Updated: Jul 28, 2009
Since 1924, osteitis pubis has been known as a noninfectious inflammation of the pubis symphysis (also known as the pubic symphysis, symphysis pubis, or symphysis pubica) causing varying degrees of lower abdominal and pelvic pain. Osteitis pubis was first described in patients who had undergone suprapubic surgery and remains a well-known complication of invasive procedures about the pelvis. However, it may occur as an inflammatory process in athletes. The incidence and etiology of osteitis pubis as an inflammatory process versus an infectious process continues to fuel debate among physicians when confronted by a patient who presents complaining of abdominal pain or pelvic pain and overlapping symptoms. (See image below and Image 1.)
Osteitis pubis is thought to result from inflammation of the pubis symphysis and is characterized by sclerosis and bony changes of the pubis symphysis.1 (See image below and Image 2.)
No available statistics are found in the literature for this condition.
No available international data exist; however, osteitis pubis may be more common in Europe due to the popularity of kicking sports such as soccer.
While rare instances of mortality have been reported in the obstetric literature from femoral artery involvement, morbidity is observed more commonly secondary to pain and difficulty with ambulation.
The literature suggests that osteitis pubis is more prevalent in men. However, as women continue to lead more active lifestyles, and become more involved in sports such as soccer, the incidence and prevalence of the condition may change.
Although osteitis pubis can affect all age groups, it is rarely encountered in the pediatric population. The disorder occurs most commonly in men aged 30-50 years. Women are more frequently affected in their mid-30s.
Adductor Strain
Osteomyelitis of the pubis symphysis
Ischial intersection syndrome
Snapping hip syndrome
Stress fracture
Groin strain
Pelvic and hip fracture
Muscle contusions
Tendon injuries
Acetabular labral tears
Bursitis
Chronic symphyseal injury
Rest and time are the primary healing mechanisms. Physical therapy (PT) may be useful during the early stage. Modalities, such as heat or ice, may provide symptomatic relief. Progressive ambulation with the aid of an assistive device (eg, cane, crutches) and possible orthoses (eg, lumbar/sacral corset, sacroiliac belt) to unload the pelvis for pain relief and to maintain correct anatomical alignment may be necessary.5
Avoidance of any therapeutic exercise that may place stress on the pelvic ring is prudent. A home exercise program that includes pelvic tilts may be prescribed. Experienced therapists may attempt dynamic stabilization techniques.
Different surgical approaches have been described, including curettage, arthrodesis, wedge resection, and wide resection.5,6 A report by Radic and Annear suggested that curettage is an effective treatment for athletes with osteitis pubis in whom nonoperative therapy has been unsuccessful.7 The investigators found that 21 of the study's 23 athletes were able to run without pain one and a half to 6 months following curettage of the pubis symphysis, while 17 of them returned to training two and half to 7 months after the procedure, and 16 of the athletes resumed full activity two and a half to 12 months after curettage.
Wedge resection of the pubis symphysis is another technique that can be performed on patients in whom conservative management has failed; however, the natural progression of osteitis pubis may require months, and in some cases years, to improve. Surgical intervention is associated with early improvement of symptoms but may lead to later posterior pelvic instability. This instability may then require a second surgical procedure for stabilization.
Nonsteroidal anti-inflammatory agents (NSAIDs) are the DOCs for treatment of osteitis pubis. Narcotics also are employed for pain control in some cases, usually in the obstetric or postsurgical patient. Limited case reports suggest that use of antibiotics and heparin also has been successful.
Most commonly used for relief of mild to moderate pain. Although ibuprofen is the DOC for initial therapy, other options include, but are not limited to, ketoprofen and naproxen.
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
200-400 mg PO q4-6h; some patients may require doses as large as 800 mg PO q8h; not to exceed 3.2 g/d
<12 Months: Not established
12 months to 12 years: 10 mg/kg q6-8h; not to exceed 40 mg/kg/d
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; renal insufficiency; peptic ulcer disease; recent GI bleeding; high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Pregnancy category D in third trimester; caution in congestive heart failure; renal and hepatic dysfunction; hypertension; anticoagulation therapy (monitor levels)
For relief of mild to moderate pain and inflammation.
Small dosages initially are indicated in small and elderly patients and in those with renal or liver disease. Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Pregnancy category D in third trimester; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.
500 mg PO, followed by 250 mg q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Pregnancy category D in third trimester; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.
Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.
