June 2012

ACL injury and OA risk: Surgery’s complicated role

istockphoto.com #11232345

Given the accumulating evidence linking anterior cruciate ligament injury to early-onset osteoarthritis, one might reason that surgical repair of the injured joint would decrease that risk. But too often that isn’t the case. This two-part series explores the complicated ways, both negative and positive, that surgery can influence OA risk.

By Cary Groner

Orthopedists and athletic trainers typically understand that the long-term consequences of anterior cruciate ligament (ACL) injury may include osteoarthritis. The meniscal damage frequently associated with ACL rupture and surgery to address that damage both compound the risk.1 Nevertheless, the biomechanical and chemical processes that lead from a torn ACL to degenerative joint disease are only now being elucidated, and many clinicians still disagree about what’s going on and what to do about it.

Contentious issues include the nature of the initial injury to cartilage and subchondral bone; if biochemical processes or stabilization issues are more to blame for OA; whether surgical intervention is superior to conservative care in preventing the progression from the initial ligament injury to osteoarthritis; and, when ACL reconstruction is done, whether certain approaches are superior to others for stabilizing the joint and reducing OA risk.

“This is a problem we thought we had under control, but it turns out we don’t,” said Jonathan Chang, MD, a clinical associate professor of orthopedics at the University of Southern California in Los Angeles. “In sports medicine we are looking for new directions to see if there is a way to stanch what looks potentially like a coming epidemic of arthritis in reconstructed knees. At the moment, we’re just trying to get a handle on how big the problem is, and what some of the risk factors are.”

shutterstock.com #47837272

According to Stefan Lohmander, MD, a professor in the Department of Orthopedics at Lund University in Sweden, dealing with an ACL tear involves two stages.

“First is what happens at the moment of acute injury, and second is what happens down the road,” he said. “Researchers are trying to find out if there are interventions we could do in the first hours or days after injury, similar to how we intervene when someone is having a heart attack or a stroke. Then later, when the biomechanics and dynamic movements of the joint are not normal, what can we do? If we can’t put it right again, then every remaining step in the individual’s lifetime will put an abnormal load onto the knee joint.”

Scope of the problem

Ten to 20 years after an ACL injury or meniscal tear, some studies report that roughly half of patients have osteoarthritis.1 Other research suggests even higher rates. For example, in a cohort of 19 elite athletes with untreated ACL ruptures who were symptomatically stable, all had meniscectomies by 20 years; by 35 years all had degenerative changes associated with OA, and eight (42%) had undergone total knee replacement.2

Clinicians and researchers do agree on the rough parameters of the physical catastrophe. The initial ACL rupture damages the cartilage of the tibial plateau and the lateral femoral condyle; this appears to trigger cytokine and protease cascades in the joint, which increases the catabolism of chondrocytes.3 Postrupture knee instability may further damage the meniscus and the articular cartilage, particularly in the medial compartment, where most OA occurs.4,5

Research shows that by 10 years, all patients with an untreated ACL rupture will have a medial meniscal tear, though this includes those who incurred meniscal damage at the initial injury.6 That damage, particularly loss of the posterior horn of the meniscus, increases the anterior displacement of the tibia on the femur, concentrates the axial load in specific areas, and increases shear forces. Not everyone with a meniscal injury will develop OA, of course, but about half do by 20 years postinjury, and the risk is affected by factors including the presence of finger osteoarthritis (a hereditary marker for generalized OA), obesity, and sex.1

shutterstock.com #1717682

In a 2007 paper in the American Journal of Sports Medicine (AJSM), Lohmander summarized in three categories the reasons for the variation in reported long-term OA outcomes in patients with ACL and/or meniscal tears. The first category includes the injury itself, reconstructive surgery and rehab, return to sport, chronic instability, and later injuries associated with these variables. The second category comprises the individual’s activity level, strength, body mass index (BMI) and personality. The third consideration is that the way OA is diagnosed and assessed—for example, using x-ray, magnetic resonance imaging (MRI), or patient symptom scores—can produce inconsistent results.1

To cut or not to cut

Experts have long debated the relative value of ACL reconstruction in preventing OA. Much of the research suggests that it has a protective effect; for example, in one study of patients with reconstructed knees at 20 years follow up, the reported risk of osteoarthritis ranged from 14% to 26% with a normal medial meniscus and up to 37% after meniscectomy. By contrast, those with untreated ruptures developed OA 60% to 100% of the time.1

The problem with assessing such statistics is the time lag between injury (with or without surgery) and the appearance of either radiographic or symptomatic osteoarthritis. It’s a little like astronomers viewing a star, knowing that the light reaching their eyes was actually set in motion millions of years before. Clinicians are now seeing the results of surgeries performed two or three decades ago, when techniques were less refined.

