Bone Non Neoplastic

Last updated: 4/3/20 Prepared by Kurt Schaberg MD
Non-Neoplastic Bone & Joint Lesions

Infectious
Acute Osteomyelitis
aka Suppurative or Pyogenic osteomyelitis
Acute Inflammation with Bone Destruction
Necrotic bone with empty osteocyte lacunae.
May see brisk osteoclast activity.
Bone often appears “moth eaten” (irregular
erosions) with lots of “rat bites.”
Often caused by bacteria (usually Staph)
Can get from hematogenous spread (“primary,”
often in kids in metaphysis of long bones or adults Can also be from direct inoculation, often from
in spine). trauma or ulceration (“secondary,” often adults)
Chronic Osteomyelitis
Chronic Inflammation with Bone Destruction
Marrow replaced by fibrosis with plasma cells and lymphocytes
Often bone remodeling with osteoclasts and osteoblasts
Plasma cells are polytypic (mixture of kappa and lambda)!
Similar irregular rat/moth-eaten appearance
Often granulation tissue
Necrotizing granulomas→ consider Tuberculosis (“Pott’s
disease” in spine),
Can have sinus tract to surface line by squamous epithelium→
can turn into squamous cell carcinoma.
Septic Arthritis
Neutrophilic inflammation of synovium with accumulation of pus in joint space. Often clinical/lab Dx.
Caused by bacteria, often Staph (esp. S. epidermidis with prosthetic joints).
Leads to rapid cartilage destruction→ acute medical emergency that needs rapid treatment.
Periprosthetic Joint Infection

Can cause prosthetic loosening, requiring revision arthroplasty
If there is concern for infection, will often send joint capsule
for frozen section neutrophil count (cutoff often >5
neutrophils/single HPF in 5 separate HPFs, excluding surface
fibrin).
Be SURE it is PMN—lymphocytes can be twisty and mimic
PMNs. Treatment = prosthesis removal and subsequent
reimplantation after eradiation.
Also evaluated for clinically based on physical exam, culture,
ESR, CRP, and synovial fluid studies.
Degenerative/Reparative Changes
Degenerative Joint Disease Eburnated bone surface
(exposed, worn, smooth bone)
aka “DJD” or Osteoarthritis (“OA”)
Non-inflammatory loss joint cartilage,
subchondral bone sclerosis, periarticular bone Geode (bone cyst)
cysts (Geodes), osteophyte formation, and
synoviocyte hypertrophy/hyperplasia.
Common result of a variety of factors including
trauma, “wear and tear,” metabolic diseases,
avascular bone necrosis, and altered
loading/anatomy.
If treated surgically→ joint arthroplasty
Ganglion Cyst
Cysts composed of fibrous tissue without a lining.
Contain myxoid/mucous material.
Can be unilocular or multilocular.
Seems to arise from joint capsule.
Most often on wrists and hand/feet.
Most common in young adults.
Can surgically excise if bothersome.
Historically, could strike and rupture with a large heavy
book (e.g., a Bible)→ “Bible bump”
Fracture Callus
Reparative changes seen at a site of prior Granulation tissue
bone fracture and fibrosis
Immediately after fracture→ hemorrhage
and hematoma→ gradually replaced by
organization and granulation tissue
Woven bone, fibrosis, and cartilage with
ossification
Cartilage
Prominent osteoblastic rimming and
bone remodeling Bone
Fracture can be seen on imaging.
Should NOT see: atypical mitoses,

significant cytologic pleomorphism
Avascular Necrosis
Geographic area of subchondral bone
and marrow necrosis with partially
separated articular cartilage surface
(“crescent sign”).
Risk factors: Trauma, Steroids, Alcohol,

Chemotherapy, Collagen vascular
disease, Pregnancy, etc…
→ Leads to DJD/OA→ requires joint

replacement
Marrow & Bone Necrosis
Aseptic Joint Loosening

Foreign material wear particles (fragments of
prosthetic that have broken off: metal,
polyethylene glycol, cement, ceramic, etc..) are
ingested by macrophages→ causes
inflammation around joint → Osteolysis →
Joint loosening
Abundant foamy histiocytes, Foreign body
giant cells, and inorganic particles.
Wear particles from metal articular surfaces
are small and appear black. Accumulate in
macrophages and fibrous tissue→ “Metallosis”
Metal can even make its way to regional lymph

