
2008). The risk factors for progression of OA are not well
understood. However, knee OA represents a substantial burden to society. The cost of treating OA in developed countries is between 1% and 2.5% of the gross domes­tic product (GDP) (Hiligsmann etal. 2013; March and Bachmeier 1997). Total knee arthroplasty (TKA) is an extremely successful and cost-effective treatment for
8
advanced knee OA but is not without complications (Price etal. 2018). While there are many additional eti­ologies of arthritis, including post- traumatic arthritis, osteonecrosis, infectious, and inammatory arthritis, this chapter will focus on primary osteoarthritis. In the rst section, we will examine patient and lifestyle factors that may contribute to the development of knee OA.In the second section, we will review the most common rea­sons for failure of cemented TKA and the correlation of individual patient variables.
8.2 Patient andLifestyle Risk Factors
Associated withtheDevelopment ofKnee Osteoarthritis
8.2.1 Patient Factors
8.2.1.1 Genetics
Genetic studies offer a partial explanation for the devel­opment of knee OA. Multiple genome-wide associa­tion studies (GWAS) have been conducted in the hopes of identifying the molecular pathogenesis of knee OA. Over 30 genetic loci have been associated with OA (Gonzalez and Valdes 2018; Kerkhof et al. 2010; Panoutsopoulou and Zeggini 2013; Zengini etal. 2018), but these have been found to explain only about 25% of heritability (Gonzalez and Valdes 2018), often as a result of differential genetic expression (Zengini etal. 2018). Other genetic efforts have focused on studies of identi­cal twins to quantify the contribution of genetics. When controlling environmental confounders, one study esti­mated that up to 65% of the variance in knee OA could be attributable to genetic factors (Spector etal. 1996). A second twin study, however, found that twins with OA of the knee were up to ve kilograms (kg) heavier than their co-twin without the disease, supporting more of an
inuence of weight than genetics (Cicuttini etal. Thus, while there is likely a component of genetic con­tribution to the development of knee OA, much remains to be investigated prior to clinical application.
8.2.1.2 Gender Dierences
> There do seem to be clear gender differences between
the burden of knee OA in men and women.
The Framingham study found that there was a slightly greater preponderance of radiographic knee OA in women (34%) than men (31%) (Felson et al. 1987). Additionally, in this study, the presence of symptom­atic knee OA was greater in women than men (11.4% vs. 6.8%). There also appear to be differences in pre­sentation between genders. Women demonstrate lower preoperative functional scores before undergoing TKA compared to men (O’Connor 1846), including reduced quadriceps strength, 6-min walk test, and stair-climbing times (Petterson etal. 2007). Additionally, women have lower preoperative Western Ontario and McMaster Universities Arthritis Index (WOMAC) scores (Lingard etal. 2004; MacDonald etal. 2008).
Gender differences among knee OA have lead many researchers to investigate the role of sex hormones in OA development. Menarche at younger age (Leung etal. 2019) and childbirth (Leung etal. 2019; Wise etal.
2013) have been associated with increased knee OA.In
fact, in the Million Women study, each additional birth was associated with an 8% increase in relative risk of knee replacement (Liu etal. 2009). Interestingly, age at menopause does not appear to alter the risk of knee replacement (Hussain etal. 2018; Liu etal. 2009), sug­gesting a temporal effect of estrogen exposure at a younger age on the risk of OA development in women. If this is true, then one may expect exogenous sex hor­mone supplementation to also inuence knee OA.While estrogen-containing oral contraceptives (OCPs) have been reported to reduce the risk of ACL injuries (Herzberg etal. 2017), studies accessing OCP use and risk of TKA compared to nonusers have demonstrated conicting results (Hussain et al. 2018; Leung et al.
2019; Liu etal. 2009). Similarly conicting ndings have
been reported with hormone replacement therapy (HRT) for postmenopausal women. In the Million Women study, patients treated with HRT had signi­cantly increased incidence of knee replacement (Liu etal. 2009), but other studies have reported a reduced risk of OA at the knee after HRT treatment (Spector etal. 1997). Therefore, the currently available evidence does not support a role for HRT in the primary preven­tion of OA.
In the male population, there is a paucity of evidence on testosterone levels and the development of OA.Testosterone levels have been associated with other
1996).
