enthesis meaning greek

• 1.1 Etymology
• 1.2 Pronunciation
• 1.3.1 Derived terms
• 1.3.2 Translations
• 1.4 Anagrams

English [ edit ]

Etymology [ edit ].

From Ancient Greek ἔνθεσις ( énthesis , “ putting in, insertion ” ) .

Pronunciation [ edit ]

• Hyphenation: en‧the‧sis

Noun [ edit ]

enthesis ( plural entheses )

• 2004 , Erbil Ünsal, “Chapter II: Andersson Lesion in Early Juvenile Spondyloarthropathies”, in Frank Columbus, editor, Focus On Arthritis Research ‎ [1] , page 26 : Like arthritis, peripheral enthesitis occurs predominantly in the lower extremities, particularly in the foot, at single sites at onset, and then at several entheses throughout the course of the disease.
• 2007 , Philip Helliwell, James Woodburn, The Foot And Ankle in Rheumatoid Arthritis: A Comprehensive Guide ‎ [2] , page 64 : Functional entheses occur where tendinous and ligamentous structures, while not actually attaching to bone, are adjacent and in a close relationship to the underlying bone.
• 2010 , Richard J. Wakefield, Maria Antonietta D′Agostino, Essential Applications of Musculoskeletal Ultrasound in Rheumatology ‎ [3] , page 211 : Inflammation of the enthesis , when associated with arthritis in children, is called the syndrome of seronegative enthesopathy associated with arthritis (SEA). The entheses most commonly involved in children are the plantar aponeurosis, calcaneal enthesis , and distal and proximal patellar ligament insertions.

Derived terms [ edit ]

• entheseal , enthesial
• enthesopathy
• enthesophyte

Translations [ edit ]

Anagrams [ edit ].

• Theisens , Thiessen , in sheets , seen shit

• English terms derived from Ancient Greek
• English 3-syllable words
• English terms with IPA pronunciation
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• English lemmas
• English nouns
• English countable nouns
• English nouns with irregular plurals
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• English undefined derivations
• Japanese terms with redundant script codes

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anthesis noun

• Hide all quotations

Earlier version

• anthesis in OED Second Edition (1989)

What does the noun anthesis mean?

There is one meaning in OED's entry for the noun anthesis . See ‘Meaning & use’ for definition, usage, and quotation evidence.

How common is the noun anthesis ?

How is the noun anthesis pronounced, british english, u.s. english, where does the noun anthesis come from.

Earliest known use

The earliest known use of the noun anthesis is in the late 1700s.

OED's earliest evidence for anthesis is from 1783, in C. Linnaeus' Syst. Veg.

anthesis is a borrowing from Latin.

Etymons: Latin anthesis .

Nearby entries

• antheridium, n. 1818–
• antheriferous, adj. 1799–
• antheriform, adj. 1802–
• antherine, n. 1689–
• antherless, adj. 1798–
• antherogenous, adj. 1847
• antheroid, adj. 1818–
• antherozoid, n. 1853–
• antherozoidal, adj. 1865–
• anther valve, n. 1839–
• anthesis, n. 1783–
• anthias, n. 1601–
• anthill, n. Old English–
• ant-hillock, n. 1656–
• ant-hilly, adj. 1796–
• anthine, n. & adj. 1601–1768
• ant-hive, n. 1817–
• antho-, comb. form
• anthobian, n. & adj. 1835–
• anthocarpous, adj. 1835–
• anthocephalous, adj. 1847

Meaning & use

The Anthesis [Latin Anthesis ] takes place, when the burnt Anthers scatter their bags of Dust upon the Stigma.

Bractea of the female flowers very much enlarged after anthesis , when the spike presents the appearance of a pine-apple; bright yellow, with red apices.

The term anthesis is sometimes used to indicate the period at which the flower-bud opens.

There were both delayed and extended antheses and most of the time the flowers were semi-open.

Histologically the ovary and style are relatively simple at anthesis .

From the time of anthesis , when the floral parts open to receive pollen, the developing grain becomes the dominant sink.

A later planting date reduced pre-anthesis moisture stress by reducing the number of days..for the crop to reach anthesis .

• efflorescence 1626– The process of producing flowers, or bursting into flower; the period of flowering.
• blow 1748– Manner, style, or time of blossoming. Also figurative .
• anthesis 1783– The stage at which a flower is open, allowing fertilization to occur. Also: an instance of this.
• florescence 1793– The process of producing flowers or bursting into flower; the period or state of flowering. Also concrete . Flowers collectively.

Pronunciation

Plural: antheses.

• ð th ee
• ɬ rhingy ll

Some consonants can take the function of the vowel in unstressed syllables. Where necessary, a syllabic marker diacritic is used, hence <petal> /ˈpɛtl/ but <petally> /ˈpɛtl̩i/.

• a trap, bath
• ɑː start, palm, bath
• ɔː thought, force
• ᵻ (/ɪ/-/ə/)
• ᵿ (/ʊ/-/ə/)

Other symbols

• The symbol ˈ at the beginning of a syllable indicates that that syllable is pronounced with primary stress.
• The symbol ˌ at the beginning of a syllable indicates that that syllable is pronounced with secondary stress.
• Round brackets ( ) in a transcription indicate that the symbol within the brackets is optional.

View the pronunciation model here .

* /d/ also represents a 'tapped' /t/ as in <bitter>

Some consonants can take the function of the vowel in unstressed syllables. Where necessary, a syllabic marker diacritic is used, hence <petal> /ˈpɛd(ə)l/ but <petally> /ˈpɛdl̩i/.

• i fleece, happ y
• æ trap, bath
• ɑ lot, palm, cloth, thought
• ɔ cloth, thought
• ɔr north, force
• ə strut, comm a
• ər nurse, lett er
• ɛ(ə)r square
• æ̃ sal on

Simple Text Respell

Simple text respell breaks words into syllables, separated by a hyphen. The syllable which carries the primary stress is written in capital letters. This key covers both British and U.S. English Simple Text Respell.

b, d, f, h, k, l, m, n, p, r, s, t, v, w and z have their standard English values

• arr carry (British only)
• a(ng) gratin
• o lot (British only)
• orr sorry (British only)
• o(ng) salon

Inflections

anthesis typically occurs about 0.2 times per million words in modern written English.

anthesis is in frequency band 4, which contains words occurring between 0.1 and 1 times per million words in modern written English. More about OED's frequency bands

Frequency of anthesis, n. , 1810–2010

* Occurrences per million words in written English

Historical frequency series are derived from Google Books Ngrams (version 2), a data set based on the Google Books corpus of several million books printed in English between 1500 and 2010.

The overall frequency for a given word is calculated by summing frequencies for the main form of the word, any plural or inflected forms, and any major spelling variations.

For sets of homographs (distinct entries that share the same word-form, e.g. mole , n.¹, mole , n.², mole , n.³, etc.), we have estimated the frequency of each homograph entry as a fraction of the total Ngrams frequency for the word-form. This may result in inaccuracies.

Smoothing has been applied to series for lower-frequency words, using a moving-average algorithm. This reduces short-term fluctuations, which may be produced by variability in the content of the Google Books corpus.

