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Correspondence response
Response to: ‘The role of infrapatellar fat pad resection in total knee arthroplasty’ by White et al
  1. Weiyu Han1,2,
  2. Faming Pan3,4,
  3. Zhenhua Liu1,2,
  4. Zhaohua Zhu1,
  5. Xia Wang1,
  6. Shuang Zheng1,
  7. Benny Antony1,
  8. Changhai Ding1,4,5
  1. 1Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia
  2. 2Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China
  3. 3Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, Anhui, China
  4. 4Arthritis Research Institute, 1st Affiliated Hospital, Anhui Medical University, Hefei, Anhui, China
  5. 5Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia
  1. Correspondence to Professor Changhai Ding, Private Bag 23, Hobart, Tasmania 7000, Australia; Changhai.Ding{at}utas.edu.au

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We thank White and Melhuish1 for their interest in our original paper2 and our response3 to Bai et al.4

There is moderate level evidence in a recent systematic review showing that infrapatellar fat pad (IPFP) preservation improves clinical outcomes post total knee arthroplasty (TKA), whereas IPFP resection increases post-TKA knee pain.5 This is contradictory with a previous systematic review suggesting that there were no differences in function, range of motion and anterior knee pain between preservation and resection groups after TKA in knee osteoarthritis (OA).6 This new evidence is consistent with our findings that the IPFP maximal area was associated with reduced knee pain, decreased loss of cartilage volume and reduced risks of increases in cartilage defects cross-sectionally in older adults7 and longitudinally in older women,2 indicating a beneficial effect of IPFP size.

More epidemiological and clinical studies are emerging to show that IPFP size or preservation in TKA may have protective roles for knee symptoms and structural changes in knee OA. Teichtahl et al8 reported that a larger IPFP at baseline was significantly associated with reduced knee pain at follow-up and decreased lateral tibial cartilage volume loss, and Cai et al9 reported that greater IPFP volume was associated with greater tibial and patellar cartilage volume, and fewer cartilage defects, bone marrow lesions and osteophytes in patients with knee OA. The findings from Gwyn et al's retrospective study10 showed that complete resection of IPFP was associated with patellar tendon shortening 1 year after TKA, while there was no significant change in tendon length with partial resection of IPFP.

In contrast, IPFP with abnormal quality may play a detrimental role in knee OA. Our recent study demonstrated that IPFP signal intensity alteration, which was negatively associated with maximum area of IPFP, was associated with increased knee cartilage defects, subchondral bone marrow lesions and knee pain, and decreased knee cartilage volume cross-sectionally and longitudinally in older adults.11 Consistently, we reported that some IPFP signal intensity measures, assessed using a semi-automated quantitative method, were consistently associated with increased structural abnormalities of the knee in patients with knee OA.12

All these evidences support our hypothesis that IPFP would have biphasic effects in knee OA: it may have a beneficial role physiologically through increased size, but could be detrimental when pathological changes are observed as signal intensity alteration on MRI. We proposed that IPFP with normal qualities, rather than abnormal qualities, should be preserved or not damaged during knee surgery,3 which needs to be tested by well-designed randomised controlled trials.

In summary, we cannot totally agree with White's view that ‘practice should transition to favour IPFP preservation where possible’, but suggest to have IPFP quality evaluated using MRI before an action (IPFP preservation or resection) is taken in TKA. If there are no significant signal intensity alterations within IPFP, IPFP should be preserved during TKA. High quality randomised controlled trials with appropriate sample size and outcome measures are required to determine our hypothesis.

References

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Footnotes

  • Contributors All authors contributed to this article.

  • Competing interests None declared.

  • Patient consent Obtained.

  • Ethics approval Approved by the Southern Tasmanian Health and Medical Human Research Ethics Committee.

  • Provenance and peer review Commissioned; internally peer reviewed.

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