Non-Ossifying Fibroma

                                  Dr. KS Dhillon

Introduction

Non-ossifying fibroma (NOF) and fibrous cortical defect (FCD) are common bone lesions. They are usually found in skeletally immature patients under the age of 15 years (1). They are generally asymptomatic. They are typically discovered incidentally. They are the most common lesions that are referred to orthopedic oncology clinics (2). Their radiographic features are usually very characteristic. If these lesions are detected incidentally a biopsy is not required.

The two lesions have different imaging characteristics. FCDs are small lesions primarily located in the bone cortex, larger NOFs are on the other hand located eccentrically in the medullary cavity (1,3,4). NOFs are large and usually symptomatic. FCDs are small and usually asymptomatic (3).

FCD and NOF are present in up to 30% of children during their skeletal growth period (1,5). However, it is difficult to draw definitive prevalence

rates. Larger lesions can cause pain (1). The association between lesion size and pain is not well known.

Non‑ossifying fibromas and fibrous cortical defects

NOFs and FCDs are benign, well-circumscribed radiolucent lesions that are present in the metaphyseal portions of long bones. The lesions are usually located in the distal femur, proximal and distal tibia, and proximal humerus (3). Usually, the diagnosis can be made from characteristic radiographic findings (6). NOF can diagnosed if there is an oval, rounded or polycyclic, sharply marginated, intramedullary radiolucency in the metaphyseal portion of the distal femur or proximal tibia, with or without a rim of sclerotic bone.

FCD can be diagnosed if there is an oval or rounded, sharply marginated,  eccentric radiolucent zone in the medial metaphyseal cortex of the distal

femur.

The prevalence of NOF increases and that of FCD decreases with advancing age. About half of the patients with FCD complain of spontaneous pain. The lesion size and spontaneous pain, however, may not be associated.

NOF and FCD are metaphyseal fibrous defects. They have been considered to be synonymous because of similar pathologic findings, although they differ in size and primary locations in the long bones (4,9). NOF lesions are principally metaphyseal in location. The most common sites include the distal femur, proximal tibia, distal tibia, proximal humerus, fibula, and radius (3). About less than 5% of NOFs are multifocal. Most multifocal NOFs often develop sporadically. They also develop in patients with neurofibromatosis type 1 and Jafe-Campanacci syndrome (1).

More recently, NOF has been considered to be a neoplasm because of

Ras-MAPK activation by somatic mutation (10). Hence, these two lesions are different entities because of their differing clinical and biological characteristics. FCD maintains the same position (11), while NOF advances proximally or distally with age. FCD most likely occurs when tendons are inserted into the perichondrium of the epiphyseal plate (7,11,12). There is a male predominance (6,7,12). It has been estimated that NOF may be present in up to 30% of children (1,5). This prevalence may not be accurate because previous studies were retrospectively case series. Sontag and Pyle (11) examined the skeletal roentgenograms of healthy children until the age of 18 years. They found cystic lesions (consistent with FCD) in 22% of the girls and 53% of the boys. No similar research has been conducted on NOF. No ethnic prevalence has been described (3). The Ritschl classification of NOF is based on the clinical course of the healing process. According to Ritschl's classification stage A is the

most common (6).

FCD and NOF differ in terms of size and clinical course. These two lesions usually disappear with advancing age. NOFs are large and typically symptomatic, while FCDs are generally small and asymptomatic (3). 

Pathologic fractures occur in up to 20% of NOFs (13). Fractures are likely to occur in NOFs that are more than 33 mm long (9). It is, however, unclear whether the lesion size is associated with the occurrence of fracture (14). 

Absolute size parameters may be useful in predicting pathologic fracture rates. They however do not imply a requirement for prophylactic curettage and bone grafting. Patients with a stage B lesion have an increased risk of pathologic fractures (6). Thus, combining lesion size and Ritschl classification may be important for evaluating and predicting pathologic fracture.

Conclusion

Non-ossifying fibroma (NOF) and fibrous cortical defect (FCD) are common bone lesions. They are usually found in skeletally immature patients under the age of 15 years. They are often discovered incidentally. FCD and NOF are present in up to 30% of children during their skeletal growth period. These two lesions usually disappear with advancing age. NOFs are large and typically symptomatic, while FCDs are generally small and asymptomatic (3). Pathologic fractures occur in up to 20% of NOFs. Prophylactic curettage and bone grafting is not required.

References

1. Baumhoer D, Rogozhin DV. Non-ossifying fibroma. In: WHO Classification of Tumours of Soft Tissue and Bone. 5th ed. Lyon: IARC Press; 2020. P.447–8.