“Prior to the late 1980s, football players didn’t want to get their ACLs reconstructed because it was an open procedure followed by six weeks in a cast, and it was six months before you could walk,” said Leo Pinczewski, MD, an associate professor of orthopedics at the University of Notre Dame in Sydney, Australia. “A combination of the surgery, and the fact that the patients lost their menisci, led to a hundred percent incidence of osteoarthritis at ten years. I was almost ready to give up ACL surgery, because even though we were making our patients more stable and allowing them a higher level of activity, we were abetting the development of osteoarthritis.”

The advent of arthroscopic surgery changed all that, Pinczewski said.

“Between 1988 and 1992, I did eighteen hundred bone-patellar tendon-bone [BPTB] reconstructions, and we could use interference screws to fix the graft. That meant we could get rid of casts and bracing and get patients moving straight away,” he said. “We found that if you operated on the ACL before the patient damaged their meniscus or articular cartilage due to instability, it took a lot longer to develop any arthritis, and not everyone did. Now we know that patients who have surgery within four months of their ACL injury have significantly less osteoarthritis at fifteen years than those who have their surgery later than four months [unpublished data]. The longer you wait, the more meniscal and articular cartilage damage there is.”

James Murray, MD, an orthopedic knee specialist at the Avon Orthopaedic Center and Frenchay Hospital in North Bristol, UK, agreed that the four-month window to surgery is important.

“When you have an unstable knee with rotational laxity, the chance of damaging the meniscus is higher on the medial side, and meniscal injury after untreated ACL injury is roughly one percent per month,” he said.4 “People who’ve had nonoperative treatment of ACLs progress to medial arthritis.”

Naturally, not everyone in the field concurs. In 2010, Lohmander, Richard Frobell, PhD, and their colleagues published a paper in The New England Journal of Medicine that provoked a lively exchange of letters to the editor in that and other journals. The paper concluded that a strategy of rehabilitation with early ACL reconstruction wasn’t any better than rehab plus optional delayed reconstruction in affecting an array of two-year outcomes, including pain, symptoms, function in sports, and knee-related quality of life.7

Detractors took issue with several aspects of the study. Not the least of these was that, of the 59 subjects in the optional delayed-reconstruction group, 23 ultimately chose to have ACL reconstruc­tion, at an average of about a year after randomization.

Of course, two years isn’t enough time to glean much information about OA risk, and the authors didn’t evaluate this variable directly. However, critics noted that in a pivot-shift test, just 47% of the delayed group scored normal, versus 75% of those in the immediate surgery group. Because pivot shift is a measure of stability that may affect later OA risk, the statistic could have implications for osteoarthritis prevention. Nevertheless, in one of the responses to the letters regarding their article, Lohmander and his colleagues wrote, “there is insufficient evidence to show whether ACL reconstruction is associated with less or more post-injury osteoarthritis compared with nonsurgical treatment.”8

Lohmander is polite, soft-spoken, and composed when discussing his research; you don’t get the feeling you’re talking to a firebrand with an ax to grind. His point is simply about evidence.

“There will be continued development in terms of finding the optimal way to reconstruct the ACL and rehabilitate patients, whether they have a surgical reconstruction or not,” he told LER. “I think our study provides the best evidence so far, but that doesn’t mean it’s the last word.”


Of course, many surgeons (including Pinczewski) believe that by stabilizing the knee, prompt ACL reconstruction helps prevent further meniscal and chondral injuries that could increase the risk of osteoarthritis.

“In our practice, the incidence of osteoarthritis after ACL reconstruction has dropped from a hundred percent to less than ten percent—and when we use hamstring tendons, less than five percent,” Pinczewski said. “To determine how surgical repair versus nonsurgical treatment affects the risk can’t be studied ethically, because you’d have to send the nonsurgical group back out to be as active as the surgical group—and if they are, they’ll tear their menisci, which is a death sentence to the knee as far as arthritis is concerned.”