Frequency of anthesis, n. , 2017–2023

Modern frequency series are derived from a corpus of 20 billion words, covering the period from 2017 to the present. The corpus is mainly compiled from online news sources, and covers all major varieties of World English.

Smoothing has been applied to series for lower-frequency words, using a moving-average algorithm. This reduces short-term fluctuations, which may be produced by variability in the content of the corpus.

Compounds & derived words

• synanthesis , n. 1880– Simultaneous ripening of the stamens and pistils in a flower.

Entry history for anthesis, n.

anthesis, n. was revised in March 2016.

anthesis, n. was last modified in July 2023.

oed.com is a living text, updated every three months. Modifications may include:

• further revisions to definitions, pronunciation, etymology, headwords, variant spellings, quotations, and dates;
• new senses, phrases, and quotations.

Revisions and additions of this kind were last incorporated into anthesis, n. in July 2023.

Earlier versions of this entry were published in:

OED First Edition (1885)

• Find out more

OED Second Edition (1989)

• View anthesis in OED Second Edition

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Citation details

Factsheet for anthesis, n., browse entry.

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• Review Article
• Published: 21 November 2017

Enthesitis: from pathophysiology to treatment

• Georg Schett 1 ,
• Rik J. Lories 2 ,
• Maria-Antonietta D'Agostino 3 ,
• Dirk Elewaut 4 ,
• Bruce Kirkham 5 ,
• Enrique R. Soriano 6 &
• Dennis McGonagle 7  

Nature Reviews Rheumatology volume  13 ,  pages 731–741 ( 2017 ) Cite this article

18k Accesses

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• Immunopathogenesis
• Medical imaging
• Spondyloarthritis

Entheses are predominantly extra-articularly localized structures that represent a key target of musculoskeletal inflammation in diseases such as psoriatic arthritis (PsA) and spondyloarthritis (SpA)

Entheses contain a specific immune microenvironment, which is activated by a combination of factors that include mechanical stress, genetic susceptibility and microbial-triggered immune activation

Enthesitis arises from robust activation of prostaglandin E2 and the IL-23–IL-17 axis, leading to the influx of innate immune cells and homing of inflammation into the entheses, which is followed by mesenchymal tissue responses and new bone formation

Clinical and imaging instruments have been developed that enable the reliable detection and monitoring of enthesitis in patients with PsA and SpA

Inhibition of the key effector cytokines of enthesitis — IL-17, IL-23 and TNF — has shown to be effective in supporting the resolution of enthesitis in PsA and SpA

Entheses are the insertion sites of tendons and ligaments to the bone surface and are essential structures for locomotion. Inflammation of the entheses (enthesitis) is a key feature of psoriatic arthritis and spondyloarthritis. To date, our conceptual understanding of enthesitis remains limited. This Review provides an insight into the pathophysiology of enthesitis, addressing the role of biomechanics, prostaglandin E2-mediated vasodilation and the activation of innate immune cells in the initiation phase of enthesitis, as well as the role of entheseal IL-23-responsive cells that augment inflammation by producing pro-inflammatory mediators such as IL-17A, IL-22 and TNF. In addition, the molecular steps that translate inflammation into resident tissue responses, resulting in new bone formation, are discussed. The second part of the article summarizes the clinical features of enthesitis, and the role of clinical and imaging instruments in detecting enthesitis are discussed together with their challenges and limitations. Finally, the Review summarizes the current treatment possibilities for enthesitis based on the aforementioned pathophysiological concepts, focusing on the role of cytokine-blocking agents.

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Acknowledgements

This work is supported by the Collaborative Research Center (CRC) 1181 of the German Research Council (Deutsche Forschungsgemeinschaft-DFG). D.M.'s work is funded by the Leeds NIHR Biomedical Research Centre.

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Schett, G., Lories, R., D'Agostino, MA. et al. Enthesitis: from pathophysiology to treatment. Nat Rev Rheumatol 13 , 731–741 (2017). https://doi.org/10.1038/nrrheum.2017.188

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Introduction

Enthesitis is a central feature of spondyloarthritis (SpA). Although enthesitis has traditionally been considered to be a focal insertional disorder, advanced imaging and pathologic findings suggest that enthesitis is a diffuse process with effects on adjacent bone and soft tissue. As a result of repeated biomechanical stress, it appears that microdamage at the enthesis triggers an inflammatory response in the synovium, leading to synovitis. Along with mechanical stress, exogenous bacteria may play a role in activating the immune response, especially in genetically predisposed individuals whose major histocompatibility locus encodes the class I molecule HLA–B27. Recent studies in animal models suggest that autoimmunity against versican and fibrocartilage proteins, and bone morphogenetic protein (BMP) signaling play roles in enthesitis development. Finally, interleukin-23 (IL-23) has been implicated in enthesitis with inflammatory effects mediated through IL-17 and tumor necrosis factor (TNF), and new bone formation driven by IL-22.

Although prior therapeutic choices were limited to nonsteroidal antiinflammatory drugs (NSAIDs) and activity modification, in recent years TNF inhibitors have proven to be useful. Further research on the effects of IL-22 and IL-23 blockade is needed to understand the effects on the treated patient. While enthesitis is underdiagnosed by physical examination alone, the use of ultrasound has proven to be highly sensitive for the detection of enthesitis, with utility in monitoring response to therapy, and will be an invaluable tool for assessing the efficacy of newer treatments. This review summarizes the substantial progress that has been made in addressing the pathophysiology, molecular mechanisms, genetic associations, clinical features, diagnostic modalities, and treatment of enthesitis.

Definitions and evolution of the enthesis concept

Historic definition.

Although the adjective “enthetic” derives from the ancient Greek word “enthetikos,” meaning “introduced into the body from without,” in the nineteenth century the adjective was increasingly used to refer to diseases that were “implanted into the body from external sources” ( 1 ). It was not until the twentieth century that the term “enthesis” was used as it is today, referring to focal insertional abnormalities at sites of bony attachments to tendons, ligaments, fascia, muscles, or joint capsules ( 2 , 3 ). The first suggestion that the enthesis is centrally affected in SpA was made by Ball in 1971 and was substantiated after a review of pathologic tissues from both patients with rheumatoid arthritis (RA) and patients with ankylosing spondylitis (AS), where he noted the presence of a unique inflammatory enthesopathy that could help to distinguish SpA from RA ( 2 ).

Broadening the definition of enthesis with the concept of the “enthesis organ”

Magnetic resonance imaging (MRI) and ultrasound findings have suggested that enthesopathy encompasses pathologic changes extending to the adjacent bone and soft tissues ( 4 ). Likewise, it has been argued that this entity should be considered an “enthesis organ” encompassing not only the enthesis itself, but also the fibrocartilage, bursa, fat pad, adjacent trabecular bone networks, and deeper fascia ( 5 ) ( Figure 1 ). Representing areas where hard and soft tissues meet, entheses are sites of concentrated stress with effects not only on the bony attachment interface and the enthesis itself, but also on these neighboring tissues ( 4 – 7 ).

Illustration of the Achilles enthesis organ.