2. Stacy GS, Dixon LB. Pitfalls in MR image interpretation prompting referrals to an orthopedic oncology clinic. Radiographics. 2007;27(3):805–26.

3. Mankin HJ, Trahan CA, Fondren G, Mankin CJ. Non-ossifying fibroma, fibrous cortical defect, and Jafe-Campanacci syndrome: a biologic and clinical review. Chir Organi Mov. 2009;93(1):1–7.

4. Betsy M, Kupersmith LM, Springfield DS. Metaphyseal fibrous defects. J Am Acad Orthop Surg. 2004;12(2):89–95.

5. Mallet JF, Rigault P, Padovani JP, Touzet P, Nezelof C. Non-ossifying fibroma in children: a surgical condition? Chir Pediatr. 1980;21(3):179–89.

6. Herget GW, Mauer D, Krauß T, El Tayeh A, Uhl M, Südkamp NP, Hauschild O. Non-ossifying fibroma: natural history with an emphasis on a stage-related growth, fracture risk and the need for follow-up. BMC Musculoskelet Disord. 2016;17:147.

7. Ritschl P, Karnel F, Hajek P. Fibrous metaphyseal defects–determination of their origin and natural history using a radiomorphological study. Skeletal Radiol. 1988;17(1):8–15.

8. Cafey J. On fibrous defects in cortical walls of growing tubular bones: their radiologic appearance, structure, prevalence, natural course, and diagnostic significance. Adv Pediatr. 1955;7:13–51.

9. Arata MA, Peterson HA, Dahlin DC. Pathological fractures through nonossifying fibromas. Review of the Mayo Clinic experience. J Bone Joint Surg Am. 1981;63(6):980–8.

10. Baumhoer D, Kovac M, Sperveslage J, Ameline B, Strobl AC, Krause A, Trautmann M, Wardelmann E, Nathrath M, Höller S, et al. Activating mutations in the MAP-kinase pathway define non-ossifying fibroma of bone. J Pathol. 2019;248(1):116–22.

11. Sontag LW, Pyle SI. The Appearance and nature of cyst-like areas in the distal femoral metaphyses of children. Am J Roentgenol. 1941;46:185–8.

12. Goldin A, Muzykewicz DA, Dwek J, Mubarak SJ. The aetiology of the non-ossifying fibroma of the distal femur and its relationship to the surrounding soft tissues. J Child Orthop. 2017;11(5):373–9.

13. Mulder JD, Schutte HE, Kroon HM, Taconis WK. Fibrous cortical defect and non-ossifying fibroma. In: Radiologic Atlas of Bone Tumors. Amsterdam: Elsevier; 1993. p. 627–38.

14. Easley ME, Kneisl JS. Pathologic fractures through nonossifying fibromas: is prophylactic treatment warranted? J Pediatr Orthop. 1997;17(6):808–13.

        Patellar Tendon Rupture

                                  Dr. KS Dhillon

Introduction

The patellar tendon is a ligament that connects two bones, the patella and the tibia. A patellar tendon rupture involves a complete tear of the tendon between the patella's inferior pole and the tibial tubercle. Such raptures are usually seen in males in their third or fourth decade. These ruptures result from an overall weakened tendon placed under high tensile forces. These ruptures are classified into acute and chronic tears, depending on the time from rupture. Since the patellar tendon is a part of the extensor mechanism such injuries require prompt diagnosis and surgical repair. For function of the lower extremity, including ambulation, the extensor mechanism of the knee is crucial. It is responsible for extending and straightening the knee and resisting knee flexion which is crucial for standing with a flexed knee and ambulation (1). Without a properly functioning knee extensor mechanism, the patient is severely limited functionally (2). Surgical intervention depends on the location of the rupture and timing. Acute ruptures can be treated by primary repair. Chronic ruptures often require reconstruction of the tendon.

Anatomy

The knee extensor mechanism consists of the quadriceps muscle, quadriceps tendon, medial and lateral patellar retinaculum, patella, patellar tendon, and the tibial tubercle (3). The quadriceps muscle consists of 4 separate muscles with different origins but a common insertion point on the patella.

