Osteitis Pubis

Etiology

Osteitis pubis has an incomplete understanding of the exact cause of the condition. However, it is commonly believed to result from overuse stress injury of the pubic symphysis.[1][2][3][4][5] The pubic symphysis is a fulcrum for muscles inserting and originating from the anterior pelvis, such as the rectus abdominis and adductor muscle complex, which are antagonistic.[2][4][5] Repetitive use causing microtrauma or injury of anterior pelvic musculature results in muscle imbalance between the 2. This imbalance disrupts the force distribution across the pubic symphysis, altering the joint’s biomechanics. The altered biomechanics of the joint result in stress injury to the pubic bone and eventual cartilage degeneration. Altered hip biomechanics, such as those seen with FAI, may also lead to osteitis pubis, although its relationship is less delineated.[6][7][8] Other less commonly cited reasons for the development of osteitis pubis are rheumatologic disorders, prior urologic and gynecologic procedures, or pregnancy.[9][10]

Epidemiology

To date, no epidemiological study has determined the true incidence of osteitis pubis. The incidence of injuries in athletes has been reported as 0.5% to 8%, with a higher incidence in distance runners and athletes in kicking sports, particularly male soccer players, who account for 10% to 18% of injuries per year.[1][5] However, it is commonly accepted to be of higher incidence in previously mentioned athletic activities. In 1 study of 189 athletes experiencing groin pain, osteitis pubis was the primary cause in 14%.[4][5] In an MRI study of 97 athletes with groin pain, isolated osteitis pubis was found in 9.3% of subjects, and osteitis pubis with associated adductor microtear was found in 42.3% of patients.[5] Classically, osteitis pubis is more common in men than women. Previous studies found it to be 2 to 5 times more common in men. However, this discrepancy is believed to decrease as women's athletic participation has increased.[4]

More recently, the relationship between FAI and athletic pubalgia has been interesting. Eighty-six percent of those diagnosed with osteitis pubis undergoing operative intervention had FAI on radiographs.[11] In an MRI study of nonathletic subjects, those with FAI were 13.89 times more likely to have osteitis pubis.[6] This result is also supported by Verrall et al, who found that those with a decreased hip range of motion had a higher incidence of pubic bone stress injury than those with a normal hip range of motion.[12] Saito et al demonstrated that approximately 68% of soccer players with symptomatic FAI had radiographic evidence of osteitis pubis.[13] Finally, Larson et al demonstrated that those with increasing cam hip deformity showed a statistically higher prevalence of osteitis pubis symptoms.[14] Regarding urological procedures resulting in osteitis pubis, the Marachall-Marchetti-Kranz (MMK) urethropexy has an incidence of 2.5% in the literature review. It occurs in less than 1% of those undergoing urologic procedures.[9]

Pathophysiology

The pubic symphysis is a non-synovial amphiarthrodial joint with an interposed fibrocartilaginous disc separating hyaline cartilage. The joint normally has minimal motion due to the static ligamentous complex. The pubic symphysis serves as the insertion point of the rectus abdominis and the origin of the adductor complex. The antagonistic nature of the rectus abdominis, which elevates the pubic symphysis while the adductors depress the joint, serves as a nidus for the development of osteitis pubis—the repetitive use of the anterior pelvic musculature results in chronic tendinosis. The chronic muscle imbalance results in abnormal forces across the pubic symphysis, causing symphyseal instability, pubic bone stress reaction, and eventually degeneration of the hyaline cartilage. Another emerging theory poses that osteitis pubis develops secondary to increased compensatory motion across the joint because of limited motion elsewhere in the kinetic chain, such as in FAI.[12][13][8][14] Birmingham et al found increased rotational motion at pubic symphysis when cam-type FAI was mimicked in cadaveric pelvis specimens.[8] Also, in intimate contact with the pubic symphysis periosteum in the inguinal ligament, which is an important suture for the inguinal canal. Urological procedures may result in injury to the inguinal ligament; in the case of MMK procedure, sutures through the pubic bone may result in chronic irritation. Finally, osteitis pubis can result from direct trauma to the pubic symphysis.

