Fatty lesions in intra-articular loose bodies: a histopathological study of non-primary synovial chondromatosis cases

Matsukuma, Susumu; Takeo, Hiroaki; Okada, Kenji; Sato, Kimiya

doi:10.1007/s00428-011-1172-0

Cited by 5 publications

(8 citation statements)

References 18 publications

(39 reference statements)

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“…25 In the current study, MFN was identified in 58 d-AVs (83%) and in 63% of nd-AVs, which are higher than or almost equal to the reported incidences (38-75%) of MFN in subcutaneous tissues affected by some underlying diseases. 18 Therefore, AV is one of the previously unrecognized common target organs of MFN.…”

Section: Discussionmentioning

confidence: 72%

Fat cells and membranous fat necrosis of aortic valves: A clinicopathological study

Matsukuma

Takeo

Kono

et al. 2013

Pathology International

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We examined 152 aortic valves (AVs), which included 82 postmortem non-dysfunctional AVs (nd-AVs) and 70 surgically removed dysfunctional AVs showing aortic stenosis (AS), aortic regurgitation (AR), or combined AS and AR (AS-R). Fat cells, membranous fat necrosis (MFN), and fat-MFN-related lesions composed of fat cells and/or MFN were found in 127 (83.6%), 110 (72.4%), and 140 (92.1%) of 152 AVs, respectively, and all were associated with older age (P = 0.010, P = 0.022, and P = 0.003, respectively). MFN was associated with fibrous thickening and calcification (both, P = 0.001). Nd-AV fat cells and fat-MFN-related lesions were not correlated with body mass index. Compared with ageand sex-matched control cases, MFN in AS and AS-R cases was more frequent (P = 0.030 and P = 0.045, respectively), but MFN in AR cases showed no significant differences. Fat-MFN-related lesions, possibly representing true preceding fat cells, showed no differences in AVs with and without dysfunction or in dysfunctional types. These data suggest that AV fat cells are age-related, obesity-independent, and AV dysfunction-unrelated common phenomenon. MFN is also age-dependent and could be caused by AS and AS-R, which is probably concerned with AV thickening and calcification.Key words: aortic valve, fat, fat necrosis, heart, membranous dystrophy, membranous fat necrosis, valvular dysfunction Lipid deposits or accumulation of aortic valves (AVs) has been reported to be related to aging and/or calcific changes 1-6 and tumorous fatty lesions of AVs have been rarely reported.7-11 However, the clinicopathological features of non-tumorous AV fat cells remain poorly understood, 11,12 although they may be scarce and represent a metaplastic condition associated with calcified or ossified valves. 12,13Recently, our routine examination of stenotic AVs incidentally disclosed not only fat cells, but also small bodies with eosinophilic serpiginous membranes closely resembling the histological features of membranous fat necrosis (MFN) [14][15][16] (unpublished data). MFN, also called membranous lipodystrophy-like changes, membranocystic changes, membranocystic fat necrosis, or lipomembranous fat necrosis, [16][17][18][19] was initially considered a morphologic hallmark of 'membranous dystrophy,' 'lipomembranous polycystic osteodysplasia,' or 'Nasu-Hakola disease,' 12,[16][17][18][19][20] and is now known to be a peculiar form of fat necrosis. 16 However, to the best of our knowledge, MFN has not been mentioned previously in AVs with or without valvular dysfunction. We questioned whether or not AV fat cells and/or MFN-like bodies are concerned with AV dysfunction. Therefore, we examined the clinicopathological characteristics of these lesions in postmortem non-dysfunctional AVs (nd-AVs) and surgically removed dysfunctional AVs (d-AVs). MATERIALS AND METHODSEighty-two postmortem nd-AVs were available from 10% buffered formalin-fixed heart specimens in 82 patients without AV dysfunction (52 men and 30 women with a mean age of 70.6 years; range, 40-95 years), ...

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Section: Discussionmentioning

confidence: 72%

Fat cells and membranous fat necrosis of aortic valves: A clinicopathological study

Matsukuma

Takeo

Kono

et al. 2013

Pathology International

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“…In a study by Matsukuma et al (56), LFN was observed in 3 (43%) of 7 loose bodies showing fatty metaplasia. Thus, intra-articular loose bodies may be encountered under hypoxic or malnourished conditions resembling ischemia (56). Furthermore, aortic valves are similarly avascular (59,60) and receive nutritious permeation directly from the blood flow.…”

Section: Coagulation-like Necrosismentioning

confidence: 89%

“…LFN is found in necrotic bone marrow within intra-articular loose bodies related to osteochondritis dissecans ( 43 ). Matsukuma et al ( 56 ) reported LFN in 7 (13%) of 55 intra-articular loose bodies; 4 were found in necrotic bone marrow derived from osteochondral fracture, and the other 3 were associated with viable fat cells without bone marrow structures.…”