The four quadriceps muscles with different origins include (3):

1. Rectus femoris – anterior superior iliac spine and superior acetabular rim

2. Vastus lateralis – greater trochanter and lateral linea aspera

3. Vastus intermedius – proximal femoral shaft

4. Vastus medialis – intertrochanteric line and medial linea aspera

The lateral and medial patellar retinaculum are on the sides of the patella and are continuous with the vastus fascia to the tibia and the patella (3). They are minor patellar stabilizers. If intact they can provide knee extension and straight leg raising despite a patellar or quadriceps tendon rupture. The patella is the largest sesamoid bone in the body. It is embedded in the quadriceps tendon. It increases the moment arm from the knee joint axis and increases the mechanical advantage and quadriceps pull-in extension. The patella begins to engage the trochlea of the femur at 20 degrees of knee flexion and is fully engaged at 40 degrees. Joint reaction forces in the patellofemoral joint can be up to 3 times the body weight with stair climbing. It can be 7 times the body weight with deep bending (4). The patellar tendon, by definition, is a ligament since it connects bone (patella) to bone (tibial tubercle). It is approximately 30 mm wide and 50 mm long. It is 5 to 7 mm in thickness. The origin on the inferior pole of the patella is juxtaposed with the articular cartilage on the deep side. It becomes confluent with the periosteum of the patella anteriorly. The tibial insertion is narrower and it covers the entire tibial tubercle. It connects the quadriceps muscles to the leg.

Etiology

Chronic inflammation leads to patellar tendonitis. The inflammation weakens the tendon which increases the likelihood of tendon rupture. Certain medical conditions can weaken the tendon and predispose an individual to tendon rupture.

These risk factors include:

Systemic lupus erythematosus

Rheumatoid arthritis

Chronic corticosteroid use

Chronic renal disease

Diabetes mellitus

Renal dialysis

Fluoroquinolone antibiotics

Corticosteroid injections

Patellar tendinopathy

Previous injury

Overuse injury

Patellar degeneration (2,5,6,7)

Epidemiology

The knee extensor mechanism disruption can occur at different locations within the extensor mechanism. The 3 most common areas of disruption include the patella tendon, the quadriceps tendon, and the patellar (8). Patella fractures are twice as common as tendon ruptures (9). Quadriceps tendon rupture is more common than patellar tendon ruptures, especially in individuals over the age of 40 years (10). In the USA, quadriceps tendon ruptures affect 1.3% of the population every year, whereas patellar tendon ruptures tend to affect less than 0.5% of the population per year. Males are more often affected than females. 

Pathophysiology

Tensile overload on the extensor mechanism causes patella tendon ruptures. There are numerous risk factors for patella tendinopathy such as sex, hours of training, hamstring flexibility, previous patellar tendon rupture, previous knee injury, current/previous back pain, family history, and age (11). Patella tendinopathy predisposes to patella tendon ruptures. The usual circumstance for patella tendon rupture is sudden quadriceps muscle contraction. This can be seen in individuals who are running up a set of stairs, landing from a jump, or suddenly stopping to change directions when running. The greatest force on the patellar tendon is when the knee is flexed more than 60 degrees. Most patellar tendon ruptures occur when the knee is in a flexed position. Patellar tendon rupture can occur at 3 distinct locations. A proximal avulsion of the tendon, with or without bone from the inferior pole of the patella, is the most common (6). The strain at the tendon-inferior pole patella interface is 3 to 4 times higher than that at the mid-substance of the tendon. The other 2 rupture locations include the tendon's mid-substance and an avulsion of the patellar tendon from the tibial tubercle.

History and Physical

Patients with an acute patellar tendon tear present with the complaint of infrapatellar knee pain, swelling, difficulty with weight-bearing, and difficulty in straightening the leg. The patient may report a “pop” sound or a sensation of the knee giving way during an event where there is a sudden contraction of the quadriceps with the knee in a flexed position, such as with jumping sports or missing a step on the stairs. Obtaining a detailed history of the patient's symptoms is essential. The history should include the specific location of the pain, the duration of the pain and symptoms, characteristics of the pain, alleviating and aggravating factors, any radiation of pain, and the severity of the symptoms. Some patients may report pre-existing pain at the patella or patellar tendon level due to underlying tendinosis. A thorough history may reveal an underlying risk factor or predisposition to a tendon rupture (12). Opinions differ on the definition of acute versus chronic tendon rupture. Generally, however, it is thought that chronic ruptures present 6 weeks after injury. Physical examination should include an inspection of the knee and evaluation of the surrounding skin for any signs of direct trauma. Swelling or knee effusion should be looked for. A large hemarthrosis and surrounding ecchymosis are often associated with patella tendon ruptures. The patellar height should be compared with the unaffected side. A patellar tendon rupture is likely to be associated with an elevation of the patellar height compared to the uninjured side. Palpation of the bony and soft tissue structures is essential. The palpatory examination can be broken down into the knee's lateral, medial, and midline structures.