nodes!
Aseptic Lymphocytic Vasculitis-associated

Lesion (AVAL)
Seen with metal-on-metal articulations.
Despite name, no true vasculitis.
Three defining features:
1) Prominent lymphoid aggregates, often near
venules
2) Absence of obvious metal debris
3) Necrosis of synovium
Loose Bodies
Loose fragments of tissue found free within the joint space
Can result from trauma, DJD, or neoplasm.
Most common in knee→ cause locking and pain
Fibrinous Loose bodies (“Rice Bodies”)
Consist of laminated fibrin. Grossly resemble rice grains.
Osteochondral or Cartilaginous Loose bodies
Detached fragments of articular cartilage ± bone.
Result from trauma. Often solitary.
Synovial Chondromatosis
Locally aggressive neoplasm. Multiple hyaline cartilage nodules within
synovium or loose in joint space. Chondrocytes cluster together in groups.
FN1-ACVR2A fusions.
Autoimmune Diseases
Rheumatoid Arthritis
Most common primary inflammatory arthropathy.
Chronic, idiopathic erosive symmetric polyarthropathy.
Impacts all joints, but worst impacted are small joints of
hands (MCP & PIP), feet, and C-spine.
Many extra-articular manifestations (e.g., Lung disease)
Serology: Positive Rheumatoid Factor (RF)
Chronic Synovitis:
Expands synovium with chronic inflammation
(lymphocytes and plasma cells), often with lymphoid
aggregates.
Often reactive/hyperplastic synovium with surface
fibrin/fibrinoid necrosis and granulation tissue.
May erode nearby bone.
Sometimes occasional neutrophils.
Pannus
Synovium that erodes cartilage and other joint
structures→ characteristic marginal erosions of bone on
X-ray.
Rheumatoid nodule:
Necrotizing granulomas with central necrobiosis
DDX for nodule: Granuloma annulare, infection, and
epithelioid sarcoma (CK+, INI1 loss)
Crystalline Diseases Modified from a presentation by Scott Kilpatrick, Cleveland Clinic, USCAP 2021
Gout Pseudogout Tumoral calcinosis

Age 30-50 yrs (middle age) >50 yrs (older) 10-40yrs (young)
Site 1st MTP Knee Shoulder, Hips
Crystal Shape Needle Rhomboid Irregular gritty plates
Type Uric acid Calcium pyrophosphate Calcium hydroxyapatite
Polarizable + + -
Seen on H&E - + +
Inflammatory reaction + - +
Gout
Uric acid metabolic disorder→ hyperuricemia→ deposit
monosodium urate crystals in joint fluid and tissues
Classically middle-aged males
Most common joint: 1st MTP, but can get anywhere
Uric acid dissolves in water during staining process (so often not
seen well on H&E slides), but can be seen on fresh touch preps or
unstained slides→ “needle-shaped” yellow, negatively
birefringent crystals. Joint fluid often neutrophil-rich.
On H&E: See fluffy pink deposits with associated granulomatous
inflammation and giant cells. Soft tissue deposits = “Tophi”
Pseudogout
Calcium Pyrophosphate Dihydrate (CPPD) deposits in
cartilage and joint soft tissue.
Appear as rhomboidal purple positively birefringent
crystals. On H&E: well-demarcated basophilic material
with virtually no inflammatory response
Often associated with degenerative joint disease.
Often incidental finding in arthroplasty finding.
Tumoral Calcinosis
Calcium hydroxyapatite deposits
Common locations: shoulder, sites of pressure
Can be localized in relation to trauma or due to a systemic
disorder (e.g., renal failure or hyperphosphatemia)
Lobules of apatite-type calcifications surrounded by chronic
inflammation with a prominent foreign body giant cell
reaction
Metabolic/Endocrine/Idiopathic
Paget Disease
Localized disorder of bone remodeling characterized
by focal areas of increased turnover with excess
bone synthesis and resorption.
Often localized to a single bone in elderly men.
Early → more resorptive; Late → more synthesis.
Unusually large osteoclasts with increased nuclei and
prominent nucleoli.
Prominent osteoblastic rimming.
Paratrabecular marrow fibrosis.
Unusually thick and thin bone trabeculae
Numerous irregular reversal cement lines and bone
scalloping. Mosaic pattern.
Etiology poorly understood
Increased risk of osteosarcoma
Brown Tumor of Hyperparathyroidism

Forms a mass lesion.
Most common in Mandible and Maxilla.
Hyperparathyroidism (often due to adenoma) →
stimulates a proliferation of osteoclasts with fibrous tissue
and hemorrhage (resembles many other giant cell-rich
lesions, like reparative granuloma), so knowing PTH is key.
Treat with parathyroidectomy.
Also can see generalized bone changes with cortical bone loss → osteitis fibrosa cystica
Osteoporosis Decrease in mass of mineralized bone→ increased risk of fracture.
Frequent in postmenopausal women (due to estrogen loss) and with general aging. Can also be secondary
to a variety of conditions (e.g., hyperparathyroidism, malnutrition) and medications (esp. Steroids).
Renal Osteodystrophy
Seen in setting of chronic renal failure.
Increased osteoclast activity→
osteoporosis
With renal failure→ hyperphosphatemia →
secondary hyperparathyroidism →
increased osteoclast activity
Also, Vit D deficiency → Hypocalcemia

Bone Non Neoplastic

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Last updated: 4/3/20 Prepared by Kurt Schaberg MD

Non-Neoplastic Bone & Joint Lesions

Periprosthetic Joint Infection

If treated surgically→ joint arthroplasty

Should NOT see: atypical mitoses,

Risk factors: Trauma, Steroids, Alcohol,

→ Leads to DJD/OA→ requires joint

Marrow & Bone Necrosis

Aseptic Joint Loosening

Metal can even make its way to regional lymph

Aseptic Lymphocytic Vasculitis-associated

Gout Pseudogout Tumoral calcinosis

Site 1st MTP Knee Shoulder, Hips

Crystal Shape Needle Rhomboid Irregular gritty plates

Type Uric acid Calcium pyrophosphate Calcium hydroxyapatite

Brown Tumor of Hyperparathyroidism

Osteoporosis Decrease in mass of mineralized bone→ increased risk of fracture.

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