Inuence of Lifestyle and Risk Factors on the Development of Knee Arthritis and Outcomes…
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known OA risk factors including muscle weakness and BMI, and testosterone levels are known to decrease with age (Harman etal. 2001), but at present the role of tes­tosterone in the etiology of OA warrants further investi­gation prior to clinical application.
8.2.1.3 Malalignment
Lower extremity malalignment has demonstrated a signicant inuence on the development of knee OA.In fact, patient self-reported varus or valgus knee malalignment during young adulthood was associ­ated with subsequent development of knee OA later in life (McWilliams et al. 2010). The Multicenter Osteoarthritis Study (Sharma etal. 2010) reported an odds ratio of 3.59 for the development of medial knee OA in patients with varus alignment and an odds ratio of 4.85 for lateral OA in patients with valgus align­ment. Subsequent studies have reafrmed the potent inuence of malalignment, with particular risk of varus alignment on the development of medial knee OA (Felson etal. 2005).
8.2.1.4 Obesity
> Obesity is one of the most inuential risk factors for
the development of knee OA.
The World Health Organization (WHO) denes obesity as a body mass index (BMI)>30kg/m2 (James etal. 2001) (. Table8.1). In the WHO denition, obesity is further stratied into classes 1–3, or sometimes referred to as “moderate,” “severe,” or “very severe.” More commonly, authors have used “obesity” to describe patients with a BMI 30–39.9, “morbid obesity” for patients with BMI 40–49.9, and a new term of “super obesity” for patients with BMI greater than 50 (Sturm 2003) (. Table8.2). For the purposes of this chapter, we will utilize these lat­ter terms to provide consistency with the cited studies.
Among US adults in 2014, 35% of men and 40% of
women were obese (Flegal etal. 2016), and predictions
. Table 8.1 World Health Organization’s classication of
obesity (James etal. 2001)
Classication BMI (kg/m2)
Underweight <18.5
Normal range 18.5–24.9
Overweight
Obese class 1 30–34.9
Obese class 2 35–39.9
Obese class 3
25
40
. Table 8.2 Descriptive classication of obesity (Sturm
2003)
Description BMI (kg/m2)
Obesity 30–39.9
Morbid obesity 40–49.9
Super obesity
50
estimate will be 65 million more obese adults in the United States by 2030 (Wang etal.
2011). A 2010 report
estimated the total annual cost of obesity to the US economy exceeded $215billion, and that this was prob­ably twice the cost spent on adults of healthy weight (Hammond and Levine 2010). In fact, care for obese patients may account for as much as 21% of all US med­ical costs (Cawley and Meyerhoefer
2012).
The risk of knee OA in the obese population has been repeatedly demonstrated (Grotle etal. 2008; Mork etal. 2012; Sturmer etal. 2000). This risk is increased by
3.87in obese women and 4.78in obese men (Anderson and Felson 1988). Furthermore, increasing levels of obesity appear to confer additional risks. Patients with a
2
BMI  35kg/m
required arthroplasty 7years earlier compared to patients with BMI≤25 mg/kg2 (Gandhi etal. 2010).
The pathogenesis of OA in the obese patient is mul­tifactorial. Mechanically, two to ve times body weight is transmitted across the knee joint during daily activi­ties (Maquet and Pelzer 1977). Reactive forces across the patellofemoral joint are four times the body weight when ascending or descending stairs, and eight times when squatting (Reilly and Martens 1972). Thus these forces are compounded in the obese patient and can pre­cipitate early cartilage wear and the development of knee OA.On a molecular level, adipose tissue may pro­duce abnormal levels of certain hormones and growth factors which can affect cartilage and the underlying bone, possibly leading to degeneration. Adipose tissue releases adipokine, a protein that has been implicated in cartilage inammation and degradation (Pottie et al.
2006). Furthermore, modest associations between ele-
vated levels of insulin-like growth factor-1 (IGF-1) in the knee have been observed in patients with knee OA (Lloyd etal. 1996), although other studies have not sup­ported this association (Denko etal. 1990). A multitude of additional proinammatory cytokines is the subject of intense investigation (Courties etal. 2019). While a full discussion is beyond the scope of this chapter, this research is invaluable in elucidating the molecular pathophysiology of adiposity and its inuence on OA development.