Pinczewski’s remarks about patellar versus hamstring tendons raise the issue of whether certain approaches to ACL reconstruction provide more stability than others, and by implication reduce osteoarthritis risk. In the early days, most ACL reconstructions were performed BPTB, and many still are. Many surgeons now prefer to use hamstring tendons, however, and there are also debates about single- versus double-bundle approaches, nonanatomic versus anatomic graft positioning, and so forth. The evidence conflicts, but opinions remain strong.

“By the early 1990s, my patients were complaining about the morbidity of taking the mid-third of the patellar tendon,” Pinczewski said. “They couldn’t kneel on it, they had anterior knee pain, they got patellar tendinitis.”

There were other problems as well. After five years, some patients were developing problems achieving full knee extension. It turned out that when the patellar tendon was removed from the knee, it shrank about 10% over time—a phenomenon that has also been described in the literature.9 This changed the position of the kneecap, Pinczewski said, which created abnormal stresses and fostered osteoarthritis.

“Once you take a patellar tendon out of a patient’s knee, they don’t walk the same way,” Pinczewski said. “There’s a decreased flexion moment at heel strike and more force going through the knee. That extra force, over a million steps a year, was causing medial compartment osteoarthritis.”

In 1994, Pinczewski turned to the emerging alternative technique of using hamstring tendons instead. Initially, there were problems with the new approach, too.

“With patellar tendons, you had bone blocks you could screw into bone, and the fixation wasn’t as good with hamstring tendons,” he said. “We improved that, and once we did, we had the same stability with a lot less morbidity, so I became a champion of that approach.”

Recently published research bolsters the case for BPTB reconstructions, however. In AJSM this past February, UK investigators reported a 13-year follow-up of patients who’d received patellar-tendon ACL reconstructions. The authors found that the approach provided a good outcome, measured as IKDC (International Knee Documentation Committee) radiological grades and patient-centered subjective measures.10

Perhaps surprisingly, the study’s lead author, James Murray, said that his personal preference is usually to use hamstring tendons.

“It’s easier and quicker to harvest and it has lower morbidity,” he said. “I use BPTB more in a revision setting, and I think it’s actually a good graft for that. It goes in quicker, and there are more solids to integrate because of the bone blocks.”

Patellar vs. hamstring

The recent scientific literature doesn’t strongly favor one approach over the other—though again, some have measured not OA outcomes per se but other potentially predictive parameters. For example, a 2007 study from Pinczewski and his colleagues reported that 10 years after surgery, in 180 patients who had received either BPTB (n=90) or hamstring tendon (HT, n=90) reconstructions, radiographic osteoarthritis was more common in the former than in the latter.11 A follow-up published this year reported similar results.12

However, a 2008 study in Sweden, published in Arthroscopy, randomized 124 patients to ACL reconstructions using either BPTB or HT; at an average seven years out, radiographic OA rates were comparable between the groups.13 A year later, another Swedish study randomized 71 patients to ACL reconstruction using the two methods; researchers reported no significant differences in knee laxity seven years later.14

A 2009 meta-analysis from France, however, concluded that BPTB reconstructions were more stable (defined as a decreased pivot-shift risk) than those performed with hamstring tendons.15 In 2011, Canadian investigators performed a Cochrane review of 19 clinical trials involving 1597 subjects and found that long-term results were insufficient to compare later osteoarthritis rates. They did note, however, that while patellar tendon reconstructions were more likely to result in statically stable knees, they were also associated with more anterior knee problems (the issue encountered by Pinczewski in his practice).16 A systematic review from Duke researchers the same year reached similar conclusions.17

Two 2011 studies from researchers at La Trobe University in Melbourne, Australia, examined the effects of different ACL reconstruction methods on knee kinematics. The first study found no differences between graft types for internal-external rotation (both groups had decreased internal rotation compared to the controls and to the contralateral knee); the hamstring group had less varus rotation than the patellar tendon and control groups, but varus rotation for the involved knee in that group did not differ from the contralateral knee.18 The second study found no difference in postsurgical knee adduction moments between the two graft types.19

Research from the University of Pittsburgh, published in AJSM in 2011, found no significant difference in outcomes between graft types, but did report surprisingly high rates of radiographic osteoarthritis—39% at an average of 7.8 years after surgery. Predictors of OA risk included female sex, high BMI, longer time from injury to surgery, medial and patellofemoral compartment chondrosis, prior or concurrent meniscectomy, and longer length of follow up. (Obesity and medial compartment chondrosis of grade 2 of higher were the strongest predictors.)20