Entheses and mechanical stress

The concept of an enthesis organ was extended to that of a synovioentheseal complex ( 8 , 9 ), which refers to the relationship between the proinflammatory synovium and the avascular enthesis. In contrast to other skeletal locations, the enthesis is a site of repetitive biomechanical forces. High biomechanical stress at the enthesis triggers an inflammatory cascade with cytokine production by infiltrating monocytes and lymphocytes in the adjacent synovial tissue, resulting in an articular inflammatory response, and clinically leading to synovitis adjacent to attachment sites ( 8 , 9 ). Support for this theory of a dynamic response to biomechanical stress at the enthesis originates from animal models. In one experiment, botulinum toxin A injection delayed fibrocartilage development, suggesting that enthesis development is sensitive to mechanical environmental factors ( 10 ). In a mouse model that overexpresses TNF, enthesitis was reduced when the hind legs of the mice were made non–weight-bearing through tail suspension ( 11 ). Those authors proposed that triggering of mechanoreceptors via the MAPK pathway stimulates the production of inflammatory mediators.

As a result of biomechanical stress, adjacent bone reacts with formation of surface spurs or enthesophytes, observed both radiographically and on histologic examination ( 12 ). In early disease, there is destruction of superficial fibrocartilage, with vascular invasion and inflammatory cell infiltration, predominantly with macrophages ( 13 ). This leads to another important microanatomical feature, which is the presence of blood vessels at sites where synovium, subchondral bone, and bone marrow are close to each other. In early experiments using labeled phosphorus, Ball identified capillary-like vessels that pass through the enthesis to the marrow ( 2 ). Later studies described the presence of vascular channels penetrating cortical bone in the knees of mice adjacent to the cruciate ligaments with associated subclinical changes, including subchondral bone damage and microcyst formation. In the rat adjuvant-induced arthritis model, vascular channels provided a site for inflammatory tissue entry and osteoclast activation ( 14 ).

Whether enthesitis is a primary central lesion or a secondary process remains a matter of debate. Studies that have implicated enthesitis as the primary process include studies of TNF-transgenic mice, in which the earliest lesion appears to be in the enthesis ( 11 ). However, this may be model specific, and a number of reports have challenged the idea of enthesitis as the primary inflammatory lesion ( 15 , 16 ). In one study examining different stages of spontaneous tail spondylitis and peripheral arthritis in HLA–B27/h β 2 m–transgenic mice, histologic samples displayed destructive synovitis with neutrophils and multinucleated giant cells rather than by enthesitis or osteitis ( 16 ). Among human studies examining biopsy specimens and MRIs of sacroiliac joints, synovitis and subchondral bone marrow changes were more prominent features while enthesitis was not ( 17 , 18 ). In a subsequent study, in patients with early untreated knee or ankle arthritis, analyses revealed a higher synovitis score by MRI in SpA than in RA, whereas there were no differences in the prevalence of enthesitis as assessed by perientheseal focal tissue, entheseal enhancement, and bone marrow edema ( 15 ). However, in light of substantial data in animal models highlighting 3 stages of tendon response to injury that have been defined by distinct pathologic changes, determining the initiating event in the enthesis may be confounded by the timing of the analysis ( 19 – 21 ).

Contributing cellular and molecular mechanisms

Genetic susceptibility.

It has long been known that AS susceptibility is largely genetically determined. The strongest genetic association is with the major histocompatibility complex (MHC)–encoded class I molecule, HLA–B27, and it is postulated that HLA–B27 contributes to ~40% of the overall risk for SpA ( 22 ). Protein misfolding of nascent HLA–B27 in the endoplasmic reticulum has been hypothesized to trigger an unfolded protein response with aberrant recognition by natural killer cell receptors ( 23 ). The HLA–B27–induced unfolded protein response in macrophages has been demonstrated in HLA–B27–transgenic rats and is associated with an increase in IL-23 production by these cells ( 24 ). Although HLA–B27 remains the dominant risk factor for susceptibility to the AS phenotype, other important influences of the MHC have been observed ( 25 ). More recently, Haroon et al ( 26 ) found a positive association of B*27:05:02 with enthesitis, dactylitis, and symmetric sacroiliitis in a cohort of psoriatic arthritis (PsA) patients, whereas B*44 haplotypes were associated with a decreased frequency of enthesitis, dactylitis, and joint fusion. Finally, investigators have recently focused on genes outside of the MHC region, such as ERAP1 and ERAP2, which code for aminopeptidases that are involved in MHC class I presentation ( 25 , 27 ). Although additional HLA class I and class II alleles have also been implicated, the scale and scope of gene identification to date have not yet matched the putative total genetic risk for SpA.

Microbial factors

Microbial infection with virulent organisms remote from affected joints, as well as gastrointestinal dysbiosis without a directly invading pathogen, are known features of certain phenotypes of SpA, and it has long been appreciated that microbial factors can lead to immune activation ( 28 ). Clinically, reactive arthritis (ReA) is known to follow infections with Chlamydia , Campylobacter , Shigella , or Yersinia . AS patients consistently have been found to have subclinical gut inflammation and increased gastrointestinal permeability ( 29 , 30 ). In animal models, HLA–B27–transgenic rats raised in germ-free environments do not develop intestinal inflammatory or peripheral joint disease, yet the disease recurs if rats are reconstituted with Bacteroides , supporting the role of gut flora in the development of joint inflammation ( 31 ). In a more recent study, colonoscopic biopsies of the terminal ileum of AS patients showed a discrete microbial signature as revealed by sequencing and quantitative polymerase chain reaction analysis of the 16S ribosomal RNA (16S rRNA) gene, exhibiting higher levels of 5 families of bacteria as compared to healthy controls ( 32 ). In that study there was no significant difference in the 16S rRNA copy number between patients with AS and controls, indicating that the observed differences were not due to bacterial overgrowth. It has been postulated that the combination of bacterial adjuvants and mechanical factors act synergistically to activate the immune response, particularly in genetically predisposed individuals ( 5 ).

Fibrocartilage and versican autoimmunity

A number of studies have indicated that autoimmunity against fibrocartilage proteins, including aggrecan, may underlie enthesitis and spondylitis ( 33 ). A model of SpA induced by immunizing BALB/c mice with the G1 globular domain of versican, leading to spondylitis and enthesitis, suggests that versican autoimmunity may also play a role in enthesitis ( 34 ). The inflammatory lesions are characterized by mononuclear cell infiltration at the entheseal insertions to the vertebrae, as is seen with AS, and are associated with angiogenesis which then progresses to cause destructive discitis ( 35 ).

Role of bone morphogens

In the DBA/1 mouse model, where mice develop spontaneously occurring arthritis that culminates in bone formation and joint ankylosis, male mice in crowded conditions developed arthritis in the hind paws that was entheseal, but not synovially based, with new bone formation driven by BMP-7 signaling ( 36 ). In that experiment, the incidence of arthritis was increased in mice that were caged together in crowded conditions, yet decreased when the mice were placed in larger cages ( 37 ). Thus, in addition to a genetic predisposition for enthesitis, this observation points to the role of environmental factors in the development of arthritis. Finally, immunohistochemical studies in SpA show increased synovial expression of BMP-2 and BMP-6, which is up-regulated by proinflammatory cytokines such as IL-1 and TNF, suggesting that synovial molecules contribute to chronic arthritis and joint ankylosis ( 36 , 38 ).