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If obesity is correlated with an increased risk of knee OA, then it follows that weight loss should decrease OA risk, or at the very least symptoms of OA.Indeed, the Framingham study reported that reduction in 2 or more BMI units signicantly decreased the odds of develop­ing OA (Felson etal. 1992). Messier conducted a pro­spective, randomized trial, concluding that modest dietary weight loss in combination with moderate exer­cise leads to signicant improvement in self-reported measures of knee pain, function, and mobility (Messier et al. 2004). In this study, a 5% weight loss over an 18-month period resulted in an 18% improvement in function, and when diet was combined with exercise, this functional improvement increased to 24%. There was no difference in radiographic joint space as a prod­uct of weight loss, however. Surgically assisted weight loss offers promising results for the obese suffering from
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knee pain. In a prospective trial of vertical-banded gas­troplasty, 1year postoperatively patients lost on average 97 pounds, and 87% reported complete relief of pain in one or more joints (McGoey et al. 1990). Specically regarding the knee, in this study, 57% of patients reported pain prior to gastroplasty, which decreased to 14% at 1-year follow-up. Interestingly, the authors found no difference in patients who lost a moderate amount (< 60 pounds) of weight compared to those who lost a greater amount (>99 pounds), suggesting a possible threshold effect on weight loss. A second bariatric sur­gery report found that in patients who self-reported knee pain but did not have a formal diagnosis of OA, weight loss was associated with a rapid and dependable means of reversing the early radiologic changes associ­ated with OA (Abu-Abeid etal. 2005).
that Vitamin C may reduce the risk of cartilage loss and disease progression, but had no effect on incident OA.Vitamin K deciency has been associated with an increased risk of developing radiographic knee OA (Misra et al.
2013) and other authors have suggested
some association between lack of Vitamin K-depen­dent proteins and progression of knee OA (Shea etal.
2015). Unfortunately, while multiple replacement trials
have been conducted, no trial has demonstrated signi­cant benecial evidence in those with established knee OA.Specically, trials examining replacement of Vita­min A (Canter et al. 2007), Vitamin C (Canter et al.
2007), Vitamin D (Diao etal. 2017), Vitamin E (Wluka
et al. 2002), and selenium (Canter et al. 2007), all reported disappointing results. Therefore, the current available evidence does not support making specic recommendations regarding dietary supplementation to prevent or treat established knee OA.Turmeric is a top-selling herbal supplement (Ficke etal. 2018), the principal component of which is curcumin (Curcuma longa). Turmeric has historically been used to treat inammation through a proposed mechanism of lim­iting pro-inammatory enzymes in the cyclooxygenase and lipoxygenase families and inammatory transcrip­tion factor nuclear factor kappa beta (Aggarwal and Sung 2009; Jurenka 2009). A prospective trial of tur­meric administration in knee OA patients demonstrated decreased biochemical markers of inammation as well as improvement in patient-reported joint function, sup­porting its role as an effective herbal anti-inammatory (Belcaro etal. 2010).
There is limited, poor-quality evidence that any spe­cic diet inuences the rate of knee OA.Animal studies have shown that olive oil may lower articular cartilage degradation (Musumeci etal. 2013). A follow-up study
8.2.2 Lifestyle Factors
suggested that patients who follow a Mediterranean diet, of which olive oil is often a principle component, is
8.2.2.1 Nutrition andDietary Patterns
> Nutritional supplementation among patients suffer-
ing from musculoskeletal conditions is common, yet its efcacy is debatable.
associated with lower prevalence of knee OA (Veronese etal. 2017). High intakes of total fat and saturated fatty acids have been correlated with increased structural knee OA progression, while monounsaturated and poly­unsaturated fatty acids have been suggested to reduce
One study reported that nearly 18% of patients used some form of dietary supplements (Ficke etal. 2018). Natural vitamin supplementation has been extensively studied, but has not shown promising results. General supplementation with Vitamin D demonstrates conict­ing evidence. Felson and colleagues found that Vitamin D status was unrelated to risk of joint space or cartilage loss in knee OA (Felson etal. 2007a), while McAlindon demonstrated that low intake and low serum levels of Vitamin D each appear to be associated with increased risk for progression of knee OA (McAlindon et al.
1996). The same study found relatively poor evidence
progression (Lu et al. 2017). At present, however, spe­cic inuences of dietary patterns are of very poor and limited evidence.