200 mg/d PO qd; alternatively, 100 mg PO bid
Not established
Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Pregnancy category D in third trimester; may cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention; severe heart failure and hyponatremia, because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction, or in abnormal liver lab results
Robertson BA, Barker PJ, Fahrer M, et al. The anatomy of the pubic region revisited: implications for the pathogenesis and clinical management of chronic groin pain in athletes. Sports Med. 2009;39(3):225-34. [Medline].
Zoga AC, Kavanagh EC, Omar IM, et al. Athletic pubalgia and the "sports hernia": MR imaging findings. Radiology. Jun 2008;247(3):797-807. [Medline]. [Full Text].
Paajanen H, Hermunen H, Karonen J. Pubic magnetic resonance imaging findings in surgically and conservatively treated athletes with osteitis pubis compared to asymptomatic athletes during heavy training. Am J Sports Med. Jan 2008;36(1):117-21. [Medline].
Lovell G, Galloway H, Hopkins W, et al. Osteitis pubis and assessment of bone marrow edema at the pubic symphysis with MRI in an elite junior male soccer squad. Clin J Sport Med. Mar 2006;16(2):117-22. [Medline].
Choi H, McCartney M, Best TM. Treatment of osteitis pubis and osteomyelitis of the pubic symphysis in athletes: a systematic review. Br J Sports Med. Sep 30 2008;[Medline].
Mehin R, Meek R, O'Brien P, et al. Surgery for osteitis pubis. Can J Surg. Jun 2006;49(3):170-6. [Medline]. [Full Text].
Radic R, Annear P. Use of pubic symphysis curettage for treatment-resistant osteitis pubis in athletes. Am J Sports Med. Jan 2008;36(1):122-8. [Medline].
Andrews SK, Carek PJ. Osteitis pubis: a diagnosis for the family physician. J Am Board Fam Pract. Jul-Aug 1998;11(4):291-5. [Medline].
DiStefano VJ, Nixon JE. Osteitis pubis--a case of housemaid''s pubis?. Pa Med. Jan 1972;75(1):51-2. [Medline].
Fon LJ, Spence RA. Sportsman''s hernia. Br J Surg. May 2000;87(5):545-52. [Medline].
Fricker PA, Taunton JE, Ammann W. Osteitis pubis in athletes. Infection, inflammation or injury?. Sports Med. Oct 1991;12(4):266-79. [Medline].
Harris NH, Murray RO. Lesions of the symphysis in athletes. Br Med J. Oct 26 1974;4(5938):211-4. [Medline].
Holmgren G. The treatment of osteitis pubis with anticoagulants. A report of three cases in Africans. Cent Afr J Med. Jan 1972;18(1):10-2. [Medline].
Michiels E, Knockaert DC, Vanneste SB. Infectious osteitis pubis. Neth J Med. Jun 1990;36(5-6):297-300.
Moore RS, Stover MD, Matta JM. Late posterior instability of the pelvis after resection of the symphysis pubis for the treatment of osteitis pubis. A report of two cases. J Bone Joint Surg Am. Jul 1998;80(7):1043-8. [Medline].
Pizzarello LD, Golden GT, Shaw A. Acute abdominal pain caused by osteitis pubis. Am Surg. Nov 1974;40(11):660-1. [Medline].
Vincent C. Osteitis pubis [published erratum appears in J Am Board Fam Pract 1993 Nov-Dec;6(6):616]. J Am Board Fam Pract. Sep-Oct 1993;6(5):492-6. [Medline].
Wiley JJ. Traumatic osteitis pubis: the gracilis syndrome. Am J Sports Med. Sep-Oct 1983;11(5):360-63. [Medline].
osteitis pubis, pelvic pain, groin pain, pubis, osteitis, symphysis, pubic symphysis, pubis symphysis, symphysis pubis, symphysis pubica, symphysis dysfunction, pubis dysfunction, symphyseal separation, pubis diathesis, gracilis syndrome
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Guy W Fried, MD, Assistant Professor, Department of Rehabilitation Medicine, Thomas Jefferson University; Outpatient Medical Director, Medical Director of Incontinence and Respiratory Care Programs, Magee Rehabilitation Hospital
Guy W Fried, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Everett C Hills, MD, MS, Medical Director, Penn State Hershey Rehabilitation Hospital, Assistant Professor of Orthopaedics and Rehabilitation, Assistant Professor of Neurology, Penn State Milton S. Hershey Medical Center and Penn State University College of Medicine
Everett C Hills, MD, MS is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Congress of Rehabilitation Medicine, American Medical Association, American Society of Neurorehabilitation, Association of Academic Physiatrists, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Michael T Andary, MD, MS, Residency Program Director, Professor, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine
Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists
Disclosure: allergan Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.