In palpatory examination, the areas of focus include:

On the medial aspect of the knee-

• Vastus medialis obliquis

• Origin of the medial collateral ligament (MCL)

• Midsubstance of the MCL

• Superomedial pole patella

• The medial facet of the patella

• Broad insertion of the MCL

• Medial joint line

• Medial meniscus

• Pes anserine tendons and bursa

At the midline of the knee-

• Quadricep tendon

• Patellar mobility

• Prepatellar bursa

• Suprapatellar pouch

• Superior pole patella

• Patellar tendon

• Tibial tubercle 

At the lateral aspect of the knee

• Lateral collateral ligament (LCL)

• Iliotibial band

• Lateral facet patella

• Lateral joint line

• Lateral meniscus

• Gerdy’s tubercle (13)

Examination of patients with a patellar tendon rupture will show a palpable defect below the inferior pole of the patella and localized tenderness about the infrapatellar aspect of the knee. Range of motion (ROM) testing and muscle strength testing are essential in the setting of a suspected patellar tendon rupture. Examination will show decreased ROM of the knee due to pain and disruption of the extensor mechanism. Active knee extension is lost. When the patellar tendon is the only portion of the extensor mechanism ruptured, and the retinaculum is intact, active extension may be possible but there will be an extensor lag of a few degrees. The patients are unable to perform active straight leg raises and are also unable to maintain a passively extended knee. It is important not to miss a diagnosis of a patellar tendon rupture or any extensor mechanism disruption because a delayed diagnosis and treatment can affect the outcome. If necessary aspiration of a painful knee effusion followed by an injection of lidocaine can be carried out to aid in clinical diagnosis. Despite adequate local anesthesia a patient with an extensor mechanism disruption cannot perform a straight leg raise. A patient with a painful effusion secondary to a different cause can perform a straight leg raise.

Evaluation

The radiographic evaluation includes anteroposterior and lateral views of the knee. When there is a complete rupture, radiographs may reveal a superiorly displaced patella (patella alta). On the lateral knee radiograph, the Insall-Salvati ratio quickly determines patella alta or baja (inferiorly displaced patella). The Insall-Salvati ratio is the ratio between the patellar tendon's length and the patella's length. The measurement is done on a lateral radiograph with the knee flexed to 30 degrees. The normal ratio is between 0.8 and 1.2. The patella alta has a ratio greater than 1.2 and the patella baja has a ratio of less than 0.8 (4).

X-rays of the knee may reveal avulsion fractures or other concomitant knee injuries. A knee MRI is the appropriate diagnostic study if a patellar tendon rupture is suspected. It can differentiate partial from complete tendon tear. It helps to determine the exact location of the rupture. It will show the presence of any tendon degeneration, the position of the patella, and any concomitant intraarticular knee lesions. Ultrasound may also be used as an adjunctive study in the suspected case of acute or chronic patellar tendon rupture. It can detect and localize the tendon disruption. It is much less expensive than an MRI. 

Management

Disability from a deficient knee extensor mechanism is high. Surgical repair of the ruptured patella tendon is necessary. Although the repair is not considered a surgical emergency, prompt surgical management of acute patella tendon rupture is needed to prevent the need for reconstruction. 

Patients with an intact knee extensor mechanism with a partial tear of the tendon can be treated without surgery. Nonsurgical management should also be considered in patients who are not surgical candidates due to medical comorbidities. Non-surgical treatment is carried out by immobilizing the knee in full extension with a progressive weight-bearing exercise program.

Surgical treatment is carried out by primary tendon repair or tendon reconstruction (8). Primary repair is carried out in patients with complete patellar tendon ruptures, where the tendon ends can be approximated (14). The location of the tear determines the type of repair carried out. When the tendon tear is mid-substance an end-to-end repair is carried out. For proximal avulsions, a transosseous tendon repair, with bone tunnels drilled through the patella can be carried out. For a distal avulsion, a suture anchor tendon repair is generally done. Tendon reconstruction is required in patients with severely disrupted or degenerative patellar tendons or in cases where primary repair cannot be performed. As the time from initial injury to surgical repair increases tendon excursion, adhesion, and degeneration increases. This can lead to a more complicated patellar tendon reconstruction. Hence, it is important to treat patellar tendon ruptures with a sense of urgency. The patellar tendon can be reconstructed using an autograft or an allograft. There are multiple surgical techniques for patellar tendon reconstruction (15,16).

Autograft and Allograft tissue options include the semitendinosus, gracilis,  ipsilateral or contralateral central quadriceps tendon-patellar bone and 

Achilles tendon with a bone block.