Histopathology

The few histological studies regarding osteitis pubis come from bone and cartilage samples taken during surgical procedures on athletes with osteitis pubis. Verrall et al performed a study in which they took samples of pubic rami from Australian rugby players with pubic bone stress injuries. Surprisingly, the samples revealed a lack of inflammatory cells or signs of osteonecrosis. However, the samples did demonstrate woven immature bone with neovascularization, osteoblasts, and fibroblasts consistent with a bony stress response.[15] In a second histology study by Radic and Annear, cartilage samples obtained from 15 athletes demonstrated degenerative cartilage void of inflammatory cells. The lack of inflammatory cells in both studies contradicts the notion that osteitis pubis is primarily a disease of inflammation. As noted by Hitti et al, the idea that osteitis pubis is an inflammatory disease stemmed from the published study by Coventry and Mitchell in 1961.[5] Coventry et al found evidence of marrow fibrosis, vascular areas, and thin layers of new bone.[16] However, their subject population was not athletes but those with prior pelvic surgery and infection. Thus, this lends itself to osteitis pubis, which may result from differing etiologies causing differing histology, which can be elicited from the patient's history and presentation.

History and Physical

Patients, particularly athletes with osteitis pubis, often have concomitant pathology, making the diagnosis difficult. The entire lower extremity kinetic chain can be involved, requiring evaluation of the sacroiliac joint, hip labrum, FAI, adductors, and abdominal muscles. Pathology at any of these locations can result in osteitis pubis for the abovementioned reasons.[17] Patients with osteitis pubis often present with anterior and medial groin pain. Pertinent history information includes athletic participation, symptoms' chronicity, and aggravating movements. Surgical or procedural history should be obtained if the patient is a non-athlete. The onset of pain is usually gradual and can be debilitating, especially to the athlete. Commonly, patients state pain is elicited with rapid hip flexion from an extended position, such as with kicking or hurdles, adductor stretching, abdominal muscle strengthening exercises, or movement from a seated to standing position.[18]

The physical exam can be difficult for osteitis pubis as it overlaps with athletic pubalgia or sports hernia. However, according to Lynch et al, the 2 can be differentiated with pain elicited by direct palpation over the pubic symphysis with OP. Another exam maneuver, the spring test, where direct pressure is applied just lateral to the pubic symphysis on the ramus, evokes pain.[2] Verrall et al proposed 3 provocation tests: single adductor, squeeze, and bilateral adductor tests. If tests were positive, they highly correlated with pubic bone marrow edema on MRI. Patients may also exhibit a waddling gait due to pain and a sensation of tightness in the adductor muscles.[10] Due to osteitis pubis’s common association with FAI, the hip joint must be evaluated. Patients with limited flexion, extension, or internal and external hip rotation should undergo evaluation. Patients presenting with either sacroiliac pathology or FAI may have pain with the FABER test, which is flexion, abduction, and external hip rotation.[2][17]

Evaluation

Both radiographs and MRI aid in the diagnosis of osteitis pubis. In the early stage, plain radiographs might appear normal.[9][19] In chronic osteitis pubis, the pubic symphysis demonstrates lytic changes, sclerosis, and widening.[2][20][4][5] Dynamic instability of the pubic symphysis can be observed in the flamingo view. The flamingo view is obtained by double- and single-legged stance positions bilaterally on a pelvic anterior-posterior radiograph. Greater than 2 mm of subluxation is a positive finding for symphyseal instability.[1][19] MRI has become the imaging modality of choice.[5] In the acute setting, MRI demonstrates subchondral bone edema, typically with bilateral involvement.[6][2][4][5] In chronic cases, MRI findings are similar to plain radiographs demonstrating periosteal reaction, bone resorption, the irregular contour of the articular surface, osteophytes, and subchondral cyst formation.[6][19] MRI is highly sensitive for distinguishing between chronic and acute cases (Krishnamoorthy et al). Pubic symphyseal bone marrow edema can also be found in asymptomatic patients.[5] More symptomatic patients have found a linear subchondral T2 signal paralleling the pubis.[5]

