Pelvic rehabilitation practitioners often focus on mechanical concerns such as diastasis recti, pelvic floor weakness, and altered load transfer. However, one foundational element that deserves equal attention in the postpartum period is the ongoing effect of hormonal shifts on connective tissues and joints.

Even after delivery, hormones such as relaxin, estrogen, and progesterone continue to influence tissue behavior, joint mobility, and the body's response to rehabilitation. Understanding how these hormones affect ligament laxity, collagen turnover, and neuromuscular control helps clinicians design safer and more effective recovery programs.

Hormonal Changes in Pregnancy and Early Postpartum
Relaxin is produced by the corpus luteum and placenta, and rises significantly during pregnancy. It is known for its role in “relaxing” muscles and ligaments, especially in the pelvis, to facilitate childbirth. Estrogen and progesterone also rise and modulate connective-tissue metabolism and receptor expression in ligaments.

A recent review highlights that pregnancy-associated hormonal fluctuations (relaxin, estrogen, progesterone) contribute to increased joint laxity (Yalçınkaya et al., 2025). These hormonal effects do not cease abruptly at delivery; they taper variably and may persist for months postpartum, meaning joint and tissue behavior remains altered during rehab.

Hormones Affect Connective Tissue and Joint Mechanics
At the cellular level, relaxin increases the activity of matrix metalloproteinases (MMPs) such as MMP-1, -9, and -13, which degrade collagen and weaken ligament/tendon architecture (Parker et al., 2-22). Estrogen and progesterone increase expression of relaxin receptors in ligaments, amplifying these effects (Yalçınkaya et al., 2025).

In animal and human tendon studies, both relaxin and estrogen have been shown to reduce tendon stiffness and increase compliance, which can reduce load tolerance (Danos et al., 2023). The net mechanical effect is increased joint mobility (or perceived laxity), reduced passive stability, and a greater need for neuromuscular control to compensate.

Clinically, this manifests as more “loose-feeling” joints, increased cushioning of movement, greater reliance on muscular control for stability, and potentially slower progress of load-transfer training. A prospective cohort during pregnancy found associations between estrogen changes and increased low-back/pelvic-girdle pain and disability (Daneau et al., 2025). Although postpartum longitudinal data are sparse, the same mechanisms are likely to persist into the early postpartum period and influence rehab.

Implications for postpartum rehabilitation of joints

1. Assessment and monitoring: Include joint laxity screening (e.g., Beighton score or joint-specific tests) and ask the client about subjective joint “giveness” or instability. Recognize that normal endpoints may be slower to return.
2. Loading progression: Because connective tissues are in a transiently weakened state, adopt more conservative load progressions. Emphasize neuromuscular control (motor control, stability) before heavy mechanical loading. Use subsets such as closed-chain, low-velocity, high-control activities.
3. Tailored timeline: Do not assume pre-pregnancy tissue behavior has returned simply because the organ-based recovery period has ended. A busy schedule, hormonal fluctuations (including lactation, menses return) may continue to modulate tissue mechanics.
4. Patient education: Explain that “it’s not just about the tummy and pelvic floor” but that “your ligaments and joints are still adjusting.” This can help set realistic expectations and foster adherence to graded rehab.
5. Coordination with other practitioners: Ensure communication with obstetric, primary-care, and sports-medicine colleagues about longer-term musculoskeletal implications of hormonal and biomechanical changes. As one review concluded, many women are at elevated risk for persistent joint instability and possible long-term sequelae such as early osteoarthritis (Yalçınkaya et al.., 2025).

Case example
A 34-year-old primipara at 10 weeks postpartum presents with “clicking” in the pubic symphysis region when lifting her 9-month-old toddler and reports a sense of “unstable hips” when stepping sideways. On assessment, she has a Beighton score of 5/9 (with bilateral thumb-to-forearm and elbow hyperextension). She also reports previous hip discomfort in adolescence.

Given her history and findings, you design a graduated program: phase 1 focused on pelvic-floor activation + hip stability in non-weight-bearing by week 12; phase 2 at week 16, introducing unilateral step-downs with low amplitude; phase 3 at week 20, adding higher load functional tasks (carrying child + step).

You monitor joint symptoms, ensure neuromuscular control precedes full load, and educate her regarding ligamentous recovery timeline (~6-12 months). You explain that although the baby is 9 months old, her connective tissues may still be adjusting to hormone-mediated changes.

Conclusion
Hormonal recovery is a critical but sometimes overlooked element of postpartum rehabilitation. The lingering influence of relaxin, estrogen, and progesterone shapes how connective tissues behave and respond to loading. By integrating hormonal awareness into clinical decision-making, pelvic health practitioners can enhance precision, promote safety, and improve long-term functional outcomes. Recovery after childbirth is not limited to muscle or fascia; it is a systemic process involving hormones, tissues, and time.

For clinicians interested in expanding their postpartum rehabilitation skills, consider registering for the upcoming Postpartum Rehabilitation Remote Course scheduled for December 13-14. This course covers acute postpartum management, mental health screening, and musculoskeletal considerations. Participants will learn to modify examinations and interventions for the relevant stages of postpartum recovery. In addition to abdominal wall considerations, typical spine and extremity dysfunctions will be addressed. The course includes instruction on postpartum exercise and return to fitness, with labs covering external perineal screening as well as techniques for the abdominal wall, spine, and ribs, and upper and lower quarter dysfunction.