8.2.2.2 Smoking andAlcohol
Smoking appears to be associated with a reduction in the risk of developing knee OA, though these ndings must be interpreted with some caution. A meta-analysis reported the relative risk of developing knee OA for smokers was 0.80, with a more marked effect in men than women (Kong et al. 2017). Hui and colleagues similarly reported that smokers had a lower odds of
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developing OA at any joint, and suggested one poten­tial mechanism could be that smokers tended to have a lower BMI than nonsmokers (Hui et al. 2011). Leung similarly demonstrated a strong dose-dependent associ­ation between increased duration and dosage of smok­ing with a decreasing risk of total knee arthroplasty (Leung etal. 2014). The authors suggested that nicotine promotes proliferation and collagen synthesis in chon­drocytes. However, these results should be interpreted with extreme caution, as the primary outcome measure was patient selection for total knee replacement, which may have been biased if surgeons did not want to oper­ate on smokers due to fear of pulmonary complications or wound healing problems.
Limited evidence exists on the effects of alcohol and knee OA. One study reported that beer consumption appears to increase the risk of developing hip and knee OA, but wine consumption was associated with a reduced risk (Muthuri etal. 2015).
8.2.2.3 Exercise andMuscle Strength
Exercise and its inuence on the risk of knee OA is a complicated issue. Anecdotally, many patients and phy­sicians surmise that long-term, high-impact exercise may risk the development of OA.While this may seem plausible, the evidence for this is not wholly convincing. In fact, multiple studies of both the general population as well as recreational runners found no increased risk of knee OA in those who reported undertaking regu­lar, “moderate” physical activity (Felson et al. 2007b; Hannan etal. 1993; Lane etal. 1993; McAlindon etal.
1999; Panush etal. 1995). However, other more intense
activities, particularly those that involve deep knee exion, have shown signicant associations with knee OA. In the Framingham study, self-reported “heavy” physical activity with a threshold of greater than 4h per day had increased odds of knee OA (McAlindon etal.
1999). A second study identied patients who engaged
in cycling and prolonged squatting as higher risk for knee OA (Dahaghin etal. 2009).
> Thus, historical assumptions of activity level on knee
OA may not be accurate, and warrant further investi-
gation to determine objective threshold measure-
ments by which practitioners can guide patients.
Muscle strength also appears to play a role in the pro­gression of knee OA.Patients with symptomatic knee OA have demonstrated reduced muscle strength, par­ticularly of the quadriceps (Leyland et al. 2012; Mur­phy etal. 2008). Historically, this has been thought to be secondary to osteoarthritis-related joint symptoms, resulting in reduced activity levels and consequent mus­cle atrophy. However, more recent studies suggest that
muscle weakness predates the onset of knee OA (Oies­tad etal.
2010; Segal etal. 2010; Slemenda etal. 1998).
Specically, weakness of the knee extensor mechanism was shown to signicantly increase the odds of develop­ing symptomatic OA (Oiestad etal. 2015).
> Therefore, muscle weakness may represent an impor-
tant modiable risk factor to help slow the progres­sion of knee OA.
A systematic review of the literature provided an inter­national consensus statement on daily activities and structured exercise related to knee OA (Vignon et al.
2006) (. Table8.3). The authors concluded that activi-
ties of daily living (ADL) were a risk factor for knee OA, and that risk increases with intensity and duration of these activities. However, the strength of the supporting data was graded as moderate, and no threshold activity level was able to be dened, limiting clinical utility in patient education.
. Table 8.3 International consensus on activity level in
knee osteoarthritis patients (Vignon etal. 2006)
Parameter (Level of evidence)
ADL (Moderate)
Structured exercise (High)
Sport and recreational activities (High)
ADL activities of daily living, OA osteoarthritis
Consensus statement Recommendation
ADL is a risk factor for knee OA, which increases with intensity and duration, but no threshold could be dened
Strengthening exercises have a favorable effect on pain and function in the sedentary knee OA patient, but it was not possible to identify a specic exercise modality that produces superior results on pain and function
Sport is a risk factor for knee OA, and this risk correlates with intensity and duration of level of exposure. However, risk of OA associated with sport was lesser than that associated with trauma or obesity
Healthy subjects can pursue a high level of physical activity, providing the activity is not painful and does not predispose to trauma
Structured exercises are recommended for the sedentary patient with knee OA
OA patients can continue to engage regularly in recreational sports as long as the activ­ity does not cause pain
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8.2.2.4 Occupation
> Occupation also appears to have a signicant effect
on the risk of knee OA.
