Displaced patellar stress fracture revealing primary hyperparathyroidism: a case report

Introduction

Background

Stress fractures are partial or complete breaks in the cortical bone caused by repetitive submaximal mechanical loading, rather than by a single traumatic event. They occur when the bone’s natural repair mechanisms are unable to keep pace with ongoing mechanical stress, resulting in cumulative microdamage and eventual structural failure (1). These injuries are frequently seen in athletes or individuals undertaking high-impact or endurance physical activity, and are most commonly observed in weight-bearing bones such as the tibia, femur, metatarsals, and navicular bones (2).

Patellar stress fractures are rare and under-recognised. When they occur, they are typically classified as either vertical or transverse. Transverse fractures, in particular, have a higher propensity for displacement and complications (1). Although extrinsic factors such as overtraining, improper footwear, or biomechanical strain may contribute, intrinsic risk factors like metabolic and endocrine disorders should also be considered (2).

One such condition is primary hyperparathyroidism (PHPT), a relatively common endocrine disorder affecting up to 1% of the population, predominantly women, with a female-to-male ratio of 3:1 to 4:1 (3). PHPT is characterised by autonomous overproduction of parathyroid hormone (PTH), most often due to a solitary parathyroid adenoma, and leads to chronic hypercalcaemia (3). Excess PTH promotes calcium resorption from bone—particularly cortical bone—resulting in reduced bone mineral density and an increased risk of pathological or stress fractures (4).

The diagnosis of PHPT is frequently incidental, made during workup for complications such as nephrolithiasis, bone pain, or gastrointestinal disturbances (5). However, bone fractures, particularly in non-classical locations, may serve as an early or sole manifestation of the disease (6).

Rationale and knowledge gap

While the link between PHPT and bone fragility is well established, the presentation of PHPT through a displaced patellar stress fracture is rarely reported. Most existing literature focuses on fractures of the vertebrae, femur, or long bones in the upper limbs (6). Patellar involvement remains a highly unusual manifestation.

The non-specific presentation of stress fractures—especially in patients without prior trauma—can delay diagnosis and management. This challenge is amplified when symptoms are subtle or the fracture occurs at a site not typically associated with mechanical overuse injuries. In such scenarios, primary care clinicians must decide when to investigate beyond musculoskeletal causes and consider systemic pathologies such as PHPT. There remains a paucity of literature exploring the role of general practice in identifying endocrine causes of atypical fractures and coordinating multidisciplinary care to manage both the fracture and the underlying disease.

Objective

This case report aims to highlight the diagnostic value of primary care follow-up in uncovering systemic aetiologies of musculoskeletal complaints. Specifically, it presents a rare case of a displaced transverse patellar stress fracture in a physically active middle-aged woman, which ultimately led to the diagnosis of previously asymptomatic PHPT due to a solitary parathyroid adenoma. The report underscores the importance of vigilance for atypical fracture presentations and demonstrates the crucial role of general practitioners (GPs) in coordinating effective multidisciplinary care across orthopaedics and endocrinology. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-104/rc).

Case presentation

A 45-year-old physically active female presented to her GP with a 3-week history of gradually worsening right knee pain. She was a keen long-distance walker and had recently increased the intensity of her training in preparation for upcoming charity events. Despite experiencing discomfort, she continued to push herself, attributing the pain to muscular fatigue.

Her past medical history was unremarkable. She had no known history of fractures, bone disease, or endocrine conditions. She was premenopausal with regular menstrual cycles and was not on hormonal therapy. Her only regular medication was prophylactic-dose cholecalciferol. She reported no recent trauma or injuries.

At initial GP examination, there was no visible swelling, erythema, or deformity of the right knee. The joint was stable with full range of motion, and no tenderness was elicited over the patella or adjacent bony landmarks. The only notable finding was pain on flexion and extension. A presumptive diagnosis of muscular strain was made, and the patient was advised to rest, apply ice, and take over-the-counter analgesia.

Four weeks later, she contacted her GP again, reporting a sudden onset of sharp, debilitating pain over the anterior right knee. She was unable to fully extend the leg and found walking nearly impossible. She denied any recent falls or trauma. An urgent video consultation was arranged, and the GP suspected a possible fracture or significant intra-articular pathology. She was referred immediately to the local accident and emergency (A&E) department for imaging and orthopaedic review.

