Musculoskeletal pain often finds its origin in the enthesis. This article explains it.

The enthesis organ is a group of tissues that work together in a shared function. The function is to provide a stable anchorage of tendons and ligaments to the skeleton and to minimise damage at the insertion site which is subject to high levels of mechanical stress.

The enthesis organ is composed of the enthesis insertion and the surrounding tissues. Whilst the insertion provides firm anchorage to the underlying bone the enthesis organ comprises several other tissues.

The bone-insertion can run over tuberosities. Thus, the tendon that is located well away from the attachment site is compressed against the adjacent bone during movement. This limits stress at the actual insertion point. A variation on this is that entheses may arise from pits of depressions in the bone leading to bone stressing being spread over a wide area.

The bone and tendon surface adjacent to the enthesis are lined by fibrocartilage.

The cartilage lining the bone surface is termed the periosteal fibrocartilage and the one lining the under surface of the tendon or ligament is called a sesamoid fibrocartilage.

Soft tissues including the cartilages related to the enthesis organ that line the bone derive nourishment from a specialised tissue called synovium. This forms a structure called a Synovio-Entheseal Complex (S.E.C.). This structure forms a cavity called a bursa.

Synovium provides lubrication and oxygen and nutrition for periosteal and sesamoid fibrocartilages so aides in their nourishment and function of the enthesis. It is also responsible for the removal of micro-debris that occurs in the course of normal enthesis activity.

The Synovio-Entheseal Complex is a biological filter that clears the fluid.

The synovial cells that remove damaged tissue are termed macrophages which are potentially highly prone to initiating inflammatory reactions.

This is a major contributor to pain and inflammation in subjects with enthesitis or enthesopathy.

If a problem arises in the fibrocartilages, then this can lead to inflammation in adjacent synovium.

The implication of this is that people with diseases of the enthesis come to osteopaths with joint swelling.

Adjacent supportive tissue or fascia is also present (many insertions around the body are loaded with fat which is a liquid and shock absorber at body temperature). The supportive tissue around the enthesis is called fascia and carries blood vessels that supply the enthesis. Many insertions are connected to adjacent insertions by a band fascia.

Enthesis organs can be classified as joint related (called ‘articular’) or extraarticular, according to whether the enthesis lies internal or external to the capsule of a synovial joint. In articular enthesis organs, the synovial membrane with which the enthesis is associated is a joint cavity. In extraarticular enthesis organs, it is that of a subtendinous bursa.

Where a tendon merges with a joint capsule, there is often a simple articular enthesis organ.

This consists of the enthesis itself, a sesamoid fibrocartilage in the tendon adjacent to the attachment site, articular fibrocartilage covering a neighbouring bone, and a joint cavity that allowed movement between sesamoid and articular fibrocartilages (the latter being functional) ally equivalent to periosteal fibrocartilage typical of that seen in the Achilles enthesis organ.

Extraarticular enthesis organs are exemplified by those associated with the biceps brachii and patellar insertional tendons. A subtendinous bursa occupied the insertional angle between the tendon and the bone, and there is periosteal fibrocartilage of variable thickness near the attachment sites. Although some fat was visible in association with both the biceps and the patellar tendon entheses.

In some attachments, there is no enthesis organ. The pes anserinus enthesis is here an example.

There are many variations:

• At the insertion of biceps brachii, the fatty subsynovial tissue occasionally contains a small number of skeletal muscle fibers, together with associated ‘microtendons’.

• Where both periosteal and sesamoid fibrocartilages are prominent at the insertion of the biceps brachii tendon, they largely replaced the synovial membrane of the intervening bursa in this region.

• The Achilles insertion is a common site of disease and has rightly been described as the ‘première enthesis’. It forms part of a complex enthesis organ that comprises not only the insertion itself, but also adjacent tendon and bone fibrocartilage, together with a fat-pad, bursa, and synovium.

• The femoral enthesis of the lateral collateral ligament merges imperceptibly with that of the popliteal tendon. The 2 structures, together with the associated synovium, form an enthesis organ as complex as that of F.E. the tibialis posterior. The lateral collateral ligament enthesis could affect the inside of the joint as well.

If stress is dissipated away from a bony insertion because of the existence of an enthesis organ, this can explain why pathologic changes are seen adjacent to entheses as well as at them, why subtendinous bursae are often affected in the disease, and why bursitis can mimic enthesitis.

The complexity of enthesis organs that are intimately associated with a synovial cavity may have implications regarding the mechanisms of synovitis.

Enthesopathies can be very painful. A normal, healthy fibrocartilaginous enthesis lacks nerve fibres. Cartilages elsewhere, including the articular cartilage that lines the ends of long bones is also aneural.