In a landmark study of outcomes following TKA, Shar­key and colleagues identify the predominant etiologies of failure for modern TKA prostheses at 10-year follow­up (Sharkey etal. 2014).
Kwon and colleagues examined men over the age of 50 stratied by occupation type (Kwon etal. 2019). They classied occupations as follows:
5 White collar (WC) including managers, profession-
als, and ofce workers
5 Pink collar (PC) including service and salespersons 5 Blue collar (BC) including technicians and device/
machine operators
5 Agribusiness and low-level (AL) including skilled
workers in agriculture and shery and low-level laborers
> In the rst 2years, infection was the most common
reason for early revision.
Beyond 2 years, aseptic, or noninfectious, loosening was the predominant mode of failure, accounting for
39.9% of revisions. Additional etiologies for late fail­ure included infection (27.4%), periprosthetic fracture (4.7%), and arthrobrosis (4.5%). Similar results have also been reported by other authors (Schroer etal. 2013). While infection is undoubtedly an important etiology of TKA failure, it is beyond the scope of this chapter and is covered elsewhere in the text. In this section, we will
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They observed that the risk for knee OA was highest in AL and BC workers compared to WC.The risk for severe radiographic knee OA was highest in AL followed by BC occupations. WC occupations appeared to be least affected by knee OA and chronic knee pain. These conclu-
focus on specic variables which are thought to contrib­ute to aseptic failure of cemented TKA prostheses, and conclude with a brief discussion on factors that may contribute to functional outcomes and patient satisfac­tion.
sions support that knee OA risk was correlated with the degree of physical labor associated with an occupation. Another occupational study found that jobs requiring
8.3.1 Aseptic Loosening
repetitive kneeling and squatting, including mining and carpentry, were at increased odds of knee OA (Maetzel etal. 1997). Professional athletes have also been shown to have increased risk of developing knee OA, particularly soccer players and weight lifters (Kujala etal. 1995). How­ever, there may be confounding factors as soccer players may be more prone to knee injuries which could predis­pose them to post-traumatic arthritis, and weight lifters may be more prone to knee OA secondary to a higher BMI that may be more common in this population.
Additionally, in Vignon and colleagues’ systematic
Aseptic loosening is thought to be due to the devel­opment of excess wear particles that induce a proin­ammatory state, which in turn leads to osteoclast differentiation and macrophage production, ultimately leading to local osteolysis and consequent loosening of the prosthesis (Jiang etal. 2013). Aseptic loosening is an end result, and its etiology can and often may be multi­factorial. Causes may include preoperative factors such as obesity, intraoperative malalignment, or postopera­tive activity level.
international review of activity level in knee OA patients, the authors also concluded that there was a relationship between occupational activity (Vignon etal. 2006). This study found that physically demanding work was associ­ated with knee OA with a high level of evidence. However, the authors were not clearly able to characterize the bio­mechanical stresses leading to OA, which limits the gener­alizability of the ndings to specic work-related activities. Rather, they simply concluded that work- related activities
8.3.1.1 Obesity
The contribution of obesity to aseptic loosening has been extensively studied, with conicting results. Multiple studies have supported a positive association between obesity and aseptic loosening (Foran etal. 2004a; Ritter etal. 2011; Schiffner etal. 2019). Several other studies, meanwhile, have refuted these ndings (Chaudhry etal.
2019; Si etal. 2015).
that produce or maintain pain should be avoided.
> Part of this discrepancy may be due to the fact that
8.3 Patient Risk Factors forAdverse
Outcome Following Cemented TKA
loosening is likely multifactorial, and is at least par­tially inuenced by surgeon technique when cement­ing the prosthesis.
> Cemented TKA is a successful operation to treat end-
stage arthritis of the knee, with reported survivorship of 82% at 25years across a range of prosthetic designs (Evans etal. 2019).
This intuitively may be more difcult in the obese patient for whom exposure may be more challenging, yet this confounding variable may be difcult to objec­tively measure even in well-designed studies. Similarly,
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while aseptic loosening has been shown to be the pre­dominant reason for revision at 10years (Sharkey etal.
