BACKGROUND: The pathophysiology of posterior tibial tendon dysfunction (PTTD) is poorly understood. It has been theorized that changes in hormone physiology may be a factor influencing tendon health. Estrogen's influence on the fibroblast has been studied in other musculoskeletal tissues. Gender differences in anterior cruciate ligament (ACL) injuries have been studied and it has been discovered that the Estrogen receptor (ER) as well as Progesterone receptor (PR) are expressed in the ACL. MATERIAL AND METHODS: Eight patients with PTTD requiring surgery were enrolled in our pilot study. The mean patient age was 52.4 (range, 18 to 73) years. There were five female and three male patients. Tendon samples were harvested from diseased PTT. Tendon samples harvested from healthy PTT and healthy flexor digitorum longus (FDL) tendon were used as controls. Tendon samples were processed using specific protocols for total RNA isolation from hypocellular, dense connective tissues. ERα and ERβ transcripts were quantified using real time RT-PCR. Quantitative values were obtained from the threshold cycle (Ct) number at which the increase in fluorescent signal associated with an exponential increase of PCR products can be detected. RESULTS: Transcripts of both ERα and ERβ were reproducibly detected in RNA samples isolated from our tendon samples. There was no difference in receptor expression between diseased and control tendon samples. There was no difference in receptor expression between male and female patients. CONCLUSION: We found that the tenocyte of the PTT and FDL tendons express ERα and ERβ. Normal and diseased tendons of both male and female patients expressed both estrogen receptors. CLINICAL RELEVANCE: Identifying ERα and ERβ gene expression in the fibroblast was an initial step in discovering whether tenocytes are targets for estrogen function. Estrogen receptors were identified indirectly by measuring receptor gene expression but we were unable to show a significant difference between diseased and control tendons.
BACKGROUND: The pathophysiology of posterior tibial tendon dysfunction (PTTD) is poorly understood. It has been theorized that changes in hormone physiology may be a factor influencing tendon health. Estrogen's influence on the fibroblast has been studied in other musculoskeletal tissues. Gender differences in anterior cruciate ligament (ACL) injuries have been studied and it has been discovered that the Estrogen receptor (ER) as well as Progesterone receptor (PR) are expressed in the ACL. MATERIAL AND METHODS: Eight patients with PTTD requiring surgery were enrolled in our pilot study. The mean patient age was 52.4 (range, 18 to 73) years. There were five female and three male patients. Tendon samples were harvested from diseased PTT. Tendon samples harvested from healthy PTT and healthy flexor digitorum longus (FDL) tendon were used as controls. Tendon samples were processed using specific protocols for total RNA isolation from hypocellular, dense connective tissues. ERα and ERβ transcripts were quantified using real time RT-PCR. Quantitative values were obtained from the threshold cycle (Ct) number at which the increase in fluorescent signal associated with an exponential increase of PCR products can be detected. RESULTS: Transcripts of both ERα and ERβ were reproducibly detected in RNA samples isolated from our tendon samples. There was no difference in receptor expression between diseased and control tendon samples. There was no difference in receptor expression between male and female patients. CONCLUSION: We found that the tenocyte of the PTT and FDL tendons express ERα and ERβ. Normal and diseased tendons of both male and female patients expressed both estrogen receptors. CLINICAL RELEVANCE: Identifying ERα and ERβ gene expression in the fibroblast was an initial step in discovering whether tenocytes are targets for estrogen function. Estrogen receptors were identified indirectly by measuring receptor gene expression but we were unable to show a significant difference between diseased and control tendons.
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