A study from South Korea, published in Arthroscopy this year, followed 117 patients who had BPTB autografts and reported similar osteoarthritis rates (~40%) at a mean of 10 years out. OA onset in the medial compartment (30.7%) was correlated with partial meniscectomy and sagittal tibial tunnel position, whereas OA in the lateral compartment (9.3%) related to higher BMI.21

Graft placement

As suggested by the Korean study, tunnel position and graft placement are also contentious issues among orthopedists. The biggest question is how to best mimic native, preinjury anatomy in order to stabilize the knee.

“Getting the graft in the right place is one of the prime determinants for osteoarthritis,” said Pinczewski. “The big thrust of AAOS [American Academy of Orthopaedic Surgeons] instruction for the past two or three years has been to convert American surgeons into anterior-medial portal drillers, which gives you a more anatomical position compared to the current transtibial tunnel drilling of the femoral tunnel.”

In a 2008 paper published in the Journal of Bone and Joint Surgery (JBJS), Pinczewski and his colleagues delineated the method and reported good clinical outcomes at seven years, noting that “vertical graft inclination is associated with increased rotary instability and radiographic osteoarthritis.”22

Jonathan Chang, at USC, noted that another recent important development has been “double-bundle” reconstruction, which involves two separate limbs of graft inserted into the femur around the anatomic location of the original ACL, versus a single bundle approach. Researchers have reported that the technique restored normal rotational knee motion in pivot-shift testing, that it led to greater rotational stability, and that it was associated with both higher subjective outcome scores and better results in manual stability tests, versus single-bundle construction.23-25

“It is more anatomic, and it may function a little better,” Chang said. “But then the question becomes whether the additional time and expertise required is justified by the potential for future improvements in arthritis. The literature is rife with all kinds of so-called improvements in technique that have never panned out, and it takes ten or twenty years before we know.”

“There is a debate about double-bundle grafts,” confirmed Timothy Hewett, PhD, a professor and director of research at the Ohio State University Sports, Health, and Performance Institute, and director of the Sports Medicine Biodynamics Center at Cincinnati Children’s Hospital.

“The primary idea is that it reproduces the in situ anatomy of the native ACL better than a single-bundle graft,” Hewett said. “Five or six years ago, proponents of this approach said the only way to anatomically reconstruct the ACL is with both an anterior medial and a posterior lateral bundle. They’ve backed off a little since then; now the thought is that a single-bundle is okay as long as you get it in the anatomic positioning of the footprint of the ACL on the tibia and femur, and it angulates in such a way—about forty-five degrees as it crosses the joint from the frontal plane—that it is like the original anatomy and limits rotation of the tibia relative to the femur.” (This is the same technique described above by Pinczewski.)

As Chang noted, time will tell about the relative efficacy of such approaches.

Cary Groner is a freelance writer in the San Francisco Bay Area.

This is the first in a two-part series on surgical repair of ACL injury and osteoarthritis risk. In our next issue, Part 2 will discuss the effect of meniscal damage and surgery on OA risk, theories about the role of proprioception, and new MR findings regarding the degree of post-injury chondral damage and its implications for ACL reconstruction and later osteoarthritis.


1. Lohmander LS, Englund PM, Dahl LL, Roos EM. The long-term consequence of anterior cruciate ligament and meniscus injuries: osteoarthritis. Am J Sports Med 2007;35(10):1756-1767.

2. Nebelung W, Wuschech H. Thirty-five years of follow-up of anterior cruciate ligament-deficient knees in high-level athletes. Arthroscopy 2005;21(6):670-696.

3. Potter HG, Sain SK, Ma Y, et al. Cartilage injury after acute, isolated anterior cruciate ligament tear: immediate and longitudinal effect with clinical/MRI follow-up. Am J Sports Med 2012;40(2):276-285.

4. Louboutin H, Debarge R, Richou J, et al. Osteoarthritis in patients with anterior cruciate ligament rupture: a review of risk factors. Knee 2009;16(4):239-244.

5. Branch TP, Browne JE, Campbell JD, et al. Rotational laxity greater in patients with contralateral anterior cruciate ligament injuries than healthy volunteers. Knee Surg Sports Traumatol Arthrosc 2010;18(10):1379-1384.