In patients diagnosed with cam-type FAI with symptoms greater than 3 months, Akgun et al demonstrated a 45.56% prevalence of osteitis pubis on MRI findings compared to 5.86% in control subjects.[6] Philips et al also support this result. Those with FAI had a prevalence of osteitis pubis at 43.48% and only 12.8% in the control group.[7] However, Krishnamoorthy et al found a low prevalence (2.3%) of symphyseal changes on MRI in patients with FAI. However, when the subjects were matched for age and BMI, the findings of symphyseal changes did have clinical significance.[21] Findings on MRI also correlate with clinical outcomes in osteitis pubis patients. Patients with edema in the pubic bone and surrounding musculature had a much lower percentage of complete recovery. Meanwhile, those who had edema confined to just the bone had a much higher percentage chance of complete recovery at 18 months.[22] Finally, MRI is usually used to diagnose concomitant injuries that can contribute to osteitis pubis, such as adductor tears, FAI, rectus femoris tears, and labral tears.[1][2][13][21] Patients with FAI treated with hip arthroscopy who also had symphyseal changes, such as bone marrow edema, on MRI had inferior surgical outcomes when compared to those who do not have such changes.[21]

Treatment / Management

The management of osteitis pubis includes both conservative and surgical options. The first option remains conservative treatment.[2][18][23] Conservative management includes rest, NSAIDs, and a progressive course of physical therapy. There is no standard conservative treatment protocol, which results in various outcomes.[5] The conservative treatment of osteitis pubis can be protracted. It may take some athletes 6 months or more to return to the preinjury level, but most commonly return in 3 months.[1][23] Albeit protracted, conservative management remains the mainstay of treatment.[18][23] Only approximately 5% to 10% of athletes require surgical treatment.[2]  Steroid injections have been demonstrated as a useful adjunctive therapy.[2][24][25][26] However, their role remains controversial.[24][18][23] Two case series have demonstrated successful treatment with prolotherapy.[27][28] Even though none of the injection studies were experimental in design, all reported positive outcomes. However, the areas injected, the amount injected, the time to return to play, the number of injections, and persistent symptoms were highly variable.[24][5][23](A1)

If conservative management does fail, surgical intervention may be required. The timeframe for considering conservative treatment as a failure ranges and no set timetable has been established.[1] Commonly, a minimum of 6 months of conservative treatment is attempted before surgical options are discussed.[29] Surgical options include curettage of symphyseal fibrocartilage, symphyseal fusion, wedge resection of the symphysis with or without arthrodesis, and an array of procedures to reinforce or repair abdominal or pelvic floor musculature.[5][23] Williams et al performed arthrodesis with a compression plate and bone graft in 7 rugby players. All could return to sport and were symptom-free at a 52-month follow-up.[29] More recently, endoscopic techniques have been successfully demonstrated in case reports.[30][31] Surgical indications are not well defined as some surgeons consider osteitis pubis an isolated condition, while others attribute it to a constellation of other entities.[2][5] Also, there have been no significant differences between surgical outcomes and the differing procedures.[1][30][31] Athletes can return to unrestricted activity at approximately 6 months.[24][4](A1)

Those with symptomatic FAI and osteitis pubis may see relief when FAI is treated, supporting the notion that osteitis pubis results from altered joint motion elsewhere in the pelvis.[1] Thirty-nine percent of patients diagnosed with both conditions had complete resolution of osteitis pubis when FAI was treated alone.[1] Results from Saito et al also support this finding, where arthroscopic surgery for FAI alone resulted in a high rate of return to sports and resolution of bone marrow edema among soccer players.[13]

Differential Diagnosis

The differential diagnosis for osteitis pubis includes the following:

• Athletic pubalgia
• Osteomyelitis
• Adductor strain
• Rectus Abdominus strain

Prognosis

The prognosis of those with osteitis pubis is very good. Those treated conservatively return to sports in approximately 3 months with a low chance of recurrence.[1] Only 5% to 10% of patients with osteitis pubis require surgery. Surgical outcomes are also very favorable, with an overwhelming return to sport at approximately 3 to 4 months.[1]

Complications

Surgical treatment of osteitis pubis can result in:

• Chronic pain
• Infection
• Nonunion of fusion
• Recurrence
• Haemospremia
• Scrotal or labial swelling