Role of proinflammatory cytokines

The role of IL-23 has been addressed as a major driver of cascades that lead to inflammation and bone remodeling in SpA. Alterations in AS susceptibility are related to the existence of single-nucleotide polymorphisms in the IL-23 receptor as demonstrated in genome-wide association studies, and serum levels of the IL-12/23 p40 subunit have been shown to be significantly higher in patients with PsA compared with controls ( 39 , 40 ). IL-23 is produced in the gut, suggesting that the intestinal mucosa is a key site of IL-23 production in SpA. Additionally, Chlamydia trachomatis also leads to induction of IL-23 via CHOP10. Taken together, these findings indicate that IL-23 is a pivotal cytokine and potentially central to the pathogenesis of SpA ( 41 ). Increased IL-17 expression by innate immune cells such as mast cells and neutrophils in SpA has been shown to target the facet joints and synovial tissue ( 42 , 43 ). In a subsequent set of investigations, Sherlock et al found that IL-23 could induce SpA by acting on an isolated population of CD3+CD4−CD8− entheseal resident lymphocytes, leading to increased expression of TNF and IL-6 in the enthesis. When IL-23 was overexpressed, mice developed enthesitis with inflammation, which spread into the adjacent synovium ( 41 ). Enthesitis was associated with new bone erosion. IL-23 promoted inflammation through IL-17 and TNF, whereas new bone formation was associated with overproduction of IL-22 ( 41 , 44 ) ( Figure 2 ).

Interleukin-23 (IL-23) is activated via a variety of pathways including the HLA–B27 unfolded protein response. IL-23 then activates resident T cells within the enthesis, which then promotes inflammation and bone remodeling, with inflammation mediated by IL-17 and osteoproliferation mediated by IL-22. The net result is bone ankylosis in the spine. ROR γ t = retinoic acid receptor–related orphan nuclear receptor γ t; TNF = tumor necrosis factor. Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/journal/doi/10.1002/art.39458/abstract

Additional support for the role of IL-23 comes from the SKG mouse model, in which curdlan ( β -1,3-glucan) injections induce enthesitis and dactylitis. Arthritis and spondylitis were IL-23 dependent and were transferable to SCID mouse recipients with CD4+ T cells ( 45 ). In this model, disease severity was dependent on the external microbial environment and the host immunogenetic background. More recent work illustrates the differential impact of microbiota on specific pathologic features of SpA; ileitis development, ileal IL-23 expression, and lymph node IL-17A production were microbiota dependent, but arthritis was not ( 46 ). In curdlan-treated SKG mice, enthesitis was specifically dependent on IL-17A and IL-22 ( 47 ). The role of up-regulation of the IL-23/Th17 pathway in promoting joint inflammation and bone turnover is further supported by recent murine studies, with inhibition of the PsA phenotype after neutralization of IL-17A ( 48 , 49 ).

Clinical enthesitis in SpA

SpA is by definition a heterogeneous group of clinical entities long recognized as having unique phenotypes that include AS, ReA, PsA, enteropathic arthritis, and what has traditionally been referred to as undifferentiated arthritis. However, with advances in imaging and careful long-term followup observations, it appears that these diseases share common features, including subclinical spinal and peripheral joint inflammation, along with associations with microbes and gene identifications. In attempting to develop a model for an underlying unifying anatomical basis for SpA, an “enthesitis-based model” has been proposed as the basis for the osteitis, periostitis, and new bone formation that are seen in SpA ( 5 ). The association between enthesitis and adjacent osteitis has been further supported by imaging and cadaver studies, primarily in patients with PsA ( 50 – 52 ).

Regional sites

Patients with SpA have a remarkable propensity for inflammation at certain enthesis sites that are ubiquitous and numerous. Clinically, peripheral enthesitis is observed not only in all forms of SpA, but particularly frequently in juvenile-onset SpA. A number of patients with juvenile SpA are classified as having enthesitis-related arthritis (ERA), a heterogeneous subtype that includes some patients who predominantly have enthesitis, enthesitis and arthritis, or juvenile AS. Compared to other subtypes of juvenile idiopathic arthritis, ERA is associated with worse function, worse quality of life, and increased pain ( 53 , 54 ).

Enthesitis can be seen in 33–58% of patients with ReA and may be the only clinical manifestation in some whose disease has been triggered by an enteric infection ( 55 ). In SpA, the entheses of the lower extremities are more frequently involved than those of the upper limbs, and the heel is the most frequent site ( 55 ). In addition to the Achilles and plantar fascia insertions, identified sites of enthesitis include muscle attachments to the greater and lesser trochanters, the insertion of the quadriceps tendon at the upper patellar pole, the insertions of the patellar ligament at the lower patellar pole and the tibial tubercle, acromial and clavicular insertions of the deltoid muscle, and the insertions of the flexor and extensor tendons at the phalanges ( 55 – 57 ). It is unknown why there is a predilection for the entheses at the lower parts of the lower limbs, although it has been hypothesized that this may be due to the length, anatomy, and higher mechanical load at these sites.

Given the presumed role of repetitive biomechanical forces discussed above, it is not surprising that in patients with longstanding AS, those with occupational activities that required more bending, twisting, and stretching had more functional limitations and radiographic damage than those whose jobs required little or no dynamic flexibility ( 58 ). A recently published computer-based method that fully quantified syndesmophyte heights and volumes on computed tomography scans has revealed that syndesmophytes grow at different rates over time in AS patients, suggesting that mechanical factors local to the disc space may influence syndesmophyte formation ( 59 ). Clearly, there are sites that are not associated with SpA despite being sites of significant biomechanical stress, and perhaps it is the compressive and shear force nature of the stress as well as the putative role of antigen expression adjacent to the enthesis that may underlie this apparent discrepancy ( 5 ). Additionally, it cannot be discounted that the increased detection of enthesitis at the lower limbs is explained by the accessibility of these sites to ultrasound.

Diagnostic criteria and outcome measures

Enthesitis is often underdiagnosed in the clinic; clinical assessment and quantification of peripheral enthesitis in daily practice lacks sensitivity and specificity ( 56 , 60 , 61 ). Although both the Amor criteria ( 62 ) and the European Spondylarthropathy Study Group criteria ( 63 ) for SpA include peripheral enthesitis, there are limitations to these criteria with regard to the exact quantification of enthesitis. Two clinical methods have been designed and often implemented for evaluating enthesopathy in AS: Mander’s Entheseal Index and the Maastricht Ankylosing Spondylitis Enthesitis Score (MASES) ( 64 , 65 ). Both rely on pain elicited by local pressure of entheseal points. The intraarticular and deep location of entheseal insertions, however, makes quantification of enthesitis by physical examination alone difficult, and not surprisingly, these scoring systems have only moderate sensitivity and specificity for predicting positive sonogram results, depending on the entheseal site ( 66 ).

