An unfused cervical neural arch (MCF-PVPH 108–90) preserves a single pathological cavity on the posterolateral margin of the right prezygapophyseal facet (Fig. 1H,I). The lesion is tear-drop shaped (20×9 mm), tapering posteriorly, and up to 6 mm deep. Perilesional growth is absent and the edges are rounded. The erosion is localized and does not encroach onto the articular surface of the prezygapophysis. Rheumatoid arthritis presents as periarticular erosions with smooth inner walls and rounded edges similar to that in MCF-PVPH 108–90. New bone growth is notably absent. However, rheumatoid arthritis does not affect the zygapophyses in human subjects [9]. Infection can cause osseous erosions; however, this is usually accompanied by exuberant bone growth, which is absent in MCF-PVPH 108–90. Some forms of bacterial infection, such as tuberculosis, produce erosions with minimal new bone formation [9], [10] and, unlike rheumatoid arthritis, can affect the zygapophyses. Because tuberculosis and other infections are named for a specific bacterium (e.g. Mycobacterium tuberculosis), we refrain from giving MCF-PVPH 108–90 a more specific diagnosis and simplify classify the lesion as infectious.

MCF-PVPH 108–175 is an incomplete right dorsal rib that lacks both the head and the distal half of the element. The rib shaft is weakly expanded (overtubulated) along its medial edge approximately 10 cm from the proximal end of the bone (Fig. 1A). The expanded region is approximately 3 cm long and grades imperceptibly into the surrounding unaffected bone. The surface of the affected area also preserves an irregular-walled (i.e. not smooth), oblong lesion that does not appear to have exposed the deeper trabecular bone. The lesion measures approximately 27 mm long and 9 mm wide (Fig. 1C). Slight overtubulation of the rib is indicative of a well-healed fracture (trauma) and the presence of an erosive lesion may be indicative of secondary suppurative (pus forming) osteomyelitis.

A second incomplete dorsal rib of uncertain position (MCF-PVPH 108–220) exhibits substantial overtubulation of the shaft (Fig. 1B,D). The rib is lacking both proximal and distal ends and appears to have broken (postmortem) part way through the pathologic region. The affected area is an elongate bulge and, as preserved, measures more than 7 cm in maximal length (Fig. 1D). This bulge is restricted to one edge (?medial) of the element and grades smoothly into the surrounding unaffected bone. The bone surface along the expanded area does not differ significantly from the surrounding unaffected parts of the element; however, there is a faint interfingering of bony spicules that meander across the surface of the lesion roughly perpendicular to the long axis of the element. The smooth texture, overtubulation, and interfingering of bone is characteristic of an incomplete but well-healed fracture.

MCF-PVPH 108–181 is a partial right ilium comprising the ventral part of the body including the anterior part of the acetabulum, ischiadic peduncle, and the proximal segment of the postacetabular process (Fig. 2). Five erosional lesions are preserved on the ventrolateral surface of the ilium in the vicinity of the acetabulum and brevis shelf. All are deep (up to and exceeding 10 mm in depth), elliptical in outline, and penetrate obliquely into the bone. Because lesions penetrate at an angle to the bone surface, the margin is often marked by a sharp ‘lip’. Lesions are of variable size ranging from 8 mm to 50 mm in maximum dimension. Perilesional bone growth is absent. The internal surfaces of the cavities are smooth and do not reveal trabecular bone (Fig. 2B–D).

The ilium of Mapusaurus is highly pneumatic¹ and it is possible that one or two of these fenestrae are in fact continuous with the pneumatic diverticulae. Coria and Currie [1] also noted the presence of the pits within the margins of the brevis fossa in MCF-PVPH 108–181 and a second specimen from the bonebed (MCF-PVPH 108–245) suggesting they may be connected to the lateral caudofemoralis musculature. However, the location of the other lesions in MCF-PVPH 108–181 suggest they are pathological in origin.