Differential Diagnosis

The differential diagnosis for patellar tendon rupture includes:

Patella fracture

Quadriceps tendon rupture

Tibial tubercle avulsion fracture

Prognosis

Generally, prompt repair of the patella tendon rupture has good to excellent outcomes. Failures, poor outcomes, and complications are typically associated with missed diagnosis and delayed treatment, or technical errors during surgery.

Complications

Complications associated with patellar tendon rupture include the following:

Quadriceps atrophy

Re-rupture

Residual extensor mechanism weakness

Residual extensor lag or inability to fully extend the knee

Knee stiffness

Postoperative and Rehabilitation Care

Following are the general guidelines for post-operative rehabilitation (17). 

In the first 2 weeks, the goal is to protect the surgical repair. Weight-bearing is allowed as tolerated with crutches and knee brace locked in full extension. The treating doctor determines ROM allowances based on the quality of repair.

During weeks 2 through 6, the goal continues to protect the surgical repair of the tendon and normalize gait with crutches and knee brace. Weight-bearing is allowed as tolerated with crutches and knee brace locked in full extension. Passive ROM from 0 to 90 degrees of knee flexion, with no active quadriceps extension is started. The treating doctor will determine ROM allowances based on the quality of the repair.

During weeks 6 through 12, the goal is to normalize gait on a flat surface and wean crutches. The knee brace is opened to allow flexion and active quadriceps contraction is started. Gradual progression of weight bearing with knee flexion is carried out. Weight-bearing in the knee flexed past 70 degrees is avoided. Active ROM of knee exercises are started. Light squats, leg presses, core strengthening, and other physical therapy exercises are carried out. 

During weeks 12 through 16, the goal is to normalize gait on all surfaces without a brace, obtain full ROM, start single-leg stance with good control, and squat to 70 degrees of flexion with good control. Non-impact balance and proprioceptive drills are begun. Physical therapy exercises, quad, and core strengthening exercises are begun.

During weeks 16 and longer the goal is to obtain good quad control with no pain with sport or work-specific movements, including impact activity.

When there is dynamic neuromuscular control with multiplane activities without pain or swelling the individual can return to sports.

Conclusion

Diagnosis and treatment of patellar tendon rupture are best performed with an interprofessional team that includes orthopaedic surgeons, therapists, and nurses. Doctors have to be aware that treatment of patellar tendon rupture depends on the integrity of the tendon. Complete patellar tendon ruptures involves surgical repair, as disability from a deficient knee extensor mechanism is high. The surgery is not a surgical emergency but prompt surgical treatment of acute patella tendon ruptures is recommended to prevent the need for reconstruction. Nonsurgical treatment is only indicated when the tendon tear is partial, and there is an intact knee extensor mechanism. Rehabilitation is recommended for all patients to regain joint function and muscle strength. The outlook in most patients is generally excellent.

References

1. Redler A, Proietti L, Mazza D, Koverech G, Vadala A, De Carli A, Ferretti A. Rupture of the Patellar Tendon After Platelet-Rich Plasma Treatment: A Case Report. Clin J Sport Med. 2020 Jan;30(1):e20-e22.

2. Alqasim E, Aljowder A, Alammari N, Joudeh AA. Total patellectomy with extensor mechanism reconstruction following pathological fracture due to patellar Ewing's sarcoma. BMJ Case Rep. 2018 Feb 07;2018.

3. LaPrade MD, Kallenbach SL, Aman ZS, Moatshe G, Storaci HW, Turnbull TL, Arendt EA, Chahla J, LaPrade RF. Biomechanical Evaluation of the Medial Stabilizers of the Patella. Am J Sports Med. 2018 Jun;46(7):1575-1582.

4. Dan MJ, McMahon J, Parr WCH, Broe D, Lucas P, Cross M, Walsh WR. Evaluation of Intrinsic Biomechanical Risk Factors in Patellar Tendinopathy: A Retrospective Radiographic Case-Control Series. Orthop J Sports Med. 2018 Dec;6(12):2325967118816038.

5. Pope JD, El Bitar Y, Mabrouk A, Plexousakis MP. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Apr 22, 2023. Quadriceps Tendon Rupture.

6. Yousef MAA. Combined avulsion fracture of the tibial tubercle and patellar tendon rupture in pediatric population: case series and review of literature. Eur J Orthop Surg Traumatol. 2018 Feb;28(2):317-323. 