Imaging of the enthesis

Because of the clinical limitations described above and the poor sensitivity of markers of inflammation, it is necessary to rely on typical abnormalities seen on various imaging techniques to diagnose SpA. Plain radiographs are limited by their inability to show inflammation or soft tissue changes, although late chronic bony changes such as enthesophyte formation or occasional erosions can be seen at the attachment of the Achilles tendon or plantar aponeurosis. More sensitive methods such as ultrasound and MRI, which are useful in their ability to detect both inflammatory and chronic changes in enthesitis at both early and late stages, can be used.

MRI has changed the way we approach both the diagnosis and classification of SpA; it is particularly useful in detecting spinal disease in early AS when conventional radiographs are still normal ( 67 ). The use of fat-suppressed, fat-saturated, and water-sensitive MRI sequences has demonstrated that the extracapsular inflammation of joints quite often represents enthesitis with variable degrees of soft tissue and bone marrow edema ( 68 , 69 ) ( Figures 3 – 5 ). The typical appearance of enthesitis on MRI includes soft tissue inflammatory changes outside the joint capsule and perientheseal bone marrow edema ( 70 ). Recent studies have examined the utility of whole-body MRI, which has shown promise in the detection of subclinical axial and peripheral enthesitis ( 71 ). Of course, MRI has limitations; structures that make up entheses have a low signal on conventional MRI, with low water accumulation in the areas where fibroblasts are tightly cross-linked. MRI is further limited by its cost and availability, and therefore ultrasound remains the preferred modality for the detection of enthesitis both in the clinical setting as well as in research.

Achilles tendon insertion into the calcaneus. An abnormal signal is seen at the posterior calcaneus at the site of the Achilles entheseal insertion (encircled area) on magnetic resonance imaging using STIR sequences. Reproduced from ref. 68 .

Fat-suppressed T1-weighted sequence magnetic resonance image (MRI) of the right midfoot of a 58-year-old woman with HLA–B27–positive peripheral spondyloarthropathy. The MRI demonstrates extensive enthesitis, synovitis, and tenosynovitis of the peroneus longus, peroneus brevis, tibialis posterior, flexor digitorum longus, and extensor digitorum tendons. This is characterized by excess fluid and enhancement in and around the tendon sheaths. Arrow indicates extensive edema and enhancement at the plantar aspect of the midfoot, involving insertions of intrinsic musculature and capsular ligaments consistent with enthesitis. Image courtesy of Dr. Joseph Robinson (Cedars-Sinai Medical Center).

Ultrasound has indeed proven to be a highly useful and sensitive tool in the evaluation of enthesitis and improves the ability of the clinical examination to detect enthesopathy. In one study of 92 patients with PsA, ultrasound was useful in detecting subclinical entheseal involvement, independent of clinical examination and symptoms ( 72 ). In another study of 600 lower limb entheses, at least 1 ultrasound sign of enthesopathy was detected in 60% of clinically asymptomatic cases of enthesitis, thus demonstrating a higher sensitivity than physical examination ( 73 ).

Ultrasound may be most useful in the early diagnosis of SpA, and likewise, entheseal abnormalities can be detected prior to overt clinical disease. Nevertheless, in an older cross-sectional single-center study of 51 SpA patients and 24 controls, neither MRI nor power Doppler ultrasound (PDUS) discriminated between SpA and controls ( 74 ). In a prospective single-center cohort study of 118 patients with symptoms suggestive of SpA conducted by D’Agostino and colleagues ( 57 ), vascularization at cortical bone detected by PDUS of at least one enthesis provided good predictive value for diagnosing SpA with a sensitivity of 76.5% and a specificity of 81.3%. Indeed, PDUS is a sensitive and reliable technique used to detect increased blood flow in the enthesis revealing neovascularity and subclinical active inflammation ( 56 , 75 ) ( Figure 6 ).

A, Ultrasound image of a patient with psoriatic arthritis with enthesitis (long-axis view of the lateral epicondyle [high-frequency, 18-MHz probe]). Precise delineation of blood flow seen at the cortical interface on B-flow imaging is shown. Calcification is seen adjacent to the epicondyle. B and C, 3T magnetic resonance image of the same patient, in the same orientation as the ultrasound in A, showing proton density (B) and fat presaturation (C). Boxed areas show the region of the lateral epicondyle. Images courtesy of Dr. Ralph Thiele (University of Rochester, Rochester, NY). Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/journal/doi/10.1002/art.39458/abstract

Recent studies have indicated that ultrasound may accurately predict which patients will go on to develop SpA ( 51 , 57 , 75 ). In one investigation, ultrasound examination of Achilles erosions correlated with objective activity-based measurements of SpA outcomes, and was sensitive to change ( 76 ). In the study by D’Agostino and colleagues described above, vascularized enthesis as detected by PDUS combined with Amor’s criteria proved to be the only independent contributors to a diagnosis of SpA ( 57 ).

Finally, ultrasound may be used to monitor response to therapeutic interventions. A few studies have illustrated improvement in enthesitis shown on ultrasound after the use of TNF antagonists ( 77 , 78 ). In one investigation of 327 patients with active SpA who were treated with anti-TNF therapy for 6 months, cumulative entheseal morphologic abnormalities, intraenthesis and perienthesis, and bursitis were all significantly decreased on PDUS after 6 months of treatment ( 77 ). In another study, D’Agostino et al monitored regression of enthesitis using PDUS after treatment with infliximab ( 78 ), providing confirmatory evidence for the utility of ultrasound in a clinical research setting.

Treatment of enthesitis

Historically, treatment of clinical enthesitis had been limited to NSAIDs. Continuous use of NSAIDs not only controls symptoms of disease, but may also slow progression of bony changes in AS ( 79 , 80 ). Therefore, Assessment of SpondyloArthritis international Society/European League Against Rheumatism guidelines place optimal NSAID therapy as a cornerstone of the management plan for AS ( 81 ).

Treatment with TNF inhibitors is indicated in patients that do not respond to NSAID therapy. TNF inhibition with adalimumab, etanercept, infliximab, and golimumab has been shown to be efficacious in the treatment of enthesitis ( 82 – 87 ). Olivieri et al ( 88 ) have reported that adalimumab and etanercept are effective treatments of MRI-documented refractory heel enthesitis, with progressive improvement of bone edema in a 6-month period ( 88 ).

Agents that block IL-23 have the potential to inhibit both inflammation and altered bone remodeling, although further analysis of the effect of IL-22 and IL-23 blockade on bone pathologies in animal models and patients with PsA are needed to address this important therapeutic issue ( 89 ). Entheseal inflammation in a passive-transfer model of collagen antibody-induced arthritis was reduced by an antibody to the p19 subunit of IL-23, which was also associated with the down-regulation of several inflammatory mediators, such as IL-6 and IL-1 β , and genes such as Rankl , Ctsk , and matrix metalloproteinases known to be involved in bone erosion ( 41 ). Both ustekinumab, a monoclonal antibody directed against the common p40 subunit of IL-12 and IL-23, and secukinumab, a human anti–IL-17A monoclonal antibody, have already demonstrated promise in PsA, with significant improvements in enthesitis ( 90 , 91 ).