Why is enthesopathy associated with pain if the insertion site lacks nerve endings?

This is because the nerves endings are near or adjacent to the insertion site.

Nerve endings may be located on the surface of the attachment site within the loose connective layer that is known as the epitenon.

Nerve endings have also been documented in fat that lies deep to the attachment site - i.e. at the insertional angle. As this fat is compressed when the insertional angle is decreased with joint movement, any nerve fibres between the fat cells are likely to be stimulated.

Some types of nerve endings may sense pain, but others sense the joint position in 3D space or what is known as proprioception. It has been suggested therefore that such innervated fat has a proprioceptive role. e.g. the fat known as Kager’s fat pad that lies in the insertional angle of the Achilles tendon. So, pain and joint position may originate in this structure.

Pain may also originate from the bone underneath insertions especially when there is bone damage or pressure changes within the bone due to disease states.

Therefore, pain may originate in several locations near insertions but not from the insertion itself.

When micro damage occurs at insertions then blood vessels may invade the region containing fibrocartilage as part of the normal repair process. However, this process may go wrong with the consequence that blood vessels persist at these sites. It is thought that blood vessels may ‘piggy back’ nerve endings into the insertion site thus leading to persistent pain. This may then contribute to chronic low back pain in disc degeneration.

The fibrocartilage at the enthesis has a very low oxygen requirement. Air contains 21% oxygen. The oxygen tension in fibrocartilage is thought to be from 1% upwards. Oxygen gets into the various parts of the insertion region by diffusion. The tissues adjacent to the insertion that form part of the enthesis including ligaments or tendons also have a comparatively low density of blood vessels. Blood vessel approach the enthesis from the bone marrow, the substance of ligaments or tendons and the tissue outside the enthesis.

The upside of the lack of blood vessels at the enthesis is that this site is partially protected from inflammatory reactions or ‘immune-privileged’. The very low density of blood vessels makes it very difficult for immune cells to get near the attachment site.

The downside of the low degree of blood supply to the enthesis might be very slow or inadequate healing responses, especially with age. This may be a major contributory factor to chronic pain and disease.

In general:

Enthesis organs are present at many articular and extraarticular sites.

The intimate relationship between enthesis organs and synovial cavities and the presence of enthesis organ components in joint capsules may have important implications for understanding the clinical pattern of arthritis, including synovitis and extracapsular changes.

Luc Peeters, MSc.Ost.

Some articles:

• The “Enthesis Organ” Concept. M. Benjamin, B. Moriggl, E. Brenner, P. Emery, D. McGonagle, S. Redman. ARTHRITIS & RHEUMATISM Vol. 50, No. 10, October 2004, pp. 3306–3313 DOI 10.1002/art.20566.

• Enthesitis in spondyloarthropathy. McGonagle D., Khan M.A., Marzo-Ortega H., O’Connor P., Gibbon W., Emery P. Curr. Opin. Rheumatol. 1999; 11: 244–250.

• The concept of a “synovio-entheseal complex” and its implications for understanding joint inflammation and damage in psoriatic arthritis and beyond. McGonagle D., Lories R.J., Tan A.L., Benjamin M. Arthritis Rheum. 2007 Aug;56(8): 2482-2491.

• Normal anatomy of the heel entheses: anatomical and ultrasonographic study of their blood supply. Morel M., Boutry N., Demondion X., Legroux-Gerot I., Cotten H., Cotten A.. Surg. Radiol. Anat. 2005 Aug. 27(3): 176-183. Epub. 2005 May 26.

• Role of vascular channels as a novel mechanism for subchondral bone damage at cruciate ligament entheses in osteoarthritis and inflammatory arthritis. Binks D.A., Gravallese E.M., Bergin D., Hodgson R.J.,

• Tan A.L., Matzelle M.M., McGonagle D., Radjenovic A. Ann. Rheum. Dis. 2013 Oct. 4. doi: 10.1136/annrheumdis-2013-203972.

• The enthesis: a review of the tendon-to-bone insertion. John Apostolakos, Thomas J.S. Durant, Corey R. Dwyer, Ryan P. Russell, Jeffrey H. Weinreb, Farhang Alaee, Knut Beitzel, Mary Beth McCarthy, Mark P. Cote, and Augustus D. Mazzocca. Muscles Ligaments Tendons J. 2014 Jul.-Sep. 4(3): 333–342. Published online 2014 Nov 17.

• Enthesis: A Brief Review. Nitya Waghray. https://doi. org/10.1016/j.apme.2015.01.003.

• Structure–function relationships of entheses in relation to mechanical load and exercise. H. M. Shaw, M. Benjamin Scand. J. Med. Sci . Sports 2007: 17: 303–315.