7. Ali Yousef MA, Rosenfeld S. Acute traumatic rupture of the patellar tendon in pediatric population: Case series and review of the literature. Injury. 2017 Nov;48(11):2515-2521.

8. Camarda L, D'Arienzo A, Morello S, Guarneri M, Balistreri F, D'Arienzo M. Bilateral ruptures of the extensor mechanism of the knee: A systematic review. J Orthop. 2017 Dec;14(4):445-453. 

9. Behery OA, Feder OI, Beutel BG, Godfried DH. Combined Tibial Tubercle Fracture and Patellar Tendon Avulsion: Surgical Technique and Case Report. J Orthop Case Rep. 2018 May-Jun;8(3):18-22.

10. Chhapan J, Sankineani SR, Chiranjeevi T, Reddy MV, Reddy D, Gurava Reddy AV. Early quadriceps tendon rupture after primary total knee arthroplasty. Knee. 2018 Jan;25(1):192-194.

11. Morton S, Williams S, Valle X, Diaz-Cueli D, Malliaras P, Morrissey D. Patellar Tendinopathy and Potential Risk Factors: An International Database of Cases and Controls. Clin J Sport Med. 2017 Sep;27(5):468-474. 

12. Bhashyam AR, Weaver MJ. Knee pain after a fall. BMJ. 2018 Mar 22;360:k775.

13. Berlinberg A, Ashbeck EL, Roemer FW, Guermazi A, Hunter DJ, Westra J, Trost J, Kwoh CK. Diagnostic performance of knee physical exam and participant-reported symptoms for MRI-detected effusion-synovitis among participants with early or late stage knee osteoarthritis: data from the Osteoarthritis Initiative. Osteoarthritis Cartilage. 2019 Jan;27(1):80-89.

14. Courtney PM, Edmiston TA, Pflederer CT, Levine BR, Gerlinger TL. Is There Any Role for Direct Repair of Extensor Mechanism Disruption Following Total Knee Arthroplasty? J Arthroplasty. 2018 Jul;33(7S):S244-S248. 

15. Woodmass JM, Johnson JD, Wu IT, Krych AJ, Stuart MJ. Patellar Tendon Repair With Ipsilateral Semitendinosus Autograft Augmentation. Arthrosc Tech. 2017 Dec;6(6):e2177-e2181. 

16. Harato K, Kobayashi S, Udagawa K, Iwama Y, Masumoto K, Enomoto H, Niki Y. Surgical Technique to Bring Down the Patellar Height and to Reconstruct the Tendon for Chronic Patellar Tendon Rupture. Arthrosc Tech. 2017 Oct;6(5):e1897-e1901.

 

  The Incidence of Accessory Ossicles of the Wrist

                               Dr. KS Dhillon

In the wrist, there are more than 20 known accessory ossicles (1). Most of these accessory ossicles originate from unfused secondary ossification centers. They can be considered as developmental anomalies. These ossicles are generally asymptomatic and detected incidentally as radiological findings. They can rarely become symptomatic due to impingement, trauma, and other such causes. A more common problem in clinical practice is that accessory ossicles can be misinterpreted as avulsion fractures in patients with trauma, which can lead to overtreatment or the use of cross-sectional imaging modalities such as CT which can cause further radiation exposure. Hence it is important to know the localization, frequency, and distribution of accessory ossicles.

Although there are numerous studies on the distribution and incidence of accessory ossicles of the foot and ankle, the number of studies about the accessory ossicles of the wrist is limited (2,3). Most of the studies are case reports. There are only two studies with a large patient series (4,5,6,7). Both of these studies are considerably outdated (1932, 1953). They were performed using conventional radiography (8,9). There are no recent large patient series that investigated the distribution and incidence of accessory ossicles of the wrist using digital radiography.

In the literature, the incidence of accessory ossicles of the wrist varies.  O'Rahilly (9) conducted a study in 1953. He analyzed 743 plain radiographs. He reported that the incidence of accessory ossicles of the wrist was 1.6%.  Bogart (8) conducted a study with 1452 radiographs in 1932 and found that the incidence of accessory ossicles was 0.3%. These studies were performed when analog radiography was used. They are, therefore, considerably outdated. In another study by Gursoy et al (10), the incidence of accessory ossicles of the wrist was 9.7% among 1146 radiographs. The most important reason for the significant difference between the results of these studies is the technological advancements in radiography techniques. Better image quality in digital radiography as compared with conventional radiography has enhanced the visibility of accessory ossicles on radiographs. The studies were conducted with populations of different ethnic origins and this can be another reason for the difference between the reported incidence values. The number of existing studies are, however, not sufficient to determine if there is a difference between ethnic groups in terms of the accessory ossicles of the wrist. There are numerous studies on accessory ossicles of the foot and sesamoid bones of the hand conducted with different populations, reporting different incidences (2,3,11,12,13). 