Apremilast, an oral inhibitor of phosphodiesterase 4, which increases cAMP and thus modulates multiple proinflammatory mediators, has demonstrated efficacy in PsA, with significant improvements in the severity of both enthesitis and dactylitis evidenced by reductions in MASES over a 52-week period ( 92 ). Finally, bisphosphonates may also have a role in peripheral enthesitis felt to be refractory to NSAID therapy. In a 6-month randomized controlled comparison of intravenous pamidronate treatment of NSAID-refractory AS, patients treated with pamidronate showed symptomatic improvement with significant reductions in Bath Ankylosing Spondylitis Functional Index and Bath Ankylosing Spondylitis Disease Activity Index measurements together with regression of periarticular osteitis documented by MRI with gadolinium ( 93 ).

Treatment of patients with SpA enthesitis with currently available agents has not had universal success. In placebo-controlled trials of methotrexate and leflunomide in PsA, enthesitis measures were not assessed ( 94 , 95 ). In a randomized controlled trial, sulfasalazine was not effective for enthesitis ( 96 ). Other agents that have not demonstrated clinical efficacy in AS include tocilizumab, and lymphocyte-targeted therapies such as abatacept ( 97 , 98 ). Rituximab only showed modest therapeutic efficacy in SpA ( 99 , 100 ).

Conclusions

In summary, investigations and clinical observations uniformly point out with increasing clarity that the enthesis is much more than a simple attachment site. A number of studies have shown that it functions as a unit comprising adjacent tissues, including bone and fibro-cartilage linked to synovium, and serves as a way of dissipating stress over a wide area. Inflammation at the enthesis manifests in the adjacent synovium presumably via immunity to common antigens or via release of proinflammatory cytokines at the enthesis. Although work by Benjamin and McGonagle ( 9 ) suggests that the enthesis is the primary SpA lesion, the precise role of the enthesis in early stages of disease, especially regarding issues of cause or effect, remains an area of continued debate and discovery. Improved imaging modalities may in the future be able to detect enthesitis at different stages of disease. However, this will require a clinically diverse and large sample size to help address this question. Inflammation at the enthesis is likely modulated by multiple factors. A more complete role for genetic predisposition will require additional advances in gene sequencing and discovery. Repeated biomechanical stress with the resultant inflammatory response regulated by IL-17, IL-22, and IL-23 now provide clues as to why certain areas of the body are affected, and perhaps why others are not. The spine itself (the clinical hallmark of the disease) remains inaccessible to traditional enthesitis-focused research methodologies thus far. However, newer imaging techniques are on the horizon. Further examination into the role of the inflammatory mediators, including IL-17, IL-22, and IL-23 as well as potentially others, in driving enthesitis and bone formation will be important to direct our attention toward future therapeutic targeted pathways in patients with SpA.

Radiographic findings of enthesitis in a 21-year-old man with ankylosing spondylitis. A, Reference plain radiograph. B, Magnetic resonance image with T1 sequence showing a small erosion at the right greater trochanter. C, Axial T2 fat-saturated sequence of the right hip showing edema of the right gluteus minimus tendon at its insertion, consistent with enthesitis. Arrows indicate the region of the right greater trochanter. Images courtesy of Dr. Joseph Robinson (Cedars-Sinai Medical Center).

Acknowledgments

Supported in part by the NIH (National Institute of Arthritis and Musculoskeletal and Skin Diseases grant P01-AR-052915 and National Center for Advancing Translational Sciences grant UL1-TR-000124).

The authors wish to thank Joseph Robinson, MD (Cedars-Sinai Medical Center Department of Radiology) for assistance with MRI acquisition and interpretation.

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Enthesitis and Enthesopathy Explained

A Primary Feature of Spondyloarthritis

If you have seen the words entheses, enthesitis, or enthesopathy in your X-ray or medical reports, the terminology may have been unfamiliar to you. Let's look at the meaning and also how it relates to various types of arthritis and rheumatic diseases.

• Enthesis (plural: entheses) typically refers to the connective tissue where tendons , ligaments, or joint capsules attach to bone. Two types of entheses exist: fibrous entheses and fibrocartilaginous entheses. While that is the classic definition, a newer, broader definition suggests that enthesis is more than a simple attachment or insertion site—enthesis functions as a unit which includes adjacent tissues (for example, bone and fibrocartilage connected to synovium). The unit is referred to as the "enthesis organ complex".
• Enthesopathy is any abnormal condition that affects the entheses (e.g., inflammation of the entheses). Enthesopathy may be due to an inflammatory condition, such as psoriatic arthritis , or a condition related to injury or overload, such as plantar fasciitis.
• Enthesitis refers to inflammation of the entheses.

Enthesitis is typically associated with pain, stiffness, and tenderness at the insertion site, sometimes without much swelling. However, where there is involvement of the large insertions of lower limbs, swelling can be significant and prominent. If swelling is absent, enthesitis can be difficult to recognize or suspect during a physical examination.

Enthesitis is common at the following sites:

• Achilles tendon
• Patellar tendon
• Plantar fascia
• Elbow epicondyles
• Iliac crest

Conditions Associated With Enthesitis

Enthesitis may be linked to inflammatory conditions or it may be mechanically induced by injury. Peripheral enthesitis is characteristic of all of the spondyloarthropathies , including undifferentiated spondyloarthritis, ankylosing spondylitis , psoriatic arthritis, enteropathic arthritis, and reactive arthritis .

Reactive arthritis is a form of arthritis that results from infection. The swelling of reactive arthritis is often triggered by infection in a more remote body part, such as the urinary tract, intestines or genitals. Typically the joints of the knees, feet, and ankles are targets for inflammation secondary to reactive arthritis. More specifically, enthesitis in people with reactive arthritis usually occurs in the plantar fascia, pelvic bones or Achilles tendon. Reactive arthritis is actually uncommon and usually goes away in most people within a year after onset.

Ankylosing spondylitis is an inflammatory condition that is most prevalent in men. The inflammation of ankylosing spondylitis affects the vertebrae and causes them to fuse. Chronic enthesitis of the tendons and ligaments of the vertebrae is the first step in the eventual fusion of vertebrae, which is the main feature of ankylosing spondylitis. People with ankylosing spondylitis can also experience enthesitis of the costochondral joints , or joints of the ribs.

Other conditions associated with enthesitis include Achilles tendinitis, rheumatoid arthritis , osteoarthritis , and diffuse idiopathic skeletal hyperostosis (DISH). It may be degenerative enthesopathy that develops with osteoarthritis. The degenerative changes that occur with wear-and-tear osteoarthritis also affect the fibrocartilages.

Imaging for Diagnosis

Imaging can help diagnose enthesitis, but the imaging modality utilized depends on whether the axial or peripheral skeleton is affected. MRI is used for the axial skeleton. Ultrasound is preferred for the peripheral skeleton. MRI would again be preferable for any insertions that are inaccessible.

Treatment of enthesitis is based on the underlying condition. For example, if enthesitis is due to an inflammatory condition, treatment usually focuses on treating the inflammatory polyarthritis. Treatment, in such cases, may include:

• nonsteroidal anti-inflammatory drugs (NSAIDs)
• methotrexate
• TNF blockers
• Physical therapy

Depending on which areas are involved, local corticosteroid injections may be used if oral medications are inadequate. However, a healthcare provider would almost never use these injections for Achilles tendinitis or into the patella; this could lead to rupture.