Section: Lfn In Various Locations and Diseasesmentioning

confidence: 99%

“…Therefore, intra-articular loose bodies derived from articular hyaline cartilage remain alive and still grow. However, detached bone and bone marrow cannot survive and therefore may exhibit LFN through ischemic necrosis of bone marrow fat cells ( 43 , 56 ). Viable fat cells, which do not contain bone marrow structures, within intra-articular loose bodies are considered uncommon fatty metaplasia of detached cartilaginous cells ( 56 ).…”

Section: Pathogenesis Of Lfnmentioning

confidence: 99%

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Lipomembranous fat necrosis: A distinctive and unique morphology (Review)

et al. 2022

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Lipomembranous fat necrosis (LFN) is an uncommon but distinct form of fat necrosis, which is characterized by eosinophilic, crenulated and/or serpiginous membranes. LFN exhibits macrocystic, microcystic and/or crushed features. LFN is routinely detectable on hematoxylin and eosin (H&E)-stained sections, and is present both in the acute phase and in the later or fibrous stage of necrotic fatty lesions. Smaller crushed LFN embedded within fibrous tissues may be difficult to recognize on H&E-stained sections, but can be highlighted by some staining techniques, including Masson trichrome, periodic acid-Schiff, orcein, long Ziehl-Neelsen stain, silver impregnation, phosphotungstic acid-hematoxylin and luxol fast blue staining. LFN was initially considered a specific feature of Nasu-Hakola disease, but has since been identified in various subcutaneous or intraabdominal lesions related to ischemic conditions or venous insufficiency. In addition, LFN is detectable in intra-articular loose bodies and aortic valves with or without dysfunction, suggesting that LFN is also associated with ischemia-like hypoxic conditions or malnutrition. LFN is considered to be a histological hallmark of hidden ischemic or hypoxic/malnourished conditions in various diseases; however, the exact mechanisms of LFN remain poorly understood. The present review described the clinicopathological features of this interesting, but poorly characterized, condition.

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“…However, the detailed pathological features of aortic valvular ossification have not been fully elucidated because 1) previous examinations of aortic valvular ossification in larger series were mixed together with those in mitral valves [1,2]; 2) the neovessels have been mentioned in non-rheumatic aortic valves [5,12]; and 3) the illustrated neovessels appeared to be divided into thick-walled and thin-walled vessels [5,9]. In addition, we speculated that ossification may occur in non-neovascularized aortic valves because ossification can be found in an avascular condition, such as intra-articular free bodies without blood supply [13,14]. In this study, focusing on the presence and the histology of neovascularization, we examined ossification in surgically excised dysfunctional aortic valves.…”

Section: Introductionmentioning

confidence: 98%

Heterotopic Ossification with and without Neovascularization in Aortic Valves: A Histopathological Study

Matsukuma¹

2014

J Cytol Histol

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Heterotopic ossification can be found in neovascularized aortic valves with end-stage valvular disease, but its histopathological characteristics are not fully understood. The present study found ossification and neovessels in 21 (28%) and 54 (72%) of 75 surgically removed dysfunctional aortic valves, respectively; there was a significant association between them (P<0.001). Fatty bone marrow was found in 5 aortic valves (6.7%) and always contained neovessels. Neovessels could be divided into thick-walled, arteriole-like vessels (ThKA-Vs) and thin-walled, capillarylike vessels (ThNC-Vs). ThKA-Vs would be a hallmark of rheumatic disease, were always accompanied by ThNC-Vs, and were closely related to ossification (P=0.046). ThNC-Vs may be in part branches of ThKA-Vs, but were also identified in 23 aortic valves without ThKA-Vs. In 44 non-rheumatic dysfunctional aortic valves, such ThNC-Vs only were also associated with ossification (P=0.004). In addition, the present study revealed vessel-independent focal/ minute ossification without nearby neovessels in 6 dysfunctional aortic valves, and also in 4 of 75 age-and sexmatched postmortem non-dysfunctional aortic valves with no neovessels or prominent calcification/thickening; there were no significant differences in the incidence between them. Neovascularized vessels would consist of rheumatic neovessels (ThKA-Vs and their branches) and non-rheumatic neovessels (ThNC-Vs only), and the presence of neovessels is one of the risk factors for aortic valvular ossification. However, aortic valvular ossification can occur in various pathogeneses, such as rheumatic neovessel-dependent ossification, non-rheumatic neovessel-dependent ossification, and rarely vessel-independent focal/minute ossification.

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Fatty lesions in intra-articular loose bodies: a histopathological study of non-primary synovial chondromatosis cases

Cited by 5 publications

References 18 publications

Fat cells and membranous fat necrosis of aortic valves: A clinicopathological study

Fat cells and membranous fat necrosis of aortic valves: A clinicopathological study

Lipomembranous fat necrosis: A distinctive and unique morphology (Review)

Heterotopic Ossification with and without Neovascularization in Aortic Valves: A Histopathological Study

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