The most common accessory ossicles are os triangulare and os ulnostyloideum. Both ossicles are present close to the ulnar styloid process. A clear distinction needs to be made since ulnar styloid process fractures, various ossifications, and dystrophic/heterotopic calcifications are also localized in this area.

These ossicles may be difficult to distinguish from a fractured ulnar styloid process. Accessory bones have well-defined, regular contours, whereas the contours of a fracture are irregular. Accessory bones have a cortex. Cortical continuation cannot be seen on at least one surface of a fracture. Bogart (8) in a study of 1452 plain radiographs found only two os triangulare (0.1%). Aydinlioglu et al (14) analyzed 388 plain radiographs to investigate the incidence of os ulnostyloideum. They found the incidence to be 2.5%.

The incidence of each accessory ossicle is not known. One of the accessory ossicles that is relatively common is the os styloideum. The clinical significance of os styloideum stems from its relationship with the carpal boss. Carpal boss is a painful lump on the dorsum of the wrist. Os styloideum is defined as a separate ossicle. It may have a fibrous connection with metacarpal bones or carpus. The carpal boss is defined as a bony protuberance, fused to the base of the 2nd and 3rd metacarpal bones. 

According to Lawson (15), the incidence of os styloideum in the normal wrist is in the range of 1.3 to 3%. Greditzer et al (16) conducted a study with 16 National Hockey League players. He found os styloideum in 13 of the players (81%). This incidence is markedly higher than the results of previous studies conducted with the general population. Although the etiology of os styloideum is not entirely clear, it is believed to be due to adaptive and reactive bone formation. 

The os centrale carpi is usually associated with other congenital anomalies such as Holt–Oram syndrome, hand-foot-uterus syndrome, etc. It is rarely an isolated finding (17).  A study by Gursoy et al (10) was the first to report an incidence of os centrale carpi, which was found in seven patients, leading to an incidence of 0.6%. Os centrale carpi can be confused with scaphoid fractures. It can cause pain due to osteonecrosis (4,18,19). 

Irregular and linear lucent areas that are superposed on the scaphoid waist due to os centrale carpi may make it challenging to distinguish between this ossicle and a transverse, ununited scaphoid fracture (4). An acute scaphoid fracture usually shows irregular or noncorticated sharp margins. An os centrale carpi generally has better-defined cortical margins. It is usually dense, round, and structureless. Old fractures usually exhibit demineralization and cyst formation. It is not always possible to differentiate between these fractures and os centrale carpi, especially in patients with no history of trauma. A CT scan is useful in such cases.

Os epilunatum is another rare ossicle. It was detected only in two patients (0.2%) in a study by Gursoy et al (10). In a patient series with 1452 radiographs Bogart (8) did not find an os epilunatum. 

According to Mauler et al (6), accessory ossicles constituted an important differential diagnosis in chronic wrist pain. They presented the first case that manifested with inflammatory changes and synovitis around the os epilunatum. Another important point to consider in patients complaining about pain due to os epilunatum is concomitant scapholunate ligament tears (6). It is therefore essential to examine the adjacent anatomical structures when an accessory ossicle is identified. This is especially so in patients who planned to undergo surgical excision.

There is no significant difference between the patients with and without accessory ossicles in terms of gender and side. The mean age is higher among patients who have accessory ossicles than those who do not have the same. 

A study by Sun et al (20), investigated the distribution patterns of sesamoid bones in metatarsophalangeal (MTP) joints. The number of sesamoid bones and the number of MTP joints with sesamoids had a positive correlation with age. They found that the number of sesamoid bones and affected joints increased with age. Ossification of accessory ossicles and sesamoids usually begins before the age of 20 years and continues throughout life. These bones become visible on radiographs once they are ossified. 

In conclusion, accessory ossicles of the wrist can be confounding. They can be confused with fractures in trauma patients and are frequently ignored in patients presenting with pain. The most common accessory ossicles in the wrist are os triangulare and os ulnostyloideum, and the incidence of accessory bones increases with age.

References

1. Freyschmidt J, Sternberg A, Brossmann J, Wiens J. 4th ed. New York, NY: Thieme Verlag; 1993. Köhler/Zimmer Borderlands of Normal and Early Pathologic Findings in Skeletal Radiography; pp. 79–93.