The biomechanical aspects of enthesitis are also addressed by using insoles and cushions.

Isaacs J. Oxford textbook of rheumatology . Oxford, UK: OUP Oxford.

Creakyjoints.org. What is enthesitis? the painful arthritis symptom you should know about .

Kataria RK, Brent LH. Spondyloarthropathies . Am Fam Physician . 69(12):2853-60.

Sufka P. Reactive arthritis . American College of Rheumatology.

Holliman K. How is a person affected? . Spondylitis Association of America.

 Baraliakos X, Conaghan PG, D'Agostino MA, Maksymowych W, Naredo E, Ostergaard M, et al. Imaging in rheumatoid arthritis, psoriatic arthritis, axial spondyloarthritis, and osteoarthritis: An international viewpoint on the current knowledge and future research priorities . Eur J Rheumatol , 6(1):38-47.

Aggarwal A, Sawhney S. Pediatric rheumatology: A clinical viewpoint . New York, NY: Springer Publishing.

Bruyn, George AW, MD. PhD. Musculoskeletal Ultrasonography - Clinical Applications . Up-To-Date.

Kehl, AS, MD. et al. Enthesitis . Arthritis & Rheumatology. 68(2): 312-322.

McGonagle D. and Benjamin, M. Entheses, Enthesitis, and Enthesopathy . Arthritis Research Campaign. Topical Reviews.

By Carol Eustice Carol Eustice is a writer covering arthritis and chronic illness, who herself has been diagnosed with both rheumatoid arthritis and osteoarthritis.

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8.26.19 7:06AM

Tina Donvito

Home Living with Arthritis Symptoms

What Is Enthesitis? The Painful Arthritis Symptom You Should Know About

PUBLISHED 08/26/19 BY Tina Donvito

Certain types of arthritis are prone to pain where tendons and ligaments meet bone, which is called enthesitis. Here’s how to deal with it.

If you have ankylosing spondylitis or psoriatic arthritis , you may be familiar with the pain of enthesitis, an inflammation where tendons and ligaments attach to the bone — even if you aren’t aware it has a name. “I didn’t know what it was called!” Monica D. told us on Facebook. “I have pain all the time. Makes it difficult to walk very far.”

What Is Enthesitis?

“Enthesitis is inflammation of the ‘enthesis,’ which is where a tendon or ligament attaches to bone,” says Joan Appleyard, MD, a rheumatologist at Baylor College of Medicine in Houston, Texas. “Symptoms are pain sometimes accompanied by swelling.”

There’s a reason the enthesis is susceptible to this problem. “The enthesis has a lot of blood flow and [thus] is subject to both infection and inflammation,” says Theodore R. Fields, MD, a professor of clinical medicine at Weill Cornell Medical College and an attending rheumatologist at Hospital for Special Surgery in New York City. “Two of the most common entheses are the area where the Achilles’ tendon inserts on the back of the heel, which causes Achilles’ tendonitis, and where the sheet of connective tissue, or fascia, inserts on the bottom of the heel, which causes plantar fasciitis.”

Types of Arthritis That Cause Enthesitis

If you have rheumatoid arthritis or osteoarthritis, chances are you won’t experience enthesitis, because it generally only occurs with certain types of arthritis called spondyloarthropathies (SpA), which include non-radiographic axial spondyloarthritis, ankylosing spondylitis, psoriatic arthritis, enteropathic arthritis (a type that occurs in people with inflammatory bowel disease), and reactive arthritis (which can occur after infection, formerly called Reiter’s syndrome).

Enthesitis is actually one of the hallmark traits of SpA. “It is not a feature of rheumatoid arthritis — this is one of the ways in which SpA differs from RA,” Dr. Appleyard says.

Doctors aren’t exactly sure why SpA targets the enthesis, but it may be that a specific inflammatory response occurs in areas under biomechanical stress (stress on the joint from movement).

“About half of people with psoriatic arthritis and ankylosing spondylitis have enthesitis,” says Dr. Fields. “In both psoriatic arthritis and ankylosing spondylitis, the back and under portions of the heel are common sites of enthesitis.”

There are many other areas where enthesitis can occur, he says, including the inner and outer sides of the elbows, the area where the ribs meet the breastbone , the back of the head where it meets the neck, and in the spine in the area closest to the skin.

What Does Enthesitis Feel Like?

The main symptom of enthesis is pain, which CreakyJoints patients described as “horrible” or “burning.”

“Quite a bit of my PsA pain is due to enthesitis,” Ruth O. shared on Facebook. “It moves around from ball of my foot, to left shoulder, hands, wrists and left hip.”

Marcia G. told us, “I have [enthesitis] in my right ankle and heel mostly. My feet hurt randomly and the right toes and top of foot swell up.” Although many patients noted that enthesitis occurs in their feet, Kelly C. says it hurts “especially around my rib cage.”

Does Enthesitis Signal Worsening Disease?

Enthesitis might not mean your disease is progressing. “Enthesitis can be part of both severe and relatively mild cases of psoriatic arthritis or ankylosing spondylitis,” Dr. Fields says. It may indicate active disease, but not necessarily worsening disease, says Dr. Appleyard.

Your doctor will diagnose enthesitis based on a physical exam, in which they’ll note the location of pain, tenderness, or swelling. “Ultrasound can also be helpful in diagnosing enthesitis, and at times MRI can also be used,” Dr. Fields says.

Treatment for Enthesitis

“Managing enthesitis is important since it can cause a lot of discomfort,” Dr. Fields says. Some specific biologic therapies used to treat SpA seem to improve symptoms of enthesitis. “Treating the underlying disease with anti-TNF agents [a type of biologic] often helps with enthesitis, but traditional DMARDs such as sulfasalazine don’t treat enthesitis,” Dr. Appleyard says. Non-steroidal anti-inflammatory agents (NSAIDs) can be used for mild cases.

When deciding on a treatment regimen for SpA, Dr. Fields says it’s important to take into account all the affected areas. “In patients where enthesitis is the major issue, and more severe than the arthritis, we may skip the non-biologic agents and go directly to biologic therapies, since they tend to be more effective for enthesitis,” he says.

In addition to TNF blockers, other biologic options include blockers of the proteins IL-17, IL-12, or IL-23. “One exception is the non-biologic agent apremilast, which does not appear to cause infection and can be used in psoriatic arthritis, and which has been shown to have effectiveness in some people with enthesitis,” says Dr. Fields.

In addition, “local injection of corticosteroids can be used in enthesitis at times, but needs to be used carefully to avoid weakening of the surrounding tendons and ligaments,” Dr. Fields says.

Talk to your doctor about which medications are right for your individual case. (Here’s what one study found about picking the right treatment for enthesitis in PsA .)