6. Neyret P, Ait si Selmi T, Gluchuk Pires L. Arthrose et laxite. Conference d’enseignement, Societie Francaise d’Arthroscopie 1999:25-45.

7. Frobell RB, Roos EM, Roos HP, et al. A randomized trial of treatment for anterior cruciate ligament tears. New England J Med 2010;363(4):331-342.

9. Lohmander LS, Frobell RB, Roos EM. A scientific approach to optimal treatment of cruciate ligament injuries. Acta Orthopaedica 2011;82(3):389-392.

10. Bernicker JP, Haddad JL, Lintner DM, et al. Patellar tendon defect during the first year after anterior cruciate ligament reconstruction: appearance on serial magnetic resonance imaging. Arthroscopy 1998;14(8):804-809.

11. Murray JR, Lindh AM, Hogan NA, et al. Does anterior cruciate ligament reconstruction lead to degenerative disease? Am J Sports Med 2012;40(2):404-413.

12. Pinczewski LA, Lyman J, Salmon LJ, et al. A 10-year comparison of anterior cruciate ligament reconstructions with hamstring tendon and patellar tendon autograph: a controlled, prospective trial. Am J Sports Med 2007;35(4):564-574.

13. Leys T, Salmon L, Waller A, et al. Clinical results and risk factors for re-injury 15 years after anterior cruciate ligament reconstruction: a prospective study of hamstring and patellar tendon grafts. Am J Sports Med 2012;40(3):595-605.

14. Liden M, Sernert N, Rostgard-Christensen L, et al. Osteoarthritic changes after anterior cruciate ligament reconstruction using bone-patellar tendon-bone or hamstring tendon autografts: a retrospective, seven-year radiographic and clinical follow-up study. Arthroscopy 2008;24(8):899-908.

15. Ahlden M, Kartus J, Ejerhed L, et al. Knee laxity measurements after anterior cruciate ligament reconstruction, using either bone-patellar tendon-bone or hamstring tendon autografts with special emphasis on comparison over time. Knee Surg Sports Traumatol Arthrosc 2009;17(9):1117-1124.

16. Biau DJ, Katsahian S, Kartus J, et al. Patellar tendon versus hamstring tendon autografts for reconstructing the anterior cruciate ligament: a meta-analysis based on individual patient data. Am J Sports Med 2009;37(12):2470-2478.

17. Mohtadi NG, Chan DS, Dainty KN, Whelan DB. Patellar tendon versus  hamstring tendon autografts for anterior cruciate ligament rupture in adults. Cochrane Database Syst Rev 2011;7(9):CD005960.

18. Magnussen RA, Carey JL, Spindler KP. Does autograft choice determine intermediate-term outcome of anterior cruciate ligament reconstruction? Knee Surg Sports Traumatol Arthrosc 2011;19(3):462-472.

19. Webster KE, Feller JA. Alterations in joint kinematics during walking following hamstring and patellar tendon anterior cruciate ligament reconstruction surgery. Clin Biomech 2011;26(2):175-180.

20. Webster KE, Feller JA. The knee adduction moment in hamstring and patellar tendon anterior cruciate ligament reconstructed knees. Knee Surg Sports Traumatol Arthrosc 2011 Dec 24. [Epub ahead of print]

21. Li RT, Lorenz S, Xu Y, et al. Predictors of radiographic knee osteoarthritis after anterior cruciate ligament reconstruction. Am J Sports Med 2011;39(12):2595-2603.

22. Ahn JH, Kim JG, Wang JH, et al. Long-term results of anterior cruciate ligament reconstruction using bone-patellar tendon-bone: an analysis of the factors affecting the development of osteoarthritis. Arthroscopy 2012; Mar 13. [epub ahead of print]

23. Pinczewski LA, Salmon LJ, Jackson WF, et al. Endoscopic anatomic landmarks for tunnel placement in anterior cruciate ligament reconstruction and their relationship to seven-year clinical outcome. J Bone Joint Surg Br 2008;90(2):172-179.

24. Tsai AG, Wijdicks CA, Walsh MP, Laprade RF. Comparative kinematic evaluation of all-inside single-bundle and double-bundle anterior cruciate ligament reconstruction: a biomechanical study. Am J Sports Med 2010;38(2):263-272.