Smooth-walled erosions similar to those in MCF-PVPH 108–181 may form as a result of osteomyelitis, fungal disease, bone tumors, or cancer. Pus-draining sinuses that form as a result of infection (osteomyelitis) are typically accompanied by periosteal reaction and rapidly-formed new bone. The latter is characterized by disorganized bone texture. Fungal diseases (such as coccidioidomycosis and blastomycosis) can also produce erosions; however, these are accompanied by short, blunt spicules of new bone (osteophytes) and periosteal reaction [10]. The absence of reactive bone and periosteal reaction in MCF-PVPH 108–181 argues against either fungal disease or osteomyelitis as a possible diagnosis. Several types of malignant tumors (cancer) produce lesions similar to those seen in MCF-PVPH 108–181. Lesions associated with eosinophilic granuloma are predominantly localized in human subjects to the vertebrae and pelvis where they occur as ‘space occupying masses’ with little reactive bone growth [11]. The lesions have effaced (indistinct) trabeculae and periosteal reaction is variably absent. Myeloma produces sharply-defined, spheroid erosions with smooth borders and effaced trabeculae [12]. Lesions are variable in size and secondary bone formation and periosteal reaction does not occur. When cancer spreads to a secondary location (metastatic cancer), it often produces multiple holes of variable size [11]. These lesions are elliptical with loss of trabecular bone and periosteal reaction is usually absent [12]. Metastatic cancer and myeloma both produce lesions that coalesce. Total absence of remodeling in myeloma distinguishes it from metastatic cancer [12]. Hematologic cancer (leukemia) produces large numbers of small (up to several millimetres in diameter), smooth-walled lesions [13]. The similarity of perforative lesions in MCF-PVPH 108–181 to tumor-related neoplasia suggests a possible etiology for such abnormalities in Mapusaurus; however, bone cysts, parasitic infection, or some other unidentified disease process cannot be ruled out. Therefore the exact etiology is unknown and the lesions are diagnosed as anomalous.

A single pedal phalanx III-1 (MCF-PVPH 108–23) bears a number of erosive lesions on the proximal articular surface and the dorsal margin of the distal articular surface (Fig. 1E–G). Because of the symmetry of this element, it was not possible to identify whether MCF-PVPH 108–23 is from the left or the right pes. The entire surface of the proximal articular surface is uneven and pockmarked with erosive lesions giving it an overall disorganized appearance. Disruption of the bone surface is limited to the articular surface and reactive bone growth is altogether absent. The largest erosive features are several centimeters long with irregular walls up to 5 mm deep. The interior of the deepest cavities reveals trabecular bone with a unique ‘stringy’ texture owing to the parallel orientation of the trabeculae (Fig. 1G). A circular erosion also occurs on the dorsal margin of the distal articular surface (Fig. 1F). Some marginal thickening (sclerosis) of the periosteum is present.

Articular surface irregularities may be cause by a variety of disorders including osteochondrosis, osteoarthritis, rheumatoid arthritis, avascular necrosis ( = osteochondritis desiccans, osteochondrosis desiccans, osteonecrosis), and also infection. In osteochondrosis, the resulting lesions are smooth-walled with sharply-delimited margins [14] contrasting with the overall disorganized texture of the articular surface in MCF-PVPH 108–23. Osteoarthritis is linked to disruption of the cartilaginous lining of the joint and is non-erosive. Osteophyte formation around the periphery of the joint, characteristic of osteoarthritis, is absent in MCF-PVPH 108–23. Rheumatoid arthritis (an erosive form of arthritis) also produces similar erosions to those in MCF-PVPH 108–23. Erosions are polyarticular in distribution and occur at the margin of the joint capsule. Compromised blood supply to the bone leads to the death and subsequent loss of bony tissue in avascular necrosis [15], [16]. Structural weakening leads to the collapse of the articular surface (focal subsidence) resulting in broad depressions and an overall uneven bone surface areas that lacks restorative bone growth similar to the erosions in MCF-PVPH 108–23. Joint infection can cause the loss of bone as a result of inflammation and decreased blood flow, which is accompanied by rapid formation of new bone that has a fibrous, disorganized texture. Pyogenic (pus-generating) infection also results in the formation of pus-draining sinus tracts (cloacae). Exuberant reactive bone growth and cloacae are absent in MCF-PVPH 108–23. Conversely, non-pyogenic forms of bacterial infection (e.g. tuberculosis), can result in marginal erosions with minimal or no reactive bone formation. Lesions form at the margin of the join capsule and invade the underlying subchondral bone. Minor reactive bone is present around the periphery of lesions [10], similar to MCF-PVPH 108–23. Lesions in MCF-PVPH 108–23 are therefore diagnosed as infectious.