Terminology of Tendon Disorders

December - January 2023

Prof Anand Pillai Consultant Orthopaedic Foot & Ankle and Adult Reconstruction Surgeon Manchester, United Kingdom

Terminology of Tendon Disorders

Editorial Summary

Often, we come across random terms such as Haglund’s deformity, Pump Bump, Cucumber Heel, Knobbly Heels and high prow heels; etc. As clinicians, we tend to use such terms as tendonsis, paratendinitis, tenosynovitis, peritendinitis or tendonosis in different circumstances quite interchangeably. The suffix ‘itis’ is traditionally supposed to imply an underlying inflammatory pathology. Most currently practicing general practitioners were told and many still believe that patients who present with overuse syndromes have a largely inflammatory cause, and will benefit from anti-inflammatory medication. This dogma seems to be deep rooted. We now know that inflammation and inflammatory cytokines are more important in the acute injuries and are not universally prominent across the spectrum of some other tendon disorders.2 This article is a concise exploration of these themes.

Introduction

The ambiguity of the nomenclature appears to stem from the lack of standard terminology and the large pool of confusing terms and definitions often used interchangeably.

In this article, we highlight the use of uniform terminology which may help promote more effective communication and documentation and also could go a long way in information sharing and affording clarity to our patients. This can possibly aid progress in the management of these conditions.

Anatomy

It is important to understand the anatomy of a tendon before we talk about pathology. Anatomically, a tendon has 3 coverings named epitenon, endotenon and paratenon. The epitenon having vascular, lymphatic and nerve supply extends into the tendon between tertiary bundles as endotenon. The epitenon is covered by the paratenon (loose type 1 and 3 collagen). Together, the paratenon and epitenon are known as the peritenon.

Discussion

Historically there have been attempts to tackle this variability Hippocratic first described a ‘Tendo Magnus of Hippocrates’. In 1693, Philip Verheyen attempted to further clarify this and in 1883 Raynal’s description of ‘Cellulite Peritendineuse’, also tries to shed some light on this problem.

The first modern classification of tendon pathologies has to be credited to Lipscomb (1950) who brought in new definitions such as:

a. Paratendinitis: inflammation of tendons/ parts of tendons without sheath.

b. Tenosynovits : inflammation of tendons within a sheath.

c. Peritendinitis : general descriptor could be either a/b.

In the 1970s Perugia and in 1998 Puddu increased the focus on histology and described the terms:

a. Peritendinitis: inflammation in peritendinous sheaths, no tendon pathology.

b. Tendinosis : tendon degeneration without histological inflammation.

c. Peritendinitis associated with Tendinosis

Clain & Baxter (1992) tried to subdivide this based on anatomic location with the introduction of the terms insertional and noninsertional to further focus the pathology.

More recently, Maffulli (1998) suggested

Dr Naeem Jagani

Specialist Registrar in Trauma and Orthopaedics, Manchester University NHS Foundation Trust Manchester, United Kingdom

Tendinosis

Tendinitis/ Partial rupture

Paratenonitis

Paratenonitis with tendinosis

Intratendinous degeneration (commonly due to ageing, microtrauma, vascular compromise)

Symptomatic degeneration of tendon with vascular disruption and inflammatory repair response

‘inflammation’ of the outer layer of the tendon (paratenon) alone, whether or not the paratenon is lined by synovium

Paratenonitis associated with intratendinous degeneration.

that the diagnosis of overuse pathology should be only histological; therefore, an excision biopsy is required before any definitive nomenclature can be attributed.

Bonar in 1999 modified Clancy’s classification of tendonopathies and suggested use of terminologies like tendinosis, tendinitis/partial rupture, paratenonitis and paratenonitis with tendinosis (Table 1).2

This reiterates that overuse tendon conditions have a non-inflammatory pathology. The knowledge of the continuum of physiology to pathology makes it unambiguous that overuse and cumulative microtrauma, micro ruptures or overload have several stages / pathogenic cascades with a common pathway of neural ingrowth and neo vascularisation. It reaffirms that inflammation and degeneration are not mutually exclusive.3

Collagen disorientation, disorganisation and fibre separation by an increase in mucoid ground substance, increased prominence of cells and vascular spaces with or without neovascularization and focal necrosis or calcification.

Degenerative changes as noted above with superimposed evidence of tear, including fibroblastic and myofibroblastic proliferation, haemorrhage and organising granulation tissue.