Home Remedies for Enthesitis

A physical therapist can give you gentle stretches to do at home to help relieve the pain of enthesitis, Dr. Fields says. In addition, the doctors and patients we talked to suggested:

• Apply heat or ice to affected areas
• Maintain a healthy weight. “Weight loss can take pressure off the involved areas,” Dr. Fields says.
• Rest and elevate the affected foot. “I try to keep the swelling down by icing it, and keeping my leg and foot elevated,” Lesley P. told us on Facebook.
• Wear special shoes. “People with plantar fasciitis can benefit from shoe inserts to cushion the heel and may be helped by a consultation with a podiatrist ,” Dr. Fields says.
• Wear compression socks, braces, wraps, or even a medical boot.
• Watch salt intake to control swelling. “Salt intake does make a difference,” Ruth says.
• Over-the-counter remedies (check with your doctor first). “I love using Biofreeze on the bone in my foot — it helps!” Caroline P. told us on Facebook. Other CreakyJoints members recommended Epsom salt soaks, diclofenac gel, magnesium, or CBD products .

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enthesis in English dictionary

Meanings and definitions of "enthesis".

• (anatomy) The point at which a tendon, ligament, or muscle inserts into a bone.
• noun (anatomy) The point at which a tendon, ligament, or muscle inserts into a bone.

Grammar and declension of enthesis

• enthesis ( plural   entheses )
• enthesis ( plural entheses )

Sample sentences with " enthesis "

Available translations.

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Citation, DOI, disclosures and article data

At the time the article was created Jeremy Jones had no recorded disclosures.

At the time the article was last revised Daniel J Bell had no financial relationships to ineligible companies to disclose.

• Footprint (tendon attachment)
• Footprints (tendon attachment)

An enthesis (plural: entheses), also known, more informally, as a footprint , generally refers to the anatomic junction where connective tissue (e.g. ligament , tendon , joint capsule , bursa or a combination thereof) attaches to bone.

Entheses are commonly classified into two types 1 :

fibrocartilage

In a fibrous enthesis, the collagen fibers comprising ligament or tendon attach directly to periosteum or bone cortex 1,2 . They are usually associated with short tendons, e.g. gluteus maximus insertion onto the femur 1 . This usually occurs along a relatively wide area of a bone shaft 1 .

Fibrocartilage

A fibrocartilage enthesis represent a more complex attachment between tendon and bone. They generally occur at locations where tendon inserts onto a portion of bone lacking periosteum, e.g. an epiphysis.

They are classically divided into four zones:

collagen zone - derived from tendon or other soft tissue structure

non-calcified fibrocartilaginous zone - variable thickness where chondrocytes predominate

calcified fibrocartilaginous zone - an abrupt transition ("tidemark" or "blue line")

subchondral bone zone

The zonal organization is thought to result in decreased stress on the interface 1 .

Related pathology

enthesopathy : a pathological condition affecting the enthesis

enthesitis : an inflammatory condition causing enthesopathy

enthesophyte : bony projection at an enthesis in response to enthesopathy

• 1. Anthony S. Tadros, Brady K. Huang, Mini N. Pathria. Muscle-Tendon-Enthesis Unit. (2018) Seminars in Musculoskeletal Radiology. 22 (03): 263. doi:10.1055/s-0038-1641570 - Pubmed
• 2. D'Agostino MA, Terslev L. Imaging Evaluation of the Entheses: Ultrasonography, MRI, and Scoring of Evaluation. (2016) Rheumatic diseases clinics of North America. 42 (4): 679-693. doi:10.1016/j.rdc.2016.07.012 - Pubmed
• 3. William Palmer, Laura Bancroft, Fiona Bonar, Jung-Ah Choi, Anne Cotten, James F. Griffith, Philip Robinson, Christian W.A. Pfirrmann. Glossary of terms for musculoskeletal radiology. (2020) Skeletal Radiology. doi:10.1007/s00256-020-03465-1 - Pubmed

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• Meaning of entheses

entheses ( English)

• Plural of enthesis

This is the meaning of enthesis :

enthesis ( English)

Origin & history, pronunciation.

• IPA: /ɪnˈθiː.sɪs/
• Hyphenation: en | the | sis
• ( anatomy ) The point at which a tendon , ligament , or muscle inserts into a bone .
• 2004 , Erbil Ünsal, Chapter II: Andersson Lesion in Early Juvenile Spondyloarthropathies , Frank Columbus (editor), Focus On Arthritis Research , page 26 , Like arthritis, peripheral enthesitis occurs predominantly in the lower extremities, particularly in the foot, at single sites at onset, and then at several entheses throughout the course of the disease.
• 2007 , Philip Helliwell, James Woodburn, The Foot And Ankle in Rheumatoid Arthritis: A Comprehensive Guide , page 64 , Functional entheses occur where tendinous and ligamentous structures, while not actually attaching to bone, are adjacent and in a close relationship to the underlying bone.
• 2010 , Richard J. Wakefield, Maria Antonietta D′Agostino, Essential Applications of Musculoskeletal Ultrasound in Rheumatology , page 211 , Inflammation of the enthesis , when associated with arthritis in children, is called the syndrome of seronegative enthesopathy associated with arthritis (SEA). The entheses most commonly involved in children are the plantar aponeurosis, calcaneal enthesis , and distal and proximal patellar ligament insertions.

Automatically generated practical examples in English:

San Diego: Academic Press; 2011. locations of indicative entheses on the long bones. Osteoarchaeology: A Guide to the Macroscopic Study of Human... (Efthymia Nikita)

There is a functional analogy here with the fibrocartilaginous entheses , where strength increase with maturity results from endochondral bone invading the TL fibrocartilage (see above). International Review of Cytology - Page 106 (2000)

Additionally, Benjamin has introduced the concept of 'functional' entheses . The Foot and Ankle in Rheumatoid Arthritis: A Comprehensive... (Philip Helliwell)

▾  Further examples

This was based on the observation that there were substantial differences in the manifestation of entheses between human populations of different subsistence strate- gies. Archaeologies of Animal Movement. Animals on the Move - Page 47 (Anna-Kaisa Salmi)

Definition: A periarticular condition that affects the entheses : sites of tendinous or ligamentous attachments to bone. These may be inflammatory or degenerative and are seldom owing to endocrinopathy, trauma, or drugs. Rheumatology: Diagnosis and Therapeutics - Page 166 (John J. Cush)

Additionally, entheses are biological components that, while influenced by physical activity, are not directly involved in synovial degeneration. Activity, Diet and Social Practice: Addressing Everyday Life... - Page 73 (Sarah Schrader)

The most significant is that although the medical literature identifies two types of entheses , the Hawkey method makes no such distinction (Villotte et al. 2010; Jurmain and Villotte 2010; Henderson and Gallant 2007). PHOTOGRAPHIC REGIONAL ATLAS OF BONE DISEASE: A Guide to... (Robert W. Mann)

▾  Dictionary entries

Entries where "entheses" occurs:

enthesopathy : enthesopathy (English) Noun enthesopathy (pl. enthesopathies) (pathology) A disorder of entheses (bone attachments). Hypernyms tendinopathy Related words & phrases…

enthesis : …in the lower extremities, particularly in the foot, at single sites at onset, and then at several entheses throughout the course of the disease. 2007, Philip Helliwell, James Woodburn, The…

enthesitis : enthesitis (English) Noun enthesitis (uncountable) pathology - An inflammatory disorder of entheses (bone attachments). Related words & phrases enthesopathy

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enthesial (English)

enthesis (English)

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