2014), other studies with shorter follow-up may not
adequately capture this mode of failure. Some authors advocate for prophylactic tibial stem extension when performing cemented TKA in the obese population to help mitigate the risk of aseptic loosening, but this has not been shown to signicantly affect early failures at an average of nearly 3-year follow-up (Steere etal. 2018).
We have previously discussed the role of weight loss in reducing the incidence and symptoms associated with knee OA, and is worth discussing the role of weight loss before and after total joint arthroplasty. Many obese patients cite their knee pain as a barrier to exercise and the consequent barrier to weight loss, which presents a challenge for the surgeon. It is a commonly held belief among the medical community that patients will lose weight after undergoing knee arthroplasty, but a meta­analysis reporting 1-year follow-up presented strong evi­dence that this does not in fact occur within this time period (Inacio etal. 2013). Furthermore, one study dem­onstrated that at 12-month follow-up, while 12.5% of obese patients had achieved a clinically signicant weight loss of 5% after arthroplasty, 21% had actually gained weight. However, a longer term study looking beyond 2-year follow-up did support a statistically sig­nicant decrease in weight after TKA, suggesting that TKA may facilitate weight loss, but that these effects may not be appreciable until outside of the follow-up period utilized in prior studies (Duchman etal. 2014).
Additionally, many surgeons refer obese patients for bariatric surgery prior to elective total joint arthroplasty. Springer reported on the fate of these patients, noting that only 23% of referred patients actually attended their bariatric appointment and only 7% underwent bar­iatric surgery prior to arthroplasty. The authors of this study make an interesting point that some surgeons argue that obese patients cannot lose weight due to their musculoskeletal limitations and, therefore, we should operate on them regardless of BMI. However, the authors state that we would not consent to operate in other forms of uncontrolled disease, such as diabetes or open wounds, and that one might consider a similar stance for obesity. Parvizi et al. reported on the out­comes of patients who underwent bariatric surgery prior to TKA (Parvizi et al. 2000). The mean reduction in BMI was from 49 to 29, and mean time from bariatric surgery to joint replacement was 23 months. In this study, Knee Society scores (KSS) improved signicantly postoperatively and no patient required revision at mean follow-up of 3.7years.
> The authors conclude that morbidly obese patients
with severe osteoarthritis who are deemed unsuitable for joint replacement because of weight should be considered for bariatric surgery.
8.3.1.2 Malalignment
Malalignment after TKA has been shown to be a sig­nicant reason for revision surgery (Evans etal. 2019). Severe malalignment may predispose to early failure due to abnormal joint biomechanics, while less pronounced malalignment could predispose to implant loosening secondary to abnormal joint forces across the implant– cement or cement–bone interfaces. Preoperative align­ment is predictive of postoperative failure, with increased risk associated with greater than 8° of varus or greater than 11° of valgus (Ritter etal. 2013). In patients under­going TKA with traditional instrumentation, preopera­tive limb alignment and BMI were signicant predictive factors in postoperative limb alignment (Estes et al.
2013). Obesity has been shown in several studies to be
a risk factor for postoperative malalignment, including risk in technical errors of component malpositioning (Gaillard etal. 2017; Jarvenpaa etal. 2010), and a higher risk for varus limb malalignment with increased BMI (Gaillard etal. 2017). One study has refuted these nd­ings, showing no difference in malalignment after TKA (Ojard etal. 2018). A study of computer navigation in TKA showed no differences in postoperative limb align­ment in the obese compared to non-obese, suggesting a potential benet of computer navigation to help miti­gate the reported risks of malalignment in this popula­tion (Shetty etal. 2014).
8.3.1.3 Activity Level
As activity level has historically and perhaps erroneously been associated with increased knee osteoarthritis, simi­larly we have assumed that increased activity would lead to earlier failure of cemented TKA.In a meta- analysis of aseptic loosening after total hip arthroplasty (THA) and TKA, Chierian and colleagues found that high activity levels were a risk factor for loosening in THA, but this was not replicated in TKA (Cherian etal. 2015). In fact, using the University of California, Los Angeles Activity Scale, Crawford etal. reported that after controlling for confounding variables, highly active patients actually demonstrated increased survivorship at 5-year mini­mum follow-up compared with lower activity patients (Crawford etal. 2020). While these ndings attempt to refute historical dogma, further study is warranted to ascertain if these trends persist with longer follow-up.