Mucoid degeneration in the areolar tissue is seen. A scattered mild mononuclear infiltrate with or without focal fibrin deposition and fibrinous exudate.

Degenerative changes as noted in tendinosis with mucoid degeneration with or without fibrosis and scattered inflammatory cells in paratenon alveolar tissue.

The ‘Pathology continuum’ model of Cook et. al embraces the transition from normal through to degenerative tendinopathy and highlights the potential for reversibility early in this continuum. This reversibility is unlikely in these latter degenerative stages (Figure 1).4

This work also factors in the differences in pharmacological and physical management in early versus late tendon disrepair (Table 2).

Stage

Reactive tendinopathy/early tendon dysrepair

Late tendon dysrepair/degeneration

Pharmacological management

Tenocyte inhibitors (ibuprofen, celecoxib, corticosteroids), aggrecan inhibitors (ibuprofen, naproxen, indomethacin)

Prolotherapy (including blood), aprotinin, sclerosing therapy, glyceryl trinitrate

Physical management

Load management. Reduction in frequency +/- intensity of tendon load

Exercise with eccentric component, Extracorporeal shock wave therapy, frictions, ultrasound.

Table 1: Bonar’s modification of Clancy’s classification.

Figure 1: ‘Pathology Contiuum’ model of Cook et. al. 4

Table 2: Clinical and pharmacological treatments placed in the model.

Adding or removing load is the primary stimulus that drives the tendon forward or back along the continuum, especially in the early stages. Within the constraints of recovery proposed in the model, reducing load may allow the tendon to return to a previous level of structure and capacity within the continuum.5 Therefore, there is a long term therapeutic advantage in understanding and clarifying terminology.

Van Dijk et. al (2011) attempted rationalisation of the nomenclature by using modern imaging (Table 3).6 Thus, by using terms such as midportion tendonopathy, para tendonopathy (acute or chronic), insertional tendonopathy, retrocalcaneal bursitis and superficial bursitis localised the area of pathology. There is now more clarity along with an insight into the findings associated with these tendon disorders.

Therefore, a clear understanding of the anatomical, histological, imaging and clinical findings could go a long way in helping us correctly label conditions and possibly effectively direct the necessary therapeutic measures.

Conclusion

We would recommend that it is time to abandon the ‘tendinitis’ myth. Physicians should acknowledge that painful overuse tendon conditions have a non-inflammatory pathology.

We suggest that the nomenclature be simplified and communications be streamlined.

We suggest to use a more unified classification like that of Van Dijk . Nomenclature for the clinical presentation of tendon disorders should reflect the true histopathological basis underlying clinical presentation.

Furthermore, by allowing time for collagen turnover and remodelling inherent in the pathology of tendonosis we can provide patients with a more realistic prognosis that better reflects the findings of clinical studies.

References

1. Klatte-Schulz F, Minkwitz S, Schmock A, Bormann N, Kurtoglu A, Tsitsilonis S, Manegold

S, Wildemann B. Different Achilles Tendon Pathologies Show Distinct Histological and Molecular Characteristics. Int J Mol Sci. 2018 Jan 30;19(2):404. doi: 10.3390/ijms19020404.

2. Khan KM, Cook JL, Bonar F, et al. Histopathology of common tendinopathies: update and implications for clinical management. Sports Med. 1999;27:393-408

3. Abate M, Silbernagel KG, Siljeholm C, Di Iorio A, De Amicis D, Salini V, Werner S, Paganelli R. Pathogenesis of tendinopathies: inflammation or degeneration? Arthritis Res Ther. 2009;11(3):235. doi: 10.1186/ar2723. Epub 2009 Jun 30.

4. Cook JL, Purdam CR . Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy British Journal of Sports Medicine 2009;43:409-416.

5.Cook JL, Khan KM,Kiss ZS, et al Asymptomatic hypoechoic regions on patellar tendon ultrasound: A 4-year clinical and ultrasound followup of 46 tendons. Scand J Med Sci Sports 2001;11:321–7.

6. Van Dijk CN, van Sterkenburg MN, Wiegerinck JI, Karlsson J, Maffulli N. Terminology for Achilles tendon related disorders. Knee Surg Sports TraumatolArthrosc. 2011 May;19(5):835-41. doi: 10.1007/s00167-010-1374-z. Epub

Table 3: Classification by Van Dijk et. al.