2. Coskun N, Yuksel M, Cevener M. Incidence of accessory ossicles and sesamoid bones in the feet: a radiographic study of the Turkish subjects. Surg Radiol Anat. 2009;31(01):19–24. doi: 10.1007/s00276-008-0383-9.

3. Koo B S, Song Y, Lee S, Sung Y K, Sung I H, Jun J B. Prevalence and distribution of sesamoid bones and accessory ossicles of the foot as determined by digital tomosynthesis. Clin Anat. 2017;30(08):1072–1076. doi: 10.1002/ca.22952.

4. Abascal F, Cerezal L, del Piñal F. Unilateral osteonecrosis in a patient with bilateral os centrale carpi: imaging findings. Skeletal Radiol. 2001;30(11):643–647. doi: 10.1007/s002560100423.

5. Karmazyn B, Siddiqui A R. Painful os styloideum in a child. Pediatr Radiol. 2002;32(05):370–372. doi: 10.1007/s00247-001-0639-6.

6. Mauler F, Rahm S, Schweizer A, Nagy L. Bilateral symptomatic os epilunatum: a case report. J Wrist Surg. 2015;4(01):68–70. doi: 10.1055/s-0034-1543978.

7. Nicolodi G C, Trippia C R, Caboclo M FFS, de Lima R R, Miller W P. Carpal boss syndrome: os styloideum fused to the trapezoid. Radiol Bras. 2017;50(03):200–201. doi: 10.1590/0100-3984.2015.0160.

8. Bogart F B. Variations of the bones of the wrist. AJR Am J Roentgenol. 1932;28:638–646.

9. O'Rahilly R. A survey of carpal and tarsal anomalies. J Bone Joint Surg Am. 1953;35-A(03):626–642.

10. Gursoy M, Coban I, Mete BD, Bulut T. The Incidence of Accessory Ossicles of the Wrist: A Radiographic Study. J Wrist Surg. 2021 Oct;10(5):458-464. doi: 10.1055/s-0041-1731386. Epub 2021 Jul 5. PMID: 34631299; PMCID: PMC8489987.

11. Amar E, Rozenblat Y, Chechik O. Sesamoid and accessory bones of the hand--an epidemiologic survey in a Mediterranean population. Clin Anat. 2011;24(02):183–187. doi: 10.1002/ca.21077.

12. Dharap A S, Al-Hashimi H, Kassab S, Abu-Hijleh M F. Incidence and ossification of sesamoid bones in the hands and feet: a radiographic study in an Arab population. Clin Anat. 2007;20(04):416–423. doi: 10.1002/ca.20378.

13. Lee J H, Kyung M G, Cho Y J, Go T W, Lee D Y. Prevalence of accessory bones and tarsal coalitions based on radiographic findings in a healthy, asymptomatic population. Clin Orthop Surg. 2020;12(02):245–251. doi: 10.4055/cios19123.

14. Aydinlioglu A, Ragbetli M C, Akpinar F, Tosun N, Dogan A. The accessory ulnar styloid process. Ulus Travma Acil Cerrahi Derg. 1998;4:53–57.

15. Lawson J P. International Skeletal Society Lecture in honor of Howard D. Dorfman. Clinically significant radiologic anatomic variants of the skeleton. AJR Am J Roentgenol. 1994;163(02):249–255. doi: 10.2214/ajr.163.2.8037009.

16. Greditzer H G, IV, Hutchinson I D, Geannette C S, Hotchkiss R N, Kelly B T, Potter H G. Prevalence of os styloideum in national hockey league players. Sports Health. 2017;9(05):469–473. doi: 10.1177/1941738117707914.

17. Poznanski A K, Holt J F. The carpals in congenital malformation syndromes. Am J Roentgenol Radium Ther Nucl Med. 1971;112(03):443–459. doi: 10.2214/ajr.112.3.443.

18. Lane L B, Gould E S, Stein P D, Coffey E. Unilateral osteonecrosis in a patient with bilateral os centrale carpi. J Hand Surg Am. 1990;15(05):751–754. doi: 10.1016/0363-5023(90)90150-p.

19. Yang Z Y, Gilula L A, Jonsson K. Os centrale carpi simulating a scaphoid waist fracture. J Hand Surg [Br] 1994;19(06):754–756. doi: 10.1016/0266-7681(94)90252-6.

20. Sun T, Zhao H, Wang L, Wu W, Hu W. Distribution patterns and coincidence of sesamoid bones at metatarsophalangeal joints. Surg Radiol Anat. 2017;39(04):427–432. doi: 10.1007/s00276-016-1759-x.