Radiographs of the right knee revealed a displaced transverse fracture of the patella (Figure 1A). This was suspected to be a stress fracture that had progressed and displaced due to continued mechanical loading. The orthopaedic team recommended open reduction and internal fixation (ORIF) due to the degree of displacement and risk of non-union. The patient opted to have the procedure performed privately and underwent successful ORIF with tension band wiring and post-operative brace immobilisation (Figure 1B,1C). She was started on physiotherapy and analgesia for post-operative rehabilitation.

Figure 1 Radiological and surgical course of the displaced patellar stress fracture. (A) Lateral knee radiograph showing a displaced transverse fracture of the right patella. (B) Intraoperative image during open reduction and internal fixation using tension band wiring. (C) Post-operative radiograph confirming satisfactory alignment and fixation. (D) Radiograph following removal of metal hardware eight months later due to localised skin ulceration and irritation. R, right.

During post-operative follow-up with her GP, routine blood tests were requested. These revealed hypercalcaemia with a corrected serum calcium level of 2.9 mmol/L (reference range, 2.2–2.6 mmol/L) and serum phosphate was also found to be low at 0.64 mmol/L (reference range, 0.8–1.5 mmol/L). Further testing showed an elevated parathyroid hormone (PTH) level of 122 pmol/L and normal serum 25-hydroxycholecalciferol. She remained otherwise asymptomatic. The biochemical findings were consistent with a diagnosis of PHPT, and she was referred to endocrinology.

Subsequent imaging—including ultrasonography of the neck and a technetium-99m sestamibi scan—identified a solitary parathyroid adenoma. She underwent elective parathyroidectomy, which was completed without complication. Post-operative blood tests confirmed normalisation of her serum calcium and PTH levels.

Eight months after the initial surgery, the patient reported pain and skin irritation over the anterior right knee. Examination revealed localised ulceration over the site of the tension band wiring, suggesting hardware-related irritation. She was referred again to orthopaedics and underwent removal of the tension band and metal hardware (Figure 1D).

The patient made a good recovery following the second procedure. She resumed physiotherapy and continued to be reviewed by her GP, endocrinologist, and orthopaedic team (Table 1). Follow-up blood tests showed persistently normal calcium and PTH levels, confirming successful resolution of her PHPT.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

This case presents an unusual instance of a displaced patellar stress fracture as the first clinical manifestation of previously undiagnosed PHPT. The patient, a physically active 45-year-old woman, developed a stress fracture without preceding trauma, and routine post-operative follow-up in primary care revealed hypercalcaemia, ultimately leading to the diagnosis of PHPT caused by a solitary parathyroid adenoma. This case highlights the importance of considering systemic causes such as PHPT in patients with atypical or unexplained fracture presentations.

Strengths and limitations

A key strength of this case is the clear diagnostic trajectory, in which initial musculoskeletal symptoms led to multidisciplinary involvement and ultimately identification of a significant endocrine disorder. The involvement of general practice, orthopaedics, and endocrinology facilitated timely diagnosis and definitive treatment. The case adds to limited literature on the presentation of PHPT through patellar stress fractures.

However, limitations include its single-patient nature, limiting generalisability. The absence of formal bone mineral density assessment is a gap, although the pattern of fracture and biochemical profile were strongly suggestive of metabolic bone disease. Although the patient had recently increased her training volume, the location, nature, and progression of the fracture—together with significantly elevated calcium and PTH levels—suggest that mechanical factors alone were insufficient to cause the injury. This interpretation is consistent with data showing that PHPT increases the risk of insufficiency fractures even in the absence of major external forces (3,4).

However, bone mineral density assessment using dual-energy X-ray absorptiometry (DXA) was not undertaken. According to UK guidance, including the National Institute for Health and Care Excellence (NICE) guideline NG132 (7), DXA scanning is recommended to evaluate fracture risk in patients with confirmed PHPT. In this case, the patient had symptomatic hypercalcaemia and a fragility fracture, making her a clear surgical candidate irrespective of DXA results. Nevertheless, the omission of bone mineral density (BMD) data limits the assessment of cortical bone involvement and baseline skeletal status.

Comparison with similar research

Stress fractures most commonly affect the tibia, femur, and metatarsals, particularly in athletes or individuals undergoing repetitive mechanical loading (1,2). Patellar stress fractures are uncommon and rarely reported. They are more likely to occur as transverse fractures, particularly in the context of predisposing factors. Structural causes include patellar maltracking, previous surgery, or anatomical variations in patellofemoral alignment. Systemic contributors may involve metabolic bone disorders such as osteoporosis, vitamin D deficiency, renal osteodystrophy, or PHPT (1,3,4).

