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Updated: Apr 23, 2026

Author Spotlight: Integrating Mechanical and Biological Analysis in Tendinopathy Research
Published on: March 1, 2024
Posterior tibial tendinopathy: what are the risk factors?
Insights
Posterior tibial tendinopathy (PTT) is a common cause of adult flatfoot. Research has focused on management, but this review highlights the need to explore genetic factors alongside intrinsic and extrinsic risks for a complete PTT profile.
Area of Science:
- Orthopedics
- Podiatry
- Genetics
Background:
- Posterior tibial tendinopathy (PTT) is the primary cause of acquired flatfoot deformity in adults.
- Current research on PTT predominantly focuses on treatment strategies, neglecting underlying causal mechanisms.
- The multifactorial etiology of PTT involves both intrinsic and extrinsic risk factors.
Purpose of the Study:
- To critically evaluate reported etiologic factors for posterior tibial tendinopathy (PTT).
- To explore the potential role of genetic predisposition in the development of PTT.
- To identify gaps in current understanding regarding PTT etiology.
Main Methods:
- A comprehensive literature review was conducted.
- Searched English-language medical databases for studies published after 1936.
- Focused on identifying reported etiologic factors and genetic associations for PTT.
Main Results:
- No definitive consensus exists regarding the relative importance of identified PTT risk factors.
- Existing literature has not adequately considered a potential genetic basis for PTT.
- The interplay between known risk factors and genetic background remains unexplored.
Conclusions:
- Understanding the genetic component of PTT is crucial for a comprehensive risk profile.
- Investigating the interaction between genetic background and environmental/intrinsic factors is essential.
- Genetic association studies offer a novel approach to understanding PTT etiology.
Background:
Posterior tibial tendinopathy (PTT) is the most common cause of acquired (progressive) flatfoot deformity in adults. To date, PTT research has mainly focused on management rather than on causal mechanisms. The etiology of PTT is likely to be multifactorial because both intrinsic and extrinsic risk factors have been reported. We sought to critically evaluate reported etiologic factors for PTT and consider the concept of genetic risk factors.
Methods:
A detailed review of the literature published after 1936 was undertaken using English-language medical databases.
Results:
No clear consensus exists as to the relative importance of the risk factors reported, and neither has any consideration been given to a possible genetic basis for PTT.
Conclusions:
To date, studies have examined various intrinsic and extrinsic risk factors implicated in the etiology of PTT. The interaction of these factors with an individual's genetic background may provide valuable data and help offer a more complete risk profile for PTT. A properly constructed genetic association study to determine the genetic basis of PTT would provide a novel and alternative approach to understanding this condition.
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