References

1. Yalçınkaya, B., Sezgin, E. A., Saçıntı, K. G., & Özçakar, L. (2025). Neuromusculoskeletal disorders in pregnancy revisited. Journal of Joint Diseases and Related Surgery, 36(3), 741-750.
2. Parker, E. A., Meyer, A. M., Goetz, J. E., Willey, M. C., & Westermann, R. W. (2022). Do Relaxin Levels Impact Hip Injury Incidence in Women? A Scoping Review. Frontiers in Endocrinology, 13, 827512. https://doi.org/10.3389/fendo.2022.827512
3. Danos, N., Patrick, M., Barretto, J., Bilotta, F., & Lee, M. (2023). Effects of pregnancy and lactation on muscle-tendon morphology. Journal of Anatomy, 243(5), 860-869. https://doi.org/10.1111/joa.13916
4. Daneau, C., Nougarou, F., Abboud, J., Ruchat, M., & Descarreaux, M. (2025). Changes in pregnancy-related hormones, neuromechanical adaptations and clinical pain status throughout pregnancy: A prospective cohort study. PLOS ONE, 20(2), e0314158. https://doi.org/10.1371/journal.pone.0314158

Vaginal wall thinning associated with menopausal changes can cause vaginal burning and pain, limitations in sexual function, and vaginal redness or even changes in discharge. Because these symptoms can mimic many other conditions such as pelvic floor muscle dysfunction or an infection, it is necessary for the pelvic rehabilitation therapist to be alert to identifying vaginal atrophy as an issue to rule out so that patients can access appropriate medical care when needed.

Atrophic vaginitis (AV) is a condition of the vaginal walls associated with tissue thinning, discomfort, and inflammation. The tissue changes often extend into the vulvar area as well. Atrophic vaginitis may also be called vaginal atrophy, vulvovaginal atrophy, urogenital atrophy, or genitourinary syndrome of menopause. Although we tend to associate menopause with women who are in their 40’s or 50’s, any woman who has stopped having her menstrual cycles or who has had a significant reduction in her cycles may be at risk for vaginal atrophy. Any woman who has had a hysterectomy may also be at risk of this thinning of the vaginal walls. Common symptoms of vaginal wall thinning include vaginal dryness, tissue irritation, redness, itching, and a “burning” pain. Interruption in sleep, limitations in activities of daily living, and changes in mood and temperament have also been reported.

One common pharmacological intervention for vaginal and vulvar atrophy is the topical application of hormone creams such as estrogen. A recent study examined the effects of low dose estrogen therapy on bacteria that populates the vaginal walls.^{Shen et al., 2016} This bacteria may be causal or correlated to vaginal health, and also appears related to estrogen levels. Sixty women diagnosed with atrophic vaginitis were treated with low dose estrogen therapy and followed for four weeks to assess the vaginal microbiotia via mid-vaginal swabs. Following are highlights from the linked study’s findings,

• Prior to treatment, in symptomatic postmenopausal women the Lactobacilli species were less abundant and made up 11.2% of the community, while in asymptomatic women, the communities were more than 50% lactobacilli
• Gardnerella was more abundant than Lactobacillus in women with atrophic vaginitis
• Overall diversity of bacterial communities between healthy women and those with atrophic vaginitis was not significantly different
• In response to treatment with estrogen, women with AV reported improved symptoms and decreased vaginal pH
• Serum estradiol improved on average from approximately 42 pmol/L to 168 pmol/L by week 2, with little change from week 2 to week 4
• Lactobacillus count was negatively correlated with symptoms (i.e., more Lactobacillis = less symptoms) and Gardnerella and Atopobium counts were positively correlated with symptoms
• There were variations noted in how each woman’s vaginal bacterial communities responded to the estrogen therapy in that some women had a dominance of other bacteria after 4 weeks even though their symptoms decreased

In conclusion, the authors stated that “…a Lactobacillus-dominated vaginal community may be considered as one of the signs of AV treatment success…” along with reduced symptoms and increased serum estradiol levels. Prior studies have recognized barriers to treatment that include lack of patient knowledge of vulvar and vaginal atrophy, failure to discuss associated symptoms with physicians, concerns about safety of treatments or poor symptom relief with prescribed interventions.^{Kingsburg et al., 2013} This leaves the pelvic rehabilitation provider in a excellent role of educating women in the signs and symptoms of atrophic vaginitis, observing the tissues for changes, and communicating with referring providers and prescribers if a concern is noted. Furthermore, failure to recognize the potential for vaginal atrophy and treating these tissues with manual therapy or exercise may injure or exacerbate the problem.

Interested in learning more? Keep an eye out for a Menopause Rehabilitation and Symptom Management course with Michelle Lyons!

Changes in the Vagina and Vulva. Retrieved June 27, 2016 from http://www.menopause.org/for-women/sexual-health-menopause-online/changes-at-midlife/changes-in-the-vagina-and-vulva
Kingsberg, S. A., Wysocki, S., Magnus, L., & Krychman, M. L. (2013). Vulvar and vaginal atrophy in postmenopausal women: findings from the REVIVE (REal Women's VIews of Treatment Options for Menopausal Vaginal ChangEs) survey. The journal of sexual medicine, 10(7), 1790-1799. 
Shen, J., Song, N., Williams, C. J., Brown, C. J., Yan, Z., Xu, C., & Forney, L. J. (2016). Effects of low dose estrogen therapy on the vaginal microbiomes of women with atrophic vaginitis. Scientific reports, 6.
Vaginal Atrophy. Retrieved June 27, 2016 from http://www.mayoclinic.org/diseases-conditions/vaginal-atrophy/home/ovc-20200167