PHPT is a recognised risk factor for fragility and pathological fractures due to its effects on bone resorption, especially in cortical-rich sites (3,4). While vertebral, radial, and femoral fractures are well documented in PHPT, patellar involvement remains exceptionally rare. Liu et al. reported that pathological fractures related to PHPT were more likely to involve the limbs but did not highlight the patella as a frequent site (5). Similarly, a large Danish cohort study found increased fracture probability in patients with PHPT, especially for forearm and vertebral sites, but patellar fractures were not specifically described (6).

Stress fractures are typically caused by repetitive mechanical loading that exceeds the bone’s ability to remodel. These ‘typical’ stress fractures are usually seen in the tibia, metatarsals, or femoral necks of otherwise healthy individuals with identifiable risk factors such as abrupt increases in activity. However, a subset of stress fractures arises from compromised bone quality due to systemic pathology. PHPT contributes to this through cortical bone resorption, predisposing to insufficiency-type stress fractures. Distinguishing between fatigue and insufficiency fractures is crucial, particularly when the site is unusual or the clinical context suggests additional risk.

It is important to note that while the fracture occurred following a period of incremental physical activity, the identification of markedly elevated serum calcium and PTH levels, along with the presence of a solitary parathyroid adenoma, strongly supports a contributory role of PHPT. In premenopausal women, PHPT is less frequently diagnosed, with most cases in Western countries occurring after the age of 50 years and often detected incidentally (8). The asymptomatic nature of PHPT in younger women may delay diagnosis, making pathological fractures a possible first clinical manifestation.

Explanations of findings

In PHPT, elevated levels of parathyroid hormone increase osteoclastic activity, leading to cortical bone resorption and reduced bone strength (3,4). The patella is composed largely of cortical bone and is subject to significant tensile and compressive forces during weight-bearing activities such as walking, running, or climbing stairs. In the presence of PHPT, this mechanical stress may exceed the weakened bone’s threshold, resulting in a stress fracture.

The patient’s recent increase in long-distance walking likely contributed to the localised mechanical load, unmasking the underlying metabolic fragility. The transverse nature and displacement of the fracture suggest a chronic, fatigue-related process that progressed to structural failure. Her unremarkable clinical examination at initial presentation reflects the subtlety with which stress fractures may evolve and the importance of re-evaluation when symptoms persist.

The delayed but ultimately successful identification of PHPT was enabled by routine blood testing during post-operative follow-up in general practice. Without such testing, the underlying endocrine disorder may have remained undetected, risking further skeletal complications (Table 2).

Implications and actions needed

This case reinforces the importance of considering systemic causes such as PHPT in the evaluation of unexplained or atypical stress fractures, particularly in non-weight-bearing bones or in the absence of significant trauma. GPs should consider serum calcium and PTH testing when evaluating patients with stress fractures at uncommon sites, especially in the presence of additional risk factors or biochemical abnormalities.

While most stress fractures do not require metabolic work-up, we suggest considering targeted investigations in the following scenarios: stress fractures at uncommon anatomical sites (e.g., patella, sacrum), absence of clear extrinsic overload, or presence of red flags such as multiple fractures, abnormal biochemistry, or delayed healing. Beyond PHPT, other systemic causes of stress fractures include hypogonadism, nutritional deficiencies, celiac disease, prolonged glucocorticoid therapy, and renal osteodystrophy.

Additionally, this case illustrates the value of multidisciplinary coordination. Early collaboration between primary care, orthopaedics, and endocrinology was essential in diagnosing the fracture, identifying the underlying pathology, and delivering curative treatment.

Guidelines for the management of stress fractures may benefit from incorporating prompts to evaluate for endocrine and metabolic contributors, particularly when fractures occur outside the usual anatomical distribution or in patients without obvious extrinsic risk factors.

Conclusions

This case underscores the necessity of considering endocrine disorders, particularly PHPT, when encountering atypical stress fractures such as patellar fractures. It demonstrates the critical role of routine primary care follow-up and multidisciplinary collaboration in diagnosing and managing underlying systemic diseases. Incorporating endocrine screening in unusual fracture presentations can significantly improve patient outcomes and prevent further complications.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-104/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-104/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-104/coif). W.J. serves as an unpaid editorial board member of AME Case Reports from July 2024 to June 2026. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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