25. Siebold R, Dehler C, Ellert T. Prospective randomized comparison of double-bundle versus single-bundle anterior cruciate ligament reconstruction. Arthroscopy 2008;24(23):137-145.

26. Siebold R, Branch TP, Freedberg HI, Jacobs CA. A matched-pairs comparison of single- versus double-bundle anterior cruciate ligament reconstruction: clinical results and manual laxity testing. Knee Surg Sports Traumatol Arthrosc 2011;19(suppl 1):S4-S11.

2 Responses to ACL injury and OA risk: Surgery’s complicated role

  1. Clyde Smith says:

    Enjoyed the review.
    I have had the experience of seeing patients (40+ years in practice of Sports Physiotherapy),of Dr”s, Slocum (Eugene Oregon),Kennedy (London, Ontario), Robert Jackson (father of arthroscopic), J.P. McConkey and many others. I have some patients that I have followed for over 30 years.
    What is not discussed in you paper is the rehab techniques. The surgical techniques I have no control over but favour the hamstring tendon to any other. I have seen and treated surgeries using carbon struts, IT band, and one of the worst being electrodes wrapped around the repair. Boy did that junk in the joint give negative joint reactions. I trained when the surgeon barged about taking the whole meniscus out and being proud that they got that big thing out of there? In the mid 70’s Dr Ryan (editor of Physician and Sports Medicine) wrote and editorial on Orthopaedic surgeons should become more like gardeners and less like carpenters, and learn to preserve tissue. It was around that same time Dr. Robert Jackson (one of the finest men I ever met) was changing the surgical world lwith arthroscopic techniques.
    As rehab go’s the important factors are 1. Sub Chondral bone bruising. 2.Meniscal damage. Either of these conditions should favour a open chain movements patterns until either or both are recovered. Then move into closed chain.The patients I have followed ( one from 1978 with both ACL’s and PCL’s, with no significant OA changes as of three years ago) all had open chain work for months following the repairs (Cybex, Kin Kom, Orthotron) These did not give negative joint reactions and certainly did not create joint laxity or damage to the repairs. I understand the fears but the art is in the application. I used these techniques as they gave the least negative joint reactions along with Isometrics where needed. Closed chain became a buss word and flavour of the month type of program. There are no medical facts to show that “closed chain” is superior to open chain in early program. In a normal healthy joint , OK, but not in a joint with pathology. Sure we hope to get back to a healthy joint. I am not talking about “early return to play”. I am talking about the medically sound rehabilitation of a joint and giving it the best chance to have a healthy life. Gary Gray made it popular with his series of “Chain Reaction” seminars. It was not until the introduction of MRI that the massive bone bruises that can occur with the mechanics of ACL injury that I understood the outcomes/reasons of some post op situations. Insurance companies in the United States and Orthopaedic surgeons alike have jumped onto it, using early return to play as the bench mark. Insurance Companies will not pay if open chain is used. That saves them money so they do not have to pay for the use of such devices. It has nothing to do with facts. In my carrier I have tested well over 10,000 knees on Cybex and KinCom devices. Not one injury or ligament failure resulted. Lots of muscle soreness.
    It is my belief that all young athletes prior to maturation should have at least 1 year of recovery before return to play. Why? Growth Hormone is the reason. They still have a healthy production of the stuff that older athletes wish they could use. A year of recovery and constructive training would give the best possible wind of a healthy joint.
    I have seen nothing on the reporting of the sub chondral bone bruising and the effects of it on hyline cartilage

  2. Stoob Franziska says:

    I’m a student in physiotherapy at the SUPSI/ Dipartimento sanità/ Physiotherapie
    Graubünden in Landquart, Switzerland. Currently I’m working on my bachelor-thesis,
    which is about ” Osteoarthritis of the knee a result after a ACL tear”.
    During my research on pubMed I found your article “ACL reconstruction and risk of knee OA, part 2” and the other one „ACL injury and OA risk: Surgery’s complicated role.“
    I read the abstract and I found it really interesting. Your work would be useful for my
    bachelor thesis. That`s why I would like to ask you if you could send me a digital version of your study. Your help is much appreciated.

    If possible please send it to: f.stoob@bluewin.ch

    Kind regards,
    Franziska Stoob

Leave a Reply

Your email address will not be published.

This site uses Akismet to reduce spam